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1: Tumour Biol 2000 Nov-Dec;21(6):328-36

Changes in serum and tissue zinc levels in sex hormone-induced prostatic carcinogenesis in the noble rat.

Wong YC, Wang YZ, Lee JS, Tam NN, Lee D

Department of Anatomy, Faculty of Medicine, University of Hong Kong, SAR, People's Republic of China. Diese E-Mail-Adresse ist vor Spambots geschützt! Zur Anzeige muss JavaScript eingeschaltet sein!

We investigated the changes in serum and tissue zinc levels in the Noble rat prostate gland under different pathological conditions induced by the administration of a combination of testosterone and 17beta-estradiol. The results showed that there were significant differences in serum zinc values between normal and hormone-treated rats with prostatic hyperplasia, dysplasia and prostatic carcinoma (p < 0.05), although there was no significant difference among rats with different forms of prostatic lesions (i.e. hyperplasia, dysplasia and prostatic adenocarcinoma). There was also a difference in zinc content between the lateral prostate (LP), ventral prostate (VP) and dorsal prostate (DP) in normal rats. The zinc levels of LP were several times greater than those of either VP or DP (p < 0.01). There was also a great difference in zinc levels between the normal and the hyperplastic/dysplastic and carcinomatous LP and VP (p < 0. 05). The levels of zinc in both LP and VP were increased in hyperplasia/dysplasia and carcinoma. On the other hand, the zinc levels of LP were much higher than those of VP in hyperplasia/dysplasia and carcinoma (p < 0.01), which may be correlated with the incidence of prostate cancers in these lobes (i. e. higher in LP and much lower in VP). In contrast, in DP, the levels of zinc were not affected, which may be correlated with the very low incidence of carcinoma in this lobe. Our data suggest that the difference in zinc levels among these lobes reflect the heterogeneity in zinc content in various lobes of the rat prostate. The growth and development of prostatic lesions in LP and VP may be positively correlated with the significant increase in tissue zinc levels in these lobes. On the other hand, the lack of response of DP to carcinogenesis may be due to its relatively stable low zinc levels. It is suggested that tissue zinc content may be used as a marker for prostatic lesions, including hyperplasia, dysplasia and carcinoma, while serum zinc levels may be a useful indicator for abnormal prostatic growth. Copyright 2000 S. Karger AG, Basel.

PMID: 11006573, UI: 20463396

1: Carcinogenesis 2000 Oct;21(10):1809-12

Proliferative potential in nasopharyngeal carcinoma: correlations with metallothionein expression and tissue zinc levels.

Jayasurya A, Bay BH, Yap WM, Tan NG, Tan BK

Anatomy Department and Pharmacology Department, National University of Singapore, Kent Ridge, S119260, Pathology Department, Tan Tock Seng Hospital, Moulmein Road, S308433, Otolaryngology Department, Singapore General Hospital, Outram Road, S1696.

[Medline record in process]

Metallothionein (MT) is a cysteine-rich protein with pleiotropic functions and a high binding affinity for heavy metals. The present study was designed to examine the relationship between MT expression and tissue zinc levels in conjunction with cell proliferation in nasopharyngeal cancer (NPC). Proliferative activity in NPC was quantified by Ki67 immunolabelling and MT expression was determined by immunohistochemistry. Total zinc and subcellular zinc fractions were analysed by flame atomic absorption spectrometry. MT immunostaining was observed in the nuclei of NPC cells, with the percentage MT immunopositivity ranging from 3.0 to 59.7%. Thirteen tumours displayed weak MT staining and the remaining 11 showed moderate to strong immunostaining. There was a significant positive correlation between MT and Ki67 positivity (P: = 0.0127). Tissue zinc levels were higher in NPC as compared with benign nasopharyngeal tissues (4.800 +/- 0.4610 versus 2.889 +/- 0.4045 &mgr;g/g dry wt tissue, respectively; P: = 0.0122). Nuclear zinc levels in NPC were significantly higher than levels in membrane and cytosolic fractions (mean zinc levels 1.4840 +/- 0.1489, 0.6286 +/- 0.0789 and 0.3014 +/- 0.0250 &mgr;g/mg protein, respectively). A linear relationship was also observed between nuclear zinc levels and MT immunostaining (P: = 0.0024) as well as with Ki67 immunopositivity (P: = 0.0123). Our results show that MT and zinc are correlated with proliferative activity in NPC, providing further insights into the biology of this enigmatic and aggressive tumour.

PMID: 11023537, UI: 20477921

1: Int Clin Psychopharmacol 2000 Jul;15 Suppl 1:S19-24

Clinical experience with paroxetine in social anxiety disorder.

Baldwin DS

Department of Mental Health, University of Southampton, UK. Diese E-Mail-Adresse ist vor Spambots geschützt! Zur Anzeige muss JavaScript eingeschaltet sein!

[Medline record in process]

Paroxetine is a selective serotonin reuptake inhibitor (SSRI) with proven efficacy in the treatment of depression, panic disorder and obsessive-compulsive disorder. Evidence that paroxetine may be effective in social anxiety disorder (social phobia) first arose from open-label studies. More recently, three multicentre, randomized, placebo-controlled trials have been performed, each lasting 12 weeks, to assess the efficacy and tolerability of paroxetine in the treatment of social anxiety disorder, and these studies are reviewed here. The data from all three studies consistently demonstrated that paroxetine was effective in reducing both the symptoms of anxiety and the disability and impairment of social anxiety disorder. Paroxetine performed significantly better than placebo on all primary (Liebowitz Social Anxiety Scale, Clinical Global Impression) and secondary (Social Avoidance and Distress Scale, Sheehan Disability Scale) outcome measures. Adverse events were restricted to those already known to be associated with SSRIs, no serious adverse events associated with medication were experienced, and the numbers withdrawing from the studies were not significantly different in the paroxetine and control groups. Taken together, these studies confirm that paroxetine is an effective and well tolerated treatment for patients with social anxiety disorder.

PMID: 10994679, UI: 20448135

1: Acta Psychiatr Scand Suppl 2000;403:57-61

Antidepressant use patterns in clinical practices: comparisons among tricyclic antidepressants and selective serotonin reuptake inhibitors.

Donoghue J

School of Pharmacy and Chemistry, Liverpool John Moores University, UK.

[Medline record in process]

OBJECTIVE: Antidepressant use in clinical practice may differ from that in randomized controlled trials due to the complex interaction between patients, prescribers and the health-care system.

METHOD: A review of studies using data from actual clinical practice has found consistent differences in the prescribing patterns of tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs).

RESULTS: Patients who initiate therapy on SSRIs are more likely to complete a course of adequate dose and duration of antidepressant therapy than patients who initiate therapy on a TCA. Differences in prescribing patterns have also emerged among the most common SSRIs, fluoxetine, sertraline and paroxetine, that are also consistent over time, settings and countries.

CONCLUSION: Given that the drugs studied are one constant across all the studies, the antidepressants' underlying pharmacological differences in tolerability and other properties may provide an explanation for differences in prescribing patterns.

PMID: 11019936, UI: 20470615

1: Izv Akad Nauk SSSR Biol 1969 Nov-Dec;6:887-92

[New type of EPR signal in tumor tissues].

[Article in Russian]

Saprin AN, Kozlova LE, Shabalkin VA, Krugliakova KE, Emanuel' NM

PMID: 4317685, UI: 70257927

1: Vopr Onkol 1967;13(9):108-12

[Free radicals in the tissue of sarcomas].

[Article in Russian]

Petiaev MM, Reznikov SA, Cherepneva IE, Siusina TG, Tereshchenko TV

Publication Types: Review

PMID: 4300278, UI: 68410862

1: Health Phys 2000 Sep;79(3):257-65

90Sr and 137Cs in environmental samples from Dolon near the Semipalatinsk Nuclear Test Site.

Gastberger M, Steinhausler F, Gerzabek MH, Hubmer A, Lettner H

Institute of Physics and Biophysics, University of Salzburg, Austria. Diese E-Mail-Adresse ist vor Spambots geschützt! Zur Anzeige muss JavaScript eingeschaltet sein!

The (90)Sr and (137)Cs activities of soil, plant, and milk samples from the village of Dolon, located close to the Semipalatinsk Nuclear Test Site in Kazakhstan, were determined. The areal deposition at the nine sampling sites is in the range of <500 to 6,100 Bq m(-2) and 300 to 7,900 Bq m-2 for (90)Sr and (137)Cs, respectively. Similar values have been reported in the literature. At some of the sites both nuclides mainly have remained in the top 6 cm of the soil profiles; at others they were partly transported into deeper soil layers since the deposition. For most of the samples the (90)Sr yield after destruction of the soil matrix is significantly higher than after extracting with 6 M HCl indicating that (90)Sr is partly associated with fused silicates. The low mean (90)Sr activity concentrations of vegetation samples (14 Bq kg(-1) dw) and milk samples (0.05 Bq kg(-1) fw) suggest that this has favorable consequences in terms of limiting its bioavailability.

PMID: 10949250, UI: 20403526

1: Anticancer Res 2000 Mar-Apr;20(2B):1109-14

89Strontium in the management of painful sceletal metastases.

Kalkner KM, Westlin JE, Strang P

Department of Oncology, University of Uppsala, Sweden. Diese E-Mail-Adresse ist vor Spambots geschützt! Zur Anzeige muss JavaScript eingeschaltet sein!

PURPOSE: To make a review of the literature of 89strontium-chloride and a retrospective study of time to palliative intended external irradiation, number of portals and overall-survival after 89strontium-chloride therapy.

RESULTS: In total 93 patients were treated 116 times with 89strontium. The patients with prostatic carcinoma received 91% of all 89strontium therapies. Median over-all survival was 10 months after injection. In those cases when 89strontium was given before palliative radiotherapy, the average of total number of local fields was significantly lower (1.1 versus 4.1) compared to those cases where local fields preceded 89strontium therapy. However, time to 89new external irradiation after 89strontium injection was equal between these groups (3.8 versus 2.9 months).

CONCLUSION: A review of literature conclude that 89strontium is effective for the reduction of pain originating from osteoblastic metastases. It also reduce the need for external radiotherapy and therefore is cost-effective. However, 89strontium is more effective in an early phase of the metastatic disease and preferably as an adjuvance to external radiotherapy.

Publication Types: Review  
Review, tutorial

PMID: 10810404, UI: 20270701

1: Semin Radiat Oncol 2000 Apr;10(2):103-14

Use of radionuclides for the palliation of bone metastases.

McEwan AJ

Department of Oncology, University of Alberta, Edmonton, Alberta, Canada.

Pain palliation with bone-seeking radiopharmaceuticals is an effective and cost-effective management tool in patients with advanced cancer metastatic to bone. Strontium-89 ((89)Sr) (Metastron) and samarium-153 ((153)Sm) EDTMP (Lexidronam) are licensed for use in patients in the United States. Patients with a positive bone scan using technetium 99m methylene diphosphonate ((99m)Tc MDP) are eligible for treatment, and indications and contraindications for use are now well defined. The evidence in the literature now suggests that the radiopharmaceuticals can significantly reduce pain and analgesic requirements, can improve quality of life, can reduce lifetime radiotherapy requirements and management costs, and may slow the progression of painful metastatic lesions. Retreatment is safe and effective. Rhenium-186 ((186)Re) HEDP and Tin-117m diethylenetriaminepenta-acetic acid (DTPA) are in phase II/III trials to evaluate efficacy and compare efficacy with the licensed agents. Phosphorus-32 ((32)P) has been reassessed in two trials evaluating efficacy in comparison with (89)Sr and safety. Toxicity is reversible myelosuppression, which may be significant, and the treatments should not be given to patients with suspected disseminated intravascular coagulation.

Publication Types: Review  
Review, tutorial

PMID: 10727599, UI: 20194042

1: Arch Biochem Biophys 2000 Apr 15;376(2):377-88

Prooxidants open both the mitochondrial permeability transition pore and a low-conductance channel in the inner mitochondrial membrane.

Kushnareva YE, Sokolove PM

Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.

Mitochondria can be induced by a variety of agents/conditions to undergo a permeability transition (MPT), which nonselectively increases the permeability of the inner membrane (i.m.) to small (<1500 Da) solutes. Prooxidants are generally considered to trigger the MPT, but some investigators suggest instead that prooxidants open a Ca(2+)-selective channel in the inner mitochondrial membrane and that the opening of this channel, when coupled with Ca(2+) cycling mediated by the Ca(2+) uniporter, leads ultimately to the observed increase in mitochondrial permeability [see, e.g., Schlegel et al. (1992) Biochem. J. 285, 65]. S. A. Novgorodov and T. I. Gudz [J. Bioenerg. Biomembr. (1996) 28, 139] propose that the i.m. contains a pore that, upon exposure to prooxidants, can open to two states, one of which conducts only H(+) and one of which is the classic MPT pore. Given the current interest in increased mitochondrial permeability as a factor in apoptotic cell death, it is important to determine whether i.m. permeability is regulated in one or multiple ways and, in the latter event, to characterize each regulatory mechanism in detail. This study examined the effects of the prooxidants diamide and t-butylhydroperoxide (t-BuOOH) on the permeability of isolated rat liver mitochondria. Under the experimental conditions used, t-BuOOH induced mitochondrial swelling only in the presence of exogenous Ca(2+) (>2 &mgr;M), whereas diamide was effective in its absence. In the absence of exogenous inorganic phosphate (P(i)), (1) both prooxidants caused a collapse of the membrane potential (DeltaPsi) that preceded the onset of mitochondrial swelling; (2) cyclosporin A eliminated the swelling induced by diamide and dramatically slowed that elicited by t-BuOOH, without altering prooxidant-induced depolarization; (3) collapse of DeltaPsi was associated with Ca(2+) efflux but not with efflux of glutathione; (4) neither Ca(2+) efflux nor DeltaPsi collapse was sensitive to ruthenium red; (5) collapse of DeltaPsi was accompanied by an increase in matrix pH; no stimulation of respiration was observed; (6) Sr(2+) was able to substitute for Ca(2+) in supporting t-BuOOH-induced i.m. depolarization, but not swelling; (7) in addition to being insensitive to CsA, the collapse of DeltaPsi was also resistant to trifluoperazine, spermine, and Mg(2+), all of which block the MPT; and (8) DeltaPsi was restored (and its collapse was inhibited) upon addition of dithiothreitol, ADP, ATP or EGTA. We suggest that these results indicate that prooxidants open two channels in the i.m.: the classic MPT and a low-conductance channel with clearly distinct properties. Opening of the low-conductance channel requires sulfhydryl group oxidation and the presence of a divalent cation; both Ca(2+) and Sr(2+) are effective. The channel permits the passage of cations, including Ca(2+), but not of protons. It is insensitive to inhibitors of the classic MPT. Copyright 2000 Academic Press.

PMID: 10775426, UI: 20239639

1: Wei Sheng Yen Chiu 1997 May;26(3):172-8

[The effects of strontium in drinking water on growth and development of rat bone].

[Article in Chinese]

Xu F, Zhang X, Liu J, Fan M

Institute of Environmental Health Monitoring, Chinese Academy of Preventive Medicine, Beijing, China.

Effects of strontium at a high level in drinking water on growth and development of rat bone were studied. The results showed that Sr2+ concentration from 5 to 500 mg/L in drinking water could increase the contents of strontium in blood serum, urine, femur, mixilla and tooth in Wistar rats exposed to Sr2+ for 12 weeks with an obvious dose-response relationship. In addition, strontium at over 50 mg/L could decrease the contents of calcium in bone, increase the contents of calcium in tooth and bone density, and decrease the levels of calcium in blood serum except female rats at the 12th week. Effects of Sr2+ on body weight, body length, AKP activity of serum, calcium content of urine and breaking load of bended femur for rats were not found. However, there are differences in the effects of strontium on growth and development of bone between male and female rats. At the 12th week the content of calcium in blood serum decreased in male rats but increased in female rats in exposed groups. At the 4th and 8th weeks, urine Hop/Cr in male rats increased but it remained normal level in female rats. Sr2+ increased the bone density of mixilla in male rats but it did not increase that of femur in female rats. It is suggested that such changes may be a result of the differences in endocritic regulation and metabolic process between two sexes.

PMID: 10325628, UI: 99256385

1: Kidney Int 2000 Mar;57(3):1107-14

Increased bone strontium levels in hemodialysis patients with osteomalacia.

D'Haese PC, Schrooten I, Goodman WG, Cabrera WE, Lamberts LV, Elseviers MM, Couttenye MM, De Broe ME

Department of Nephrology-Hypertension, University of Antwerp, P/a University Hospital Antwerp, Edegem, Belgium. Diese E-Mail-Adresse ist vor Spambots geschützt! Zur Anzeige muss JavaScript eingeschaltet sein!

BACKGROUND: In this study, we report on the association between increased bone strontium levels and the presence of osteomalacia in end-stage renal failure patients treated by hemodialysis.

METHODS: We performed a histologic examination and determined the strontium content and strontium/calcium ratios in bone biopsies of 100 hemodialysis patients recruited from various centers all over the world. Aside from the bone strontium concentration, the bone aluminum content was assessed. The bone zinc concentration, a nonrelevant element for bone toxicity, was also measured.

RESULTS: Bone strontium levels and bone strontium/calcium ratios were increased in subjects with osteomalacia when compared with those with the other types of renal osteodystrophy. Bone strontium and bone calcium levels correlated with each other. The slope of the linear regression curve correlating these parameters was much steeper in the osteomalacic group (Y = 2.22X - 120) as compared with the other types of renal osteodystrophy (Y = 0.52X - 5.7). Within the group of patients with osteomalacia, bone strontium levels also significantly correlated with the bone aluminum content (r = 0.72, P = 0.018). No such correlation was found for the other types of renal osteodystrophy. The bone zinc concentration of subjects with normal renal function did not differ significantly from the values noted for the various types of renal osteodystrophy taken as separate groups, nor could increased bone zinc concentrations be associated with a particular bone lesion.

CONCLUSIONS: Our data demonstrate an association between osteomalacia and increased bone strontium concentrations in dialysis patients. Further studies are warranted to establish whether strontium plays either a primary, secondary, or contributive role in the development of the latter type of renal osteodystrophy.

PMID: 10720963, UI: 20188752

1: Tohoku J Exp Med 1999 Jul;188(3):217-25

Trace element levels in drinking water and the incidence of colorectal cancer.

Kikuchi H, Iwane S, Munakata A, Tamura K, Nakaji S, Sugawara K

The First Department of Internal Medicine, Hirosaki University School of Medicine, Japan.

We determined the levels of 15 elements in drinking water from 34 water treatment plants in Aomori Prefecture and studied how element levels relate to colorectal cancer incidence by district. Colorectal cancer incidence was calculated from the data of Aomori Colorectal Cancer Registry. Multiple regression analysis was performed by using age-adjusted incidences of rectal cancer and colon cancer by gender as object variables and each element level as an explanatory variable. The standardized partial regression coefficient was significant in gold (p < 0.01), magnesium (p < 0.01), selenium (p < 0.01) and tin (p < 0.05) for age-adjusted rectal cancer incidence in men as objective variable; in gold (p < 0.05), calcium (p < 0.01) and phosphorus (p < 0.01) with age-adjusted colon cancer incidence in men as the objective variable; and in sodium (p < 0.05), phosphorus (p < 0.05), tin (p < 0.05) and strontium (p < 0.01) with age-adjusted colon cancer incidence in women as the objective variable. These results confirm the need to further study trace elements in drinking water and food, and relationship to colorectal carcinogenesis.

PMID: 10587013, UI: 20052296

1: J Neurol Neurosurg Psychiatry 2000 Aug;69(2):254-6

Ataxia caused by mutations in the alpha-tocopherol transfer protein gene.

Usuki F, Maruyama K

Department of Clinical Medicine, National Institute for Minamata Disease, 4058-18 Hama, Minamata 867-0008, Japan. Diese E-Mail-Adresse ist vor Spambots geschützt! Zur Anzeige muss JavaScript eingeschaltet sein!

A 48 year old woman with ataxia with vitamin E deficiency is described. Gene analysis identified two point mutations in exon 1 of the alpha-tocopherol transfer protein (alpha-TTP) gene, one missense mutation and an upstream initiation codon mutation in the 5'-untranslated region (Kozak sequence). The latter mutation is the first one identified in the translation regulatory region. This mutation decreased the level of alpha-TTP protein expression. The clinical features included uncommon urinary disturbance and deafness and relatively rare retinitis pigmentosa. Supplementary therapy increased her serum vitamin E concentration to the normal range with mild improvement of the deep senses.

PMID: 10896705, UI: 20355102

1: Surv Ophthalmol 1999 Jan-Feb;43(4):321-34

Retinitis pigmentosa: defined from a molecular point of view.

van Soest S, Westerveld A, de Jong PT, Bleeker-Wagemakers EM, Bergen AA

Department of Ophthalmogenetics, The Netherlands Ophthalmic Research Institute, Amsterdam.

Retinitis pigmentosa (RP) denotes a group of hereditary retinal dystrophies, characterized by the early onset of night blindness followed by a progressive loss of the visual field. The primary defect underlying RP affects the function of the rod photoreceptor cell, and, subsequently, mostly unknown molecular and cellular mechanisms trigger the apoptotic degeneration of these photoreceptor cells. Retinitis pigmentosa is very heterogeneous, both phenotypically and genetically. In this review we propose a tentative classification of RP based on the functional systems affected by the mutated proteins. This classification connects the variety of phenotypes to the mutations and segregation patterns observed in RP. Current progress in the identification of the molecular defects underlying RP reveals that at least three distinct functional mechanisms may be affected: 1) the daily renewal and shedding of the photoreceptor outer segments, 2) the visual transduction cascade, and 3) the retinol (vitamin A) metabolism. The first group includes the rhodopsin and peripherin/RDS genes, and mutations in these genes often result in a dominant phenotype. The second group is predominantly associated with a recessive phenotype that results, as we argue, from continuous inactivation of the transduction pathway. Disturbances in the retinal metabolism seem to be associated with equal rod and cone involvement and the presence of deposits in the retinal pigment epithelium.

Publication Types: Review  
Review, academic

PMID: 10025514, UI: 99148381

1: Altern Med Rev 2000 Jun;5(3):209-23

Environmental medicine, part three: long-term effects of chronic low-dose mercury exposure.

Crinnion WJ

Healing Naturally, 11811 NE 128th St., Suite 202, Kirkland, WA 98034, USA.

Mercury is ubiquitous in the environment, and in our mouths in the form of "silver" amalgams. Once introduced to the body through food or vapor, mercury is rapidly absorbed and accumulates in several tissues, leading to increased oxidative damage, mitochondrial dysfunction, and cell death. Mercury primarily affects neurological tissue, resulting in numerous neurological symptoms, and also affects the kidneys and the immune system. It causes increased production of free radicals and decreases the availability of antioxidants. It also has devastating effects on the glutathione content of the body, giving rise to the possibility of increased retention of other environmental toxins. Fortunately, effective tests are available to help distinguish those individuals who are excessively burdened with mercury, and to monitor them during treatment. Therapies for assisting the reduction of a mercury load include the use of 2,3-dimercaptosuccinic acid (DMSA) and 2,3-dimercato-1-propanesulfonic acid (DMPS). Additional supplementation to assist in the removal of mercury and to reduce its adverse effects is discussed.

Publication Types: Review  
Review, tutorial

PMID: 10869102, UI: 20328060

1: Toxicology 1996 May 3;109(1):49-55

Sodium 2,3-dimercapto-1-propanesulfonate (DMPS) treatment does not redistribute lead or mercury to the brain of rat.

Aposhian MM, Maiorino RM, Xu Z, Aposhian HV

Department of Molecular and Cellular Biology, University of Arizona, Tuscon, AZ 85721, USA.

Since there has been concern about whether any of the chelating agents used therapeutically might cause an initial redistribution of heavy metals to the brain and since the sodium salt of 2,3-dimercapto-1-propanesulfonic acid (Dimaval, DMPS) has been used to treat heavy metal intoxication in humans, the hypothesis that DMPS does not redistribute and increase lead or mercuric ions in the brains of rats was tested. Lead acetate at a concentration of 50 mg/l was made available in the drinking water of rats for 86 days. Other rats received intraperitoneal injections of 0.50 mg Hg/kg (as mercuric chloride) each day for 5 days a week for a total of 32 or 41 days. Animals were divided into groups and given, i.p., either 0.27 mmol DMPS/kg body weight or saline, each day for 1, 2, 3 or 4 days. Lead or mercury concentrations of the brain were determined after each group received DMPS for the different number of days. DMPS treatment did not result in any initial increase of lead or mercuric ions in the brain. The mercury content of the kidney decreased. The results of these experiments demonstrated that lead or mercuric ions were not redistributed to or increased in the brains of rats during the initial days of DMPS treatment.

PMID: 8619252, UI: 96204898

1: Neurotoxicology 1996 Summer;17(2):343-9

Increased inorganic mercury in spinal motor neurons following chelating agents.

Ewan KB, Pamphlett R

Department of Pathology (Neuropathology Division), University of Sydney, Australia.

Heavy metal toxicity has been implicated in the pathogenesis of motor neuron diseases. In an attempt to assess the efficacy of chelating agents to remove mercury from motor neurons, we quantitated the effect of the chelating agents meso-2,3-dimercaptosuccinic acid (DMSA) and 2,3- dimercaptopropane-1-sulphonate (DMPS) on the burden of inorganic mercury in mouse spinal motor neurons. Mice were injected intraperitoneally with 1.0 mg HgCl2/kg body weight and one week later with either 4,400 mg/kg DMPS, 3,600 mg/kg DMSA or 5% NaHCO3 (control) over 4 weeks. Mercury deposits in motor neurons of 50 micron frozen sections of lumbar spinal cord were visualised with an autometallographic technique. Optical sections of silver-enhanced deposits were acquired using a confocal microscope in reflective mode and the volume of the deposits within the perikaryon was estimated. Mercury deposits occupied significantly more volume in motor neurons after both DMPS (7.4%, SD +/- 0.7%) and DMSA (8.0% +/- SD 0.7%) treatment than in controls (4.3%, SD +/- 1.7%). The higher levels of neuronal inorganic mercury may be due to increased entry of mercury into motor axons across the neuromuscular junction as a result of chelator-induced elevated circulating mercury.

PMID: 8856730, UI: 97009625

1: Mutat Res 1997 Dec;387(3):141-6

Mutagenicity, carcinogenicity and teratogenicity of germanium compounds.

Gerber GB, Leonard A

Teratogenicity and Mutagenicity Unit, Catholic University of Louvain, Brussels, Belgium.

The metalloid germanium has found widespread application in electronics, nuclear sciences and in medicine. General toxicity of germanium is low, except for the tetrahydride germane, and few observations on toxicity of germanium in man exist. Germanium is not carcinogenic and even appears to inhibit cancer development and, in the form of the organic germanium compound, spirogermanium, to destroy cancer cells. Germanium compounds have no mutagenic activity and may, under certain conditions, inhibit the mutagenic activity of other substances. High doses of germanium may result in an increased embryonic resorption, but possible malformations have been reported only after administration of dimethyl germanium oxide to pregnant animals. Germanium may thus be considered an element of rather low risk to man.

Publication Types: Review  
Review, tutorial

PMID: 9439710, UI: 98102883

1: Chung Hua Wai Ko Tsa Chih 1996 Apr;34(4):221-3

[Effect of dietary selenium and germanium on the precancerous lesion in rat glandular stomach induced by N-methyl-N'-nitro-N-nitrosoguanidine].

[Article in Chinese]

Ming X, Yin H, Zhu Z

Department of Surgery, Ruijin Hospital Shanghai Second Medical University.

N-Methyl-N'-nitrosoguanidine (MNNG) was administered (100 mg/L) in drinking water in 100 Wistar rats for 24 weeks to induce the precancerous lesion in glandular stomach. 77 rats with the precancerous lesion in glandular stomach were divided into 3 groups randomly at the 25 thweek. Yeast selenium (Yse, 4 mg/L) and carboxyethyl germanium sesquioxide (Ge-132, 600 mg/L) in drinking water were administered respectively in the corresponding treatment groups: 100 ml/MNNG in drinking water was administered in the treatment group, and 100 ml/MNN in drinking water was administered in the treatment group and control group for another 5 weeks. The experiment ended at the end of the 37th week. The results showed that the incidence of glandular stomach cancer in the Yse group was significantly lower than that in the control group; the infiltrating depth of glandular stomach cancer in the Yse group and the Ge-132 group was remarkably shallower than that in the control group. These findings suggest that Yse and Ge-132 have some preventive effect on the precancerous lesion in rat glandular stomach induced by MNNG.

PMID: 9387686, UI: 98048933

1: Wien Klin Wochenschr 1994;106(18):590-5

[Measuring cesium 137 concentrations in surgical specimen of gynecologic tumors and breast milk, amniotic fluid and in umbilical cords, 6 years after Chernobyl].

[Article in German]

Czerwenka KF, Heuss F, Teherani DK

Institute fur Klinische Pathologie der Universitat Wien.

In the present study, the cesium 137 content in various human tissues was examined 6 years after the Chernobyl reactor catastrophe. The measurements were performed with a gamma-ray spectrometer by means of a germanium/lithium detector. The median of cesium 137 was 20 mBq/ml in mother's milk, 60 mBq/ml in amniotic fluid, 105 mBq/g in umbilical cords, 51 mBq/g in ovarian tumours, and 140 mBq/g in mammary carcinomas. These values lay far below the permissible limit values of 528 mBq/ml or 528 mBq/g for persons not exposed to radiation. The problems of determining the upper limit were also discussed, and it was ascertained that despite the favorably low values recorded in this study a residual risk to health cannot be absolutely precluded in the light of present-day knowledge.

PMID: 7992498, UI: 95084625

1: Head Neck 1994 Jan-Feb;16(1):30-8

Multidisciplinary treatment of head and neck cancer using BCG, OK-432, and GE-132 as biologic response modifiers.

Fukazawa H, Ohashi Y, Sekiyama S, Hoshi H, Abe M, Takahashi M, Sato T

2nd Department of Oral and Maxillofacial Surgery, Niigata University, School of Dentistry, Japan.

Since 1979, we have performed multidisciplinary treatment using intensive immunotherapy with biologic response modifiers (BRM) in combination with surgical treatment of oral cancer. Chemotherapy and radiotherapy were also included as part of the therapy. A historic control study was performed. Adjuvant therapy was administered by standardized methods, and the distribution of patients at various stages was similar between groups. The immunotherapy group showed a shorter treatment period, lower rates of recurrence, metastases, and side effects, greater histologic effects at the end of the first treatment, and a higher survival rate than the nonimmunotherapy group. Immunologically, immunotherapy tended to promote positive immune reactions and inhibit negative immune reactions.

PMID: 7510275, UI: 94171557

1: Invest New Drugs 1985;3(3):303-5

A phase II study of spirogermanium in patients with metastatic malignant melanoma. An NCI Canada Clinical Trials Group Study.

Eisenhauer E, Kerr I, Bodurtha A, Iscoe N, McCulloch P, Pritchard K, Quirt I

The National Cancer Institute of Canada Clinical Trials Group conducted a phase II study of spirogermanium given daily for 5 days every 3 weeks to previously untreated patients with malignant melanoma. In 21 evaluable patients one complete response was seen (response rate 5%). Disease progression occurred in the other 20 patients. Toxicity was primarily neurologic and mild or moderate in most patients, though there was one treatment related death. In this schedule spirogermanium has extremely limited activity against malignant melanoma and will not contribute significantly to the systemic therapy of this disease.

PMID: 4066224, UI: 86058481

1: Cancer Treat Rep 1980;64(12):1207-10

Toxicity of spirogermanium in mice and dogs after iv or im administration.

Henry MC, Rosen E, Port CD, Levine BS

Toxicity of single-dose spirogermanium was evaluated after iv and im administration to CDF1 mice and beagle dogs. The im LD50 in mice was approximately threefold greater than the iv LD50. The lethal dose in dogs was the same for both routes of administration, but death was delayed after im injection. Convulsive seizures occurred only after the im doses that were lethal, but they were observed after administration of iv doses that were nonlethal. Microscopic evidence of drug toxicity (necrosis and degeneration) was found in mitotically active tissues: intestinal tract, lymphoid tissue, and bone marrow. Necrosis, hemorrhage, edema, and granulation tissue were observed in the muscle injection site.

PMID: 7471112, UI: 81135631

1: J Nutr 1976 Feb;106(2):198-203

Interactions of trace metals in mouse and rat tissues; zinc, chromium, copper, and manganese with 13 other elements.

Schroeder HA, Nason AP

Tissues  of rats and mice fed a nonessential metal in drinking water for life were analyzed for the essential metals chromium, copper, manganese and zinc. The study involved 505 rats and 843 mice. Livers, lungs, hearts, kidneys and spleens were pooled in groups according to age at death, averaging 5 for rats and 8 for mice, in order to provide adequate sample weight. Copper was significantly higher in livers of rats fed tin, germanium, niobium and zirconium than in controls. Similarly, niobium was associated with deposition of manganese in heart and zinc deposition in liver. Chromium levels were depressed in heart, kidney and spleen by germanium. In mice the greatest effects occurred when indium and rhodium were fed, all four essential trace metals exhibiting raised levels principally in kidney but also in heart and spleen. Chromium levels were raised in all organs but heart when hexavalent chromium was fed. From these data it is apparent that the ingestion of a nonessential metal can enhance the retention of an essential trace metal, perhaps thus avoiding toxicity from the nonessential one.

PMID: 1249646, UI: 76122040

1: Mol Genet Metab 2000 Oct;71(1/2):121-138

Folic Acid: Nutritional Biochemistry, Molecular Biology, and Role in Disease Processes.

Lucock M

Academic Unit of Paediatrics and Obstetrics and Gynaecology, University of Leeds, D Floor, Clarendon Wing, Leeds General Infirmary, West Yorkshire, Leeds, LS2 9NS, United Kingdom

[Record supplied by publisher]

This paper reviews the chemistry, metabolism, and molecular biology of folic acid, with a particular emphasis on how it is, or may be, involved in many disease processes. Folic acid prevents neural tube defects like spina bifida, while its ability to lower homocysteine suggests it might have a positive influence on cardiovascular disease. A role for this B vitamin in maintaining good health may, in fact, extend beyond these clinical conditions to encompass other birth defects, several types of cancer, dementia, affective disorders, Down's syndrome, and serious conditions affecting pregnancy outcome. The effect of folate in these conditions can be explained largely within the context of folate-dependent pathways leading to methionine and nucleotide biosynthesis, and genetic variability resulting from a number of common polymorphisms of folate-dependent enzymes involved in the homocysteine remethylation cycle. Allelic variants of folate genes that have a high frequency in the population, and that may play a role in disease formation include 677C --> T-MTHFR, 1298A --> C-MTHFR, 2756A --> G-MetSyn, and 66A --> G-MSR. Future work will probably uncover further polymorphisms of folate metabolism, and lead to a wider understanding of the interaction between this essential nutrient and the many genes which underpin its enzymatic utilization in a plethora of critical biosynthetic reactions, and which, under adverse nutritional conditions, may promote disease. Copyright 2000 Academic Press.

PMID: 11001804

1: Carcinogenesis 1997 Nov;18(11):2071-6

Presence and consequence of uracil in preneoplastic DNA from folate/methyl-deficient rats.

Pogribny IP, Muskhelishvili L, Miller BJ, James SJ

Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock 72205, USA.

Uracil can arise in DNA by misincorporation of dUTP into nascent DNA and/or by cytosine deamination in established DNA. Based on recent findings, both pathways appear to be promoted in the methyl-deficient model of hepatocarcinogenesis. A chronic increase in the ratio dUTP:dTTP with folate/methyl deficiency can result in a futile cycle of excision and reiterative uracil misincorporation leading to premutagenic apyrimidinic (AP) sites, DNA strand breaks, DNA fragmentation and apoptotic cell death. The progressive accumulation of unmethylated cytosines with chronic methyl deficiency will increase the potential for cytosine deamination to uracil and further stress uracil mismatch repair mechanisms. Uracil is removed by a highly specific uracil-DNA glycosylase (UDG) leaving an AP site that is subsequently repaired by sequential action of AP endonuclease, 5'-phosphodiesterase, a DNA polymerase and DNA ligase. Since the DNA polymerases cannot distinguish between dUTP and dTTP, an increase in dUTP:dTTP ratio will promote uracil misincorporation during both DNA replication and repair synthesis. The misincorporation of uracil for thymine (5-methyluracil) may constitute a genetically significant form of DNA hypomethylation distinct from cytosine hypomethylation. In the present study a significant increase in the level of uracil in liver DNA as early as 3 weeks after initiation of folate/methyl deficiency was accompanied by parallel increases in DNA strand breaks, AP sites and increased levels of AP endonuclease mRNA. In addition, uracil was also detected within the p53 gene sequence using UDG PCR techniques. Increased levels of uracil in DNA implies that the capacity for uracil base excision repair is exceeded with chronic folate/methyl deficiency. It is possible that enzyme-induced extrahelical bases, AP sites and DNA strand breaks interact to negatively affect the stability of the DNA helix and stress the structural limits of permissible uracil base excision repair activity. Thus substitution of uracil for thymine induces repair-related premutagenic lesions and a novel form of DNA hypomethylation that may relate to tumor promotion in the methyl-deficient model of hepatocarcinogenesis.

PMID: 9395204, UI: 98055582

1: Eur J Cancer B Oral Oncol 1996 Mar;32B(2):120-2

Serum vitamins' status in oral leucoplakias--a preliminary study.

Ramaswamy G, Rao VR, Kumaraswamy SV, Anantha N

Department of Biochemistry, Kidwai Memorial Institute of Oncology, Bangalore, India.

Vitamins, such as A, beta carotene, C, E, B12 and folate, are the micronutrients with the strongest evidence of having a link to cancer prevention and control. Deficiency of these vitamins at the dietary, systemic or mucosal level will interact with tobacco use and increase the risk of oral precancerous lesions. The objective of this study was to (1) establish the baseline circulating levels of these vitamins in our normal population with and without tobacco use and (2) compare these levels with the values obtained in cases of oral leucoplakias. 50 normal controls with 25 each in chewers and non-chewers, matched for age and sex, were selected. 50 cases of oral leucoplakias (clinically detectable white patches) from the field constituted the study group. Simultaneous measurement of serum vitamin B12 and folate were carried out by radioassay. The other serum vitamins were estimated spectrophotometrically. Except for serum vitamin E, all the other serum vitamin levels were significantly decreased in oral leucoplakias compared to the controls. Cancer chemopreventive agents acting as inhibitors of both initiation and promotion, as analysed in our population, is promising for further intervention trials.

PMID: 8736174, UI: 96297035

1: J Natl Cancer Inst 1992 Nov 18;84(22):1740-4

Effects of folate deficiency and supplementation on methylnitrosourea-induced rat mammary tumors.

Baggott JE, Vaughn WH, Juliana MM, Eto I, Krumdieck CL, Grubbs CJ

Department of Nutrition Sciences, University of Alabama, Birmingham 35294-3360.

BACKGROUND: There are metabolic and epidemiologic data consistent with the hypothesis that folate deficiency increases the likelihood of cancer. Conversely, it is also known that folate is necessary for cancer growth, but few experiments in laboratory animals have evaluated the effects of folate deficiency on the development of chemically induced cancers.

PURPOSE: Our purpose was to determine the effects of nutritional folate deficiency in female Fischer 344 rats on initiation and early promotion of methylnitrosourea (MNU)-induced mammary cancer.

METHODS: Rats (age, 27 days) were fed a folic acid-deficient diet (AIN-76A) supplemented with glycine and succinylsulfathiazole [FA(0)]; the FA(0) diet supplemented with 2 or 40 mg of folic acid per kilogram [FA(2) or FA(40), respectively]; or the FA(0) diet supplemented with 20 mg of folinic acid per kilogram [FL(20)]. At 57 days of age, each diet-treated group (30 rats in each group) received MNU (50 mg/kg) by intravenous injection. Immediately after MNU treatment, all animals were fed the AIN-76A complete diet containing 2 mg of folic acid per kilogram. Control groups were fed the AIN-76A complete diet throughout the entire experiment.

RESULTS: After 4 weeks, folate deficiency, but not anemia or growth suppression, was documented by lower folate levels in plasma and red blood cells in the group receiving the FA(0) diet. Cancer multiplicity (i.e., number of mammary cancers per number of tumor-bearing animals) at 180 days after MNU injection was 1.32, 1.90, 2.14, and 2.73 mammary cancers per tumor-bearing animal in the FA(0), FA(2), FA(40), and FL(20) groups, respectively; the value in the FA(0) group was statistically significant compared with the values in the other groups. The time required for 50% of the rats to develop palpable mammary cancer was 170, 142, 100, and 85 days, respectively. The value of 170 days for the FA(0) group was statistically significant compared with the values of 100 and 85 days. Mammary cancer incidence was 63%, 70%, 72%, and 73%, respectively; these percentages were not significantly different.

CONCLUSIONS: Folate deficiency suppresses and folate supplementation enhances initiation or early promotion of MNU-induced mammary cancer in rats, even when the folate-deficient rats do not have anemia or growth suppression.

IMPLICATION: Since the rat is relatively resistant to folate deficiency anemia, other animal models should be used to test the effect of folate nutriture on carcinogenesis.

PMID: 1433358, UI: 93059459

1: Wien Klin Wochenschr 2000 Jul 28;112(14):610-6

Therapeutic potential of glutathione.

Exner R, Wessner B, Manhart N, Roth E

Department of Surgery, University of Vienna, Austria.

[Medline record in process]

Reactive oxygen species, formed in various biochemical reactions, are normally scavenged by antioxidants. Glutathione in its reduced form (GSH) is the most powerful intracellular antioxidant, and the ratio of reduced to oxidised glutathione (GSH:GSSG) serves as a representative marker of the antioxidative capacity of the cell. Several clinical conditions are associated with reduced GSH levels which as a consequence can result in a lowered cellular redox potential. GSH and the redox potential of the cell are components of the cell signaling system influencing the translocation of the transcription factor NF kappa B which regulates the synthesis of cytokines and adhesion molecules. Therefore, one possibility to protect cells from damage caused by reactive oxygen species is to restore the intracellular glutathione levels. Cellular GSH concentration can be influenced by exogenous administration of GSH (as intravenous infusion or as aerosol), of glutathione esters or of GSH precursors such as glutamine or cysteine (in form of N-acetyl-L-cysteine, alpha-lipoic acid). The modulation of GSH metabolism might present a useful adjuvant therapy in many pathologies such as intoxication, diabetes, uremia, sepsis, inflammatory lung processes, coronary disease, cancer and immunodeficiency states.

PMID: 11008322, UI: 20463602

1: Prikl Biokhim Mikrobiol 1977 Sep-Oct;13(5):677-81

Influence of methylcobalamin and cyanocobalamin on the neoplastic process in rats.

Kal'nev VR, Rachkus IuA, Kanopkaite SI

The effect of methylcobalamine (5.6-dimethylbenzimidazolyl-Co-methylcobamide, CH3-B12) and cyanocobalamine (5,6-dimethylbenzimidazolyly-Co-cyanocobamide, CN-B12) on the growth of Walker's carcinosarcoma and longevity of white noninbred rats with implanted Zajdela ascites hepatoma was studied. The two agents exerted a similar effect. They 1) reduced the survival of rats with implanted Zajdela ascites hepatoma and Walker's carcinosarcoma; 2) did not increase the cell concentration in ascites; and 3) increased the total volume of ascites.

PMID: 199903, UI: 78032835

1: Neuropediatrics 1995 Oct;26(5):260-2

Oxyradical damage and mitochondrial enzyme activities in the mdx mouse.

Hauser E, Hoger H, Bittner R, Widhalm K, Herkner K, Lubec G

Department of Pediatrics, University of Vienna, Austria.

A number of studies have already been undertaken to investigate involvement of oxyradicals in muscle diseases by means of measurements of oxyradical protective enzymes. We investigated o-tyrosine, which is a biomarker for OH radical damage in vivo, in 10 mdx and 10 control mice. We also measured mitochondrial enzymes in muscle homogenates of 10 mdx and 10 control mice. Mdx mice had significantly elevated values for o-tyrosine, succinat-phenacinmetosulfat oxidoreductase. NADH O2 oxidoreductase and cytochrome C oxidoreductase. Our findings confirm the suggestion that elevated oxyradical production occurs in muscular dystrophies with lack of dystrophin. Furthermore, our results demonstrate that OH radical damage does not impair mitochondrial enzyme activities in the mdx mouse.

PMID: 8552217, UI: 96141214

1: Eur J Dermatol 1999 Apr-May;9(3):202-6

Vitamin D3 analogues improve cafe au lait spots in patients with von Recklinghausen's disease: experimental and clinical studies.

Nakayama J, Kiryu H, Urabe K, Matsuo S, Shibata S, Koga T, Furue M

Department of Dermatology, Fukuoka University School of Medicine, 7-45-1, Nanakuma, Jonan-Ku, Fukuoka, 814-0180, Japan.

Topical application of vitamin D3 analogues for 6 months was found to be effective in improving the pigmentation of cafe au lait spots in patients with von Recklinghausen's disease. Treatment of cafe au lait spots grafted onto nude mice with a vitamin D3 analogue caused suppression of bromodeoxy- uridine uptake in the cells of the basal layer. Vitamin D3 analogues also decreased melanin pigment in cafe au lait spots after 4 weeks of treatment. Thus, it is considered that long-term application of vitamin D3 analogues is effective both for improving the pigmentation of cafe au lait spots and suppressing the development of neurofibromas in patients with von Recklinghausen's disease.

Publication Types: Clinical trial

PMID: 10210785, UI: 99228818

1: Biochem Med Metab Biol 1992 Aug;48(1):69-73

Nicotinamide-induced activity of alkaline phosphodiesterase I toward tumor-derived cultured cells from neurofibromatosis patients.

Maruyama E, Takashima S, Arima M

Division of Mental Retardation and Birth Defect Research, National Institute of Neuroscience, Tokyo, Japan.

Membrane-bound alkaline phosphodiesterase I was investigated in control fibroblasts and tumor-derived fibroblasts from patients with neurofibromatosis. Alkaline phosphodiesterase I activity of tumor-derived cells increased in a dose response to nicotinamide (0-9 mM) in culture; 5'-thymidine p-nitrophenyl phosphate was used as substrate. The enzyme activity increased 1.7-fold after 30 h of incubation with 9 mM nicotinamide, and after 3 weeks increased 5-fold. The nicotinamide-dependent enhancement of alkaline phosphodiesterase I activity was inhibited by actinomycin D, which specifically blocks RNA synthesis, but not by cycloheximide. These results suggest that the increase in the enzyme activity caused by nicotinamide was due to induction of alkaline phosphodiesterase I at the transcriptional level in tumor-derived cells. The metabolic effect of nicotinamide on alkaline phosphodiesterase I may be related to tumorigenicity in neurofibromatosis.

PMID: 1326301, UI: 92399024

1: Lancet 1999 Oct 9;354(9186):1266-7

Olestra increases faecal excretion of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Geusau A, Tschachler E, Meixner M, Sandermann S, Papke O, Wolf C, Valic E, Stingl G, McLachlan M

Two patients with chloracne had concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) of 144,000 and 26,000 pg/g blood lipids. Olestra, a non-digestible, lipophilic dietary fat substitute accelerated the patients' intestinal excretion of TCDD by eight to ten fold. This is sufficient to reduce the normally observed elimination half life of TCDD from about 7 years to 1-2 years.

Publication Types: Letter

PMID: 10520643, UI: 99448953

1: Ann Epidemiol 1999 Aug;9(6):358-65

Serum ascorbic acid and cardiovascular disease prevalence in U.S. adults: the Third National Health and Nutrition Examination Survey (NHANES III).

Simon JA, Hudes ES

General Internal Medicine Section, Medical Service, Veterans Affairs Medical

Center, San Francisco, CA 94121, USA.

PURPOSE: To examine the relation between serum ascorbic acid concentration, which reflects dietary and supplement intake, and the prevalence of cardiovascular disease.

METHODS: We analyzed data from 7658 men and women enrolled in the Third National Health and Nutrition Examination Survey (NHANES III). We calculated odds ratios and 95% confidence intervals (CI) to estimate the relative prevalence of cardiovascular disease, defined as self-reported angina, myocardial infarction, or stroke. Because we detected an interaction between serum ascorbic acid concentration and alcohol intake, we performed analyses stratified by drinking status.

RESULTS: Among participants who reported no alcohol consumption, serum ascorbic acid concentrations were not independently associated with cardiovascular disease prevalence. Among participants who consumed alcohol, serum ascorbic acid concentrations consistent with tissue saturation (1.0-3.0 mg/dl) were associated with a decreased prevalence of angina (multivariate odds ratio (OR): 0.48; 95% CI: 0.23% to 1.03; p for trend = 0.06), but were not significantly associated with myocardial infarction or stroke prevalence.

CONCLUSIONS: These results suggest the possibility of a biologic interaction between ascorbic acid and alcohol and that higher intakes of ascorbic acid may be associated with a decreased risk of angina among drinkers.

PMID: 10475535, UI: 99402520

1: JAMA 1999 Jun 23-30;281(24):2289-93

Relationship of ascorbic acid to blood lead levels.

Simon JA, Hudes ES

Department of Epidemiology and Biostatistics, University of California, Veterans Affairs Medical Center, San Francisco 94121, USA. Diese E-Mail-Adresse ist vor Spambots geschützt! Zur Anzeige muss JavaScript eingeschaltet sein!

CONTEXT: Some animal studies suggest that orally administered ascorbic acid may chelate lead and decrease the risk of the toxic effects of lead. However, results from several small studies in humans have yielded inconclusive evidence of a beneficial effect of ascorbic acid on lead toxicity.

OBJECTIVE: To examine the relationship between serum ascorbic acid levels and prevalence of elevated blood lead levels.

DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional analysis of a probability sample of the US population enrolled in the Third National Health and Nutrition Examination Survey, 1988-1994 (4213 youths aged 6-16 years and 15365 adults aged > or =17 years) without a history of lead poisoning.

MAIN OUTCOME MEASURES: Elevated and log blood lead levels by serum ascorbic acid level. RESULTS: A total of 22 youths (0.5%) and 57 adults (0.4%) had elevated blood lead levels (defined as > or =0.72 micromol/L [15 microg/dL]) and > or =0.97 micromol/L [20 microg/dL], respectively). After controlling for the effects of age, race, sex, income level, and dietary energy, fat, calcium, iron, and zinc intake, youths in the highest serum ascorbic acid tertile had an 89% decreased prevalence of elevated blood lead levels compared with youths in the lowest serum ascorbic acid tertile (odds ratio, 0.11; 95% confidence interval, 0.04-0.35; P for trend = .002). Adults in the highest 2 serum ascorbic acid tertiles had a 65% to 68% decreased prevalence of elevated blood lead levels compared with adults in the lowest serum ascorbic acid tertile (P for trend = .03). As a continuous predictor, serum ascorbic acid level was independently associated with decreased log blood lead levels among adults (P<.001), but not among youths (P=.14).

CONCLUSIONS: Our data suggest that high serum levels of ascorbic acid are independently associated with a decreased prevalence of elevated blood lead levels. If these associations are related causally, ascorbic acid intake may have public health implications for control of lead toxicity.

Comment in: JAMA 1999 Jun 23-30;281(24):2340-2

PMID: 10386552, UI: 99313123 

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