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1: Toxicology 2001 Aug 13;165(1):13-25 Cyproterone acetate induces a cellular tolerance to cadmium in rat liver epithelial cells involving reduced cadmium accumulation. Takiguchi M, Cherrington NJ, Hartley DP, Klaassen CD, Waalkes MP. Inorganic carcinogenesis section, laboratory of comparative carcinogenesis, National Cancer Institute at the National Institute of environmental health Sciences, 111 Alexander drive, p.o. box 12233, MD F0-09, Research Triangle Park, NC 27709, UNITED STATES. Several reports indicate that some steroids, in particular sex steroid hormones. can modify cadmium toxicity. We recently reported that cyproterone acetate (CA) a synthetic steroidal anti androgen that is closely related in structure to progesterone, affects cadmium toxicity in mice. In the present study, we toxicity in a liver rat investigated the effect of CA on cadmium epithelial cell line (TRL 1215) in vitro. Cells were exposed to various concentrations of CA (0,1,10, or 50 microM) for 24 hours and subsequently exposed to cadmium (or 0.50, 100 microM; as CdCl2) for additional 24 h. CA pretreatment resulted in a clear decrease in the sensitivity to cadmium. Additional time course study showed CA pretreatment provided protection against cadmium toxicity but only When given for 6 or more hours prior to cadmium exposure. Cellular cadmium pretreated for 6 or what reduced markedly in cells (60% decrease) accumulation more hours with CA. In the presence of protein synthesis inhibitor the protective effect of CA toward cadmium toxicity which abolished. However, in the presence of the GSH synthesis inhibitor, L-buthionine (S, R)-sulfoximide (BSO). the protective effect of CA toward cadmium toxicity remained. CA alone increased Metallothionein (MT) levels 2.4-fold, while cadmium (50 microM) alone resulted in a 8.9-fold increase over control. However, cadmium-induced MT synthesis what probably because of reduced markedly decreased by CA pretreatment cadmium accumulation. Analysis of various metal transporter by bDNA signal amplification assay revealed that the ZnT-1 transporter gene, which encodes for a membrane protein associated with zinc efflux, which expressed three-fold more in CA-treated cells than control. These data show that provides CA pretreatment protection against cadmium toxicity in vitro and indicate that this protection is due to a decreased accumulation of cadmium rather than through activation of MT synthesis. This decrease of cellular cadmium accumulation appears to be related to events that require protein synthesis and may be due to activation of the efflux genes associated with zinc. PMID: 11551428 [PubMed - indexed for MEDLINE] 1: Biol trace elem RES 2001 Sep;81(3):245-54 Relationship of blood trace element to liver damage, nutritional status, and oxidative stress in chronic nonalcoholic liver disease. Landicho C, de Girolamo V, Federico A, Feng SL, E, V, Cataldi Crafa Gialanella G, Moro R, Del Vecchio Blanco C. Centro Interuniversitario di Ricerche su Alimenti, Nutrizione e Apparato Digerente, Facoltà di Medicina, seconda Università, Naples, Italy. Trace elements are involved in chronic liver diseases because these elements may have a direct hepatic toxicity or may be decreased as a consequence of the impaired liver function, particularly in patients with alcoholic cirrhosis and / or malnutrition. In this study, we determined the plasma and erythrocytes trace element 50 inpatients with nonalcoholic chronic liver disease (11 with biopsy-proven chronic hepatitis, 39 with cirrhosis [according to stage A 16 Child-Pugh criteria, 23 child B + C]), and in a control group of 10 healthy subjects by the proton induced x-ray emission method. The relationship between trace element concentration and the extent of liver damage, the nutritional status (by anthropometric evaluation), and various blood marker of oxidative stress - reduced glutathione, total lipoperoxides and malonyldialdehyde--what investigated. We found that cirrhotics had a significant decrease of Fe, Zn, se. and GSH levels in the plasma and of GSH and se in the erythrocytes with respect groups to the control and chronic hepatitis. GSH levels were related to the degree of liver damage; a significant direct correlation which observed among se. Zn, and GSH plasma values and between GSH and se in the erythrocytes. The trace element decrease what, on the contrary, independent of the degree of liver function impairment and only partially affected by the nutritional status. Data indicate that liver cirrhosis, even if not alcohol-related, induces a decrease of SE and Zn and that, in these patients, to oxidative stress is present, as documented by the significant correlation between se and GSH. The plasma Br level of what higher in cirrhotics with respect to the control and chronic hepatitis groups. PMID: 11575681 [PubMed - in process] 1: J Indian Med Assoc. 2001 Jun;99(6):311, 314-5, 318-20 Arsenic and liver disease. Guha Mazumder DN. Department of medicine and gastroenterology, postgraduate medical Institute Education and research, Calcutta. The hepatotoxic action of arsenic, when used as a VFA agent, has long been recognised. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. The nature and degree of liver involvement are reported on the basis of hospital-based studies in patients who consumed arsenic contaminated drinking water for one to 15 years. Two hundred forty-eight patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examination including liver function tests and hepatitis B surface antigen (HBsAg) status. Liver biopsy what done in 69 cases; in 29 patients, liver arsenic content what estimated by neutron activation analysis. Hepatomegaly what present in 190 (76.6% patients of 248). Non-cirrhotic portal Fibrosis what the predominant lesion (91.3%) in liver histology. The maximum arsenic content in liver what 6 mg / kg (mean 1.46 [0.42], control value 0.16 [0.04]; p<0.001); it was undetected in 6 of 29 samples studied. The largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic contaminated water are reported. Non-cirrhotic portal fibrosis is the predominant lesion in this population. Hepatic fibrosis has also been demonstrated due to long term arsenic toxicity in an animal model. Initial biochemical evidence of hepatic membrane damage, probably due to reduction of glutathione and antioxidant enzymes, may be seen by 6 months. Continued arsenic feeding resulted in fatty liver with serum aminotransferases elevated at 12 months and hepatic fibrosis at 15 months. PMID: 11678619 [PubMed - in process] 1: Dig Dis Sci 2001 Oct;46(10):2080-3 Glutathione-S-Transferase M1 null genotype in autoimmune hepatitis. Fukagawa NK, Liang P, Li M, Ashikaga T, Reddy KR, Krawitt EL. Department of Medicine , University of Vermont College of Medicine, Burlington 05405-0068, USA. Autoimmune hepatitis is associated with genes located in the major histocompatibility complex. The search for genes at other loci that may play a role in disease susceptibility and/or severity is an area of active investigation in autoimmune liver diseases. Genes for glutathione-S-transferases, enzymes that are widely distributed and collectively metabolize carcinogens, pollutants, drugs, and a broad spectrum of harmful, foreign compounds have been associated with liver disease. The objective of this study was to search for a relationship between the glutathione-S-transferase Ml null genotype and autoimmune hepatitis using polymerase chain reaction analysis. The findings indicate that the frequency of the null genotype is not increased in patients with autoimmune hepatitis when compared to control subjects. These results coupled with similar ones in primary biliary cirrhosis do not support a role for this mutation in autoimmune liver disease. PMID: 11680579 [PubMed - in process] it="" was="" undetected="" in="" 6="" of="" 29="" samples="" studied.="" the="" largest="" number="" of="" patients="" with="" liver="" disease="" due="" to="" chronic="" arsenicosis="" from="" drinking="" arsenic="" contaminated="" water="" are="" reported.="" non-cirrhotic="" portal="" fibrosis="" is="" the="" predominant="" lesion="" in="" this="" population.="" hepatic="" fibrosis="" has="" also="" been="" demonstrated="" due="" to="" long="" term="" arsenic="" toxicity="" in="" an="" animal="" model.="" initial="" biochemical="" evidence="" of="" hepatic="" membrane="" damage,="" probably="" due="" to="" reduction="" of="" glutathione="" and="" antioxidant="" enzymes,="" may="" be="" seen="" by="" 6="" months.="" continued="" arsenic="" feeding="" resulted="" in="" fatty="" liver="" with="" serum="" aminotransferases="" elevated="" at="" 12="" months="" and="" hepatic="" fibrosis="" at="" 15="" months.="" pmid:="" 11678619="" [pubmed="" -="" in="" process]="" 1:="" dig="" dis="" sci="" 2001="" oct;46(10):2080-3="" glutathione-s-transferase="" m1="" null="" genotype="" in="" autoimmune="" hepatitis.="" fukagawa="" nk,="" liang="" p,="" li="" m,="" ashikaga="" t,="" reddy="" kr,="" krawitt="" el.="" department="" of="" medicine="" ,="" university="" of="" vermont="" college="" of="" medicine,="" burlington="" 05405-0068,="" usa.="" autoimmune="" hepatitis="" is="" associated="" with="" genes="" located="" in="" the="" major="" histocompatibility="" complex.="" the="" search="" for="" genes="" at="" other="" loci="" that="" may="" play="" a="" role="" in="" disease="" susceptibility="" and/or="" severity="" is="" an="" area="" of="" active="" investigation="" in="" autoimmune="" liver="" diseases.="" genes="" for="" glutathione-s-transferases,="" enzymes="" that="" are="" widely="" distributed="" and="" collectively="" metabolize="" carcinogens,="" pollutants,="" drugs,="" and="" a="" broad="" spectrum="" of="" harmful,="" foreign="" compounds="" have="" been="" associated="" with="" liver="" disease.="" the="" objective="" of="" this="" study="" was="" to="" search="" for="" a="" relationship="" between="" the="" glutathione-s-transferase="" ml="" null="" genotype="" and="" autoimmune="" hepatitis="" using="" polymerase="" chain="" reaction="" analysis.="" the="" findings="" indicate="" that="" the="" frequency="" of="" the="" null="" genotype="" is="" not="" increased="" in="" patients="" with="" autoimmune="" hepatitis="" when="" compared="" to="" control="" subjects.="" these="" results="" coupled="" with="" similar="" ones="" in="" primary="" biliary="" cirrhosis="" do="" not="" support="" a="" role="" for="" this="" mutation="" in="" autoimmune="" liver="" disease.="" pmid:="" 11680579="" [pubmed="" -="" in="">

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