title: Effects of tamoxifen and levonorgestrel treatment on carbon tetrachloride induced alterations in rats.
abstract: Oestrogens cause progression in liver lesion, and thus ovariectomy improves hepatic injury both functionally and histologically. In the present study the efficacy of the antioestrogen tamoxifen (CAS 10540-29-1) was examined in chronical carbon tetrachloride damage. The results were compared with the effect of the progestogen levonorgestrel. Male Wistar rats were treated for 16 days. Blood sampling and autopsy were performed 2 h after last tamoxifen resp. levonorgestrel and 1 h after last CCl4 dosage. Tamoxifen diminished water content of the healthy liver. By fairly the same ratio it decreased high water content of the damaged liver. Levonorgestrel moderated water imbibition in CCl4 impairment. Tamoxifen caused protein synthesis in healthy and in injured liver. Levonorgestrel could not prevent protein loss associated with CCl4 damage. Tamoxifen counteracted, levonorgestrel moderated glycogen loss in liver lesion. Blood glucose was normal in all examined groups. Cytochrome P-450 decrease in CCl4 injury was moderated but not normalised by tamoxifen. Levonorgestrel was less effective. Cytochrome b5 content diminished in CCl4 lesion and both treatments restored it. Aminopyrine-N-demethylase was impaired by liver injury. An improvement was measured correlating with microsomal cytochrome P-450 content. This was significant with tamoxifen but not following levonorgestrel administration. The pathological serum bilirubin level of CCl4 lesion was normalised by tamoxifen as well as levonorgestrel treatment. The progestogen levonorgestrel moderated liver injury in reducing high water content, glycogen loss and normalising serum bilirubin. The antioestrogen tamoxifen seems to be a promising treatment in chronic hepatic impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: II. Medical Clinic, University Medical School of Debrecen, Hungary.
authors.forename: A
authors.initials: A
authors.lastname: Kulcsár
authors.forename: J
authors.initials: J
authors.lastname: Kulcsár-Gergely
mesh_terms: D000633:Aminopyrine N-Demethylase / Q000378:metabolism; D000818:Animals; D001663:Bilirubin / Q000097:blood; D001834:Body Water / Q000378:metabolism; D002252:Carbon Tetrachloride Poisoning / Q000503:physiopathology*; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D003573:Cytochrome b Group / Q000378:metabolism; D045346:Cytochrome b6f Complex; D016912:Levonorgestrel / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D008106:Liver Cirrhosis, Experimental / Q000503:physiopathology / Q000517:prevention & control; D008112:Liver Glycogen / Q000378:metabolism; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013629:Tamoxifen / Q000494:pharmacology*
chemical_list: D003573:Cytochrome b Group; D008112:Liver Glycogen; D011506:Proteins; D013629:Tamoxifen; D016912:Levonorgestrel; D045346:Cytochrome b6f Complex; D003577:Cytochrome P-450 Enzyme System; D000633:Aminopyrine N-Demethylase; D001663:Bilirubin