Effect of sodium selenite upon bromobenzene toxicity in rats. I. Hepatotoxicity.
The effects of sodium selenite on bromobenzene hepatotoxicity were examined in male rats. Rats pretreated with sodium selenite (12.5 or 30 mumol/kg, ip) 72 hr prior to injection of bromobenzene (7.5 mmol/kg, ip) showed a marked reduction in bromobenzene-induced liver injury as evidenced by decreased plasma alanine and aspartate transaminase values, sorbitol dehydrogenase activity, and reduced histologic damage. Administration of bromobenzene did not affect the selenium content of blood or liver. At 72 hr after treatment with selenite, hepatic reduced (GSH) and oxidized (GSSG) glutathione values or GSH synthetic and degradation enzyme activities were not altered. However, from 3 to 12 hr following bromobenzene administration, hepatic GSH and cysteine amounts declined less rapidly in selenite-treated rats compared to control. Thus, acute selenite treatment ameliorated bromobenzene hepatotoxicity in a manner suggesting facilitation of hepatic GSH production by selenite for use in bromobenzene detoxication.
D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D001969:Bromobenzenes / Q000037:antagonists & inhibitors / Q000633:toxicity*; D003545:Cysteine / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D007274:Injections, Intraperitoneal; D007064:L-Iditol 2-Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D020887:Selenious Acid; D012643:Selenium / Q000032:analysis / Q000494:pharmacology*
D001969:Bromobenzenes; C032036:bromobenzene; D007064:L-Iditol 2-Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D020887:Selenious Acid; D005978:Glutathione; D012643:Selenium; D003545:Cysteine