Hepatic polyamines and related enzymes following chlordecone-potentiated carbon tetrachloride toxicity in rats

✍ Scribed by Rao, Shrinivas B. ;Young, Robert A. ;Mehendale, Harihara M.

• Publisher: John Wiley and Sons
• Year: 1989
• Tongue: English
• Weight: 866 KB
• Volume: 4
• Category: Article
• ISSN: 0887-2082
• DOI: 10.1002/jbt.2570040110

✦ Synopsis

Chlordecone potentiation of the hepatotoxic and lethal effects of CC14 has been well established. Recent studies have shown that the suppression of hepatocellular regeneration results in an accelerated progression of liver injury leading to complete hepatic failure. Since polyamines are involved in cell division, these studies were designed to investigate the polyamine levels and associated enzymes in the livers of rats treated with a low-dose combination of CD and CC14. For comparison, a large toxic dose of CC14 was also employed. The extent of liver toxicity in rats fed 10 parts per million chlordecone (CD) for 15 days and subsequently injected with a single dose of CC14 (100 pLlkg body weight) or a high dose of CCl, alone (2.5 mLlkg body weight) was similar 6 and 24 hr later as assessed by plasma transaminase levels. There was significant elevation in liver ornithine decarboxylase, S-adenosylmethionine decarboxylase, and putrescine at 24 hr and spermidine N1-acetyltransferase, N1-acetylputrescine, putreanine, putrescine, and N1-acetylspermidine at 6 hr in rats treated with the high dose of CC14 alone compared to the combination treatment. Spermidine levels decreased up to 6 hr and then increased up to 24 hr for both treatments. Spermine continuously decreased up to 24 hr for the CD and CC14 low-dose combination treatment compared to rats treated with a high dose of CCl, alone. Spermidine levels were lower than in controls and rose towards control value between 6 and 24 hr after the combination treatment and the high dose of CCl, .

Results indicate that the CD and CCl, low-dose combination treatment increased liver toxicity, resulting in compromised polyamine metabolism that is coincidental with suppressed hepatocellular regenera-