Hepatic lipid peroxidation in CoCl2-treated rats, evidenced by elevated concentrations of thiobarbituric acid chromogens.

Parenteral administration of cobalt chloride (CoCl2) to male Fischer-344 rats caused hepatic lipid peroxidation, as evidenced by the thiobarbituric acid (TBA) reaction for malondialdehyde (MDA) and related chromogens in fresh liver homogenates. After a single sc injection of CoCl2 (300 mumol/kg, body wt.), hepatic concentrations of TBA-chromogens became significantly increased by 4 h and reached peak levels at 24-72 h post-injection. For example, in rats killed 48 h post-injection, hepatic TBA-chromogens (mean +/- SD, N = 7) averaged 607 +/- 141 nmol/g of tissue, wet wt., (P less than 0.01 versus 245 +/- 73 nmol/g in 19 controls). A dose-effect relationship was observed between CoCl2 dosages (100 to 450 mumol/kg, body wt.) and hepatic concentrations of TBA-chromogens in rats killed 24 h post-injection. This study indicates that hepatic lipid peroxidation develops as a consequence of acute CoCl2 toxicity in rats.