4-Hydroxynonenal and other lipid peroxidation products are formed in mouse liver following intoxication with allyl alcohol.

Some recent reports indicate that lipid peroxidation might play a crucial role in the production of allyl alcohol hepatotoxicity. Previous work from our laboratory has suggested that in the case of bromobenzene, a hepatotoxin sharing the ability of allyl alcohol to induce a marked depletion of liver glutathione, liver injury is likely to be mediated by lipid peroxidation. In particular, we demonstrated that 4-hydroxynonenal and other aldehydes derived from lipid peroxidation can be detected in the liver of bromobenzene-poisoned mice. In the present study, we report also the in vivo formation of 4-hydroxynonenal and other aldehydes after allyl alcohol poisoning. 24-h-fasted mice were intoxicated with allyl alcohol (1.5 mmol/kg body wt., i.p.) and killed 1-3 h later. 4-Hydroxynonenal and other carbonyls were looked for in liver extracts in the form of 2,4-dinitrophenylhydrazone derivatives. After fractionation of liver extracts by means of thin-layer chromatography (TLC), a well-resolved peak corresponding to standard 4-hydroxynonenal was obtained in the high-pressure liquid chromatography analysis. Total carbonyls (as 2,4-dinitrophenylhydrazones) were separated by TLC into three fractions, according to their different polarity. The amounts of carbonyls present in each fraction were determined by ultraviolet-visible spectroscopy. In addition, several products were identified in the fraction of the 'non-polar carbonyls' corresponding to alkanals and alk-2-enals.