Response of urinary lipophilic aldehydes and related carbonyl compounds to factors that stimulate lipid peroxidation in vivo.

Peroxidation of lipids results in the formation of a number of aldehydic and other carbonyl-containing secondary degradation products. The effect of peroxidative stimuli mediated by vitamin E deficiency, a diet high in polyunsaturated fatty acids (containing cod liver oil), and carbon tetrachloride administration on urinary excretion of a number of lipophilic aldehydes and related carbonyl compounds was examined in rats. These secondary lipid peroxidation products were measured as 2,4-dinitrophenylhydrazine derivatives. All three treatments increased urinary excretion of secondary lipid peroxidation products, although the pattern of excretion of these products varied somewhat among the treatments. Significant increases were found in butanal, hexanal, octanal, butan-2-one, pentan-2-one, hex-2-enal, hepta-2,4-dienal, 4-hydroxyhex-2-enal, 4-hydroxyoct-2-enal, 4-hydroxynon-2-enal, and a number of unidentified carbonyl compounds. These results suggest that urinary excretion of these lipophilic secondary lipid peroxidation products is a useful and noninvasive marker of whole-body lipid peroxidation.