URINARY MALONDIALDEHYDE AS AN INDICATOR OF LIPID-PEROXIDATION IN THE DIET AND IN THE TISSUES

Although malondialdehyde (MDA) is extensively metabolized to CO2, small amounts are nevertheless excreted in an acid-hydrolyzable form in rat urine. Urinary MDA was evaluated as an indicator of lipid peroxidation in the diet and in the tissues. MDA was released from its bound form(s) in urine by acid treatment and determined as the TBA[thiobarbituric acid]-MDA derivative by HPLC[high performance liquid chromatography]. MDA excretion by the rat was found to be responsive to oral administration of the Na enol salt and to peroxidation of dietary lipids. Urinary MDA also increased in response to the increased lipid peroxidation in vivo produced by vitamin E deficiency and by administration of Fe nitrilotriacetate. Chronic feeding of a diet containing cod liver oil led to increases in MDA excretion which were not completely eliminated by fasting or feeding a peroxide-free diet, indicating that there was increased lipid peroxidation in vivo. MDA excretion was not responsive to Se deficiency or CCl4 administration. DPPD[N,N-diphenyl-p-phenylenediamine], a biologically active antioxidant, but not BHA[butylated hydroxyanisole], a non-biologically active antioxidant, prevented the increase in MDA excretion in vitamin E deficient animals. MDA excretion may serve as an indicator of the extent of lipid peroxidation in the diet and, under conditions which preclude a dietary effect, as an index of lipid peroxidation in vivo.