Response of urinary malondialdehyde to factors that stimulate lipid peroxidation in vivo
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Malondialdehyde (MDA) derivatives occur as normal constituents of rat and human urine. In a previous study, it was found that MDA excretion in rats is responsive to MDA intake and to certain factors that increase lipid peroxidation in vivo: vitamin E deficiency, iron administration and a high concentration of cod liver oil (CLO) fatty acids in the tissues. In the present study, the effect on MDA excretion of several additional dietary and endogeneous factors was evaluated.
The composition of dietary fatty acids had a major influence on MDA excretion in fed animals, being highest for animals fed n−3 fatty acids (20∶5 and 22∶6) from CLO, intermediate for those fed n−6 (18∶2) acids from corn oil (CO) and lowest for those fed saturated acids from hydrogenated coconut oil (HCO). Diet was the main source of urinary MDA in all groups. Fasting produced a marked increase in urinary MDA, which tended to be higher in rats previously fed CLO. Fasting MDA excretion was not affected by the level of CO in the diet (5, 10 or 15%), indicating that feeding n−6 acids does not increase lipid peroxidation in vivo. Adrenocorticotropic hormone and epinephrine administration increased urinary MDA, further indicating that lipolysis either releases fatty acid peroxides from the tissues or increases the susceptibility of mobilized fatty acids to peroxidation. A decrease in fasting MDA excretion was observed in rats previously fed a high level of antioxidants (vitamin E+BHT+vitamin C) vs a normal level of vitamin E. MDA excretion increased following adriamycin and CCl4 administration. No increase was observed following short-term feeding of a choline-methionine-deficient diet, which has been reported to increase peroxidation of rat liver nuclear lipids.
This study provides further evidience that urinary MDA can serve as a useful indicator of lipid peroxidation in vivo when peroxidation of dietary lipids is precluded.
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- Response of urinary malondialdehyde to factors that stimulate lipid peroxidation in vivo
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