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Urinary malondialdehyde as an indicator of lipid peroxidation in the diet and in the tissues
Author(s) -
Draper H. H.,
Polensek L.,
Hadley M.,
McGirr L. G.
Publication year - 1984
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02534512
Subject(s) - lipid peroxidation , malondialdehyde , chemistry , excretion , vitamin e , antioxidant , in vivo , biochemistry , urine , medicine , endocrinology , pharmacology , biology , microbiology and biotechnology
Although malondialdehyde (MDA) is extensively metabolized to CO 2 , small amounts are nevertheless excreted in an acid‐hydrolyzable form in rat urine. In this study, 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‐MA derivative by HPLC. 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 iron 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 CCl 4 administration. DPPD, a biologically active antioxidant, but not BHA, a non‐biologically active antioxidant, prevented the increase in MDA excretion in vitamin E deficient animals. The results indicate that MDA excretion can 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.