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Uptake of secondary autoxidation products of linoleic acid by the rat
Author(s) -
Kanazawa Kazuki,
Kanazawa Eri,
Natake Masato
Publication year - 1985
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/bf02534231
Subject(s) - autoxidation , chemistry , thiobarbituric acid , weanling , linoleic acid , feces , urine , lipid peroxide , excretion , transaminase , lipidology , clinical chemistry , peroxide , medicine , biochemistry , endocrinology , food science , lipid peroxidation , biology , antioxidant , enzyme , microbiology and biotechnology , fatty acid , organic chemistry
Incorporation of secondary autoxidation products (SP) of linoleic acid into the rat body was investigated. Radioactive SP was administered orally to a group of 5 rats, and excretions of radioactive substances in feces, urine and respiration were measured and compared with excretions from rats fed linoleic acid and its hydroperoxides. The SP‐fed group excreted 45% and the other groups about 10% of the administered radioactivity through feces. Urinary excretion accounted for 52% of activity ingested in the SP group and less than 30% in the other groups. The 14 CO 2 produced in each group was about 25% of the ingested activity. Incorporation of the radioactive substances of SP into tissues and organs was measured periodically after administration of a single dose. The radioactive substances accumulated in the liver between 12–24 hr after administration and accounted for 2.6% of the total amount given, the highest level of all tissues and organs. This accumulation led to an elevation of serum transaminase activities, an increase in hepatic lipid peroxide, as determined by thiobarbituric acid test, and a slight hypertrophy of liver (1.5‐fold). Therefore, absorbed SP appeared to contribute to the deleterious condition of the liver.