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Non-polar lipid carbonyls of thermally oxidized coconut oil induce hepatotoxicity mediated by redox imbalance

Published on Nov 1, 2018in Prostaglandins Leukotrienes and Essential Fatty Acids2.86
· DOI :10.1016/j.plefa.2018.10.004
Arunaksharan Narayanankutty7
Estimated H-index: 7
(University of Calicut),
Anu Anil1
Estimated H-index: 1
(University of Calicut)
+ 2 AuthorsAchuthan C. Raghavamenon5
Estimated H-index: 5
(University of Calicut)
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Abstract
Abstract Thermal oxidation products of edible oils including aldehydes, peroxides and polymerized triglycerides formed during the cooking process are increasingly debated as contributory to chronic degenerative diseases. Depending on the oil used for cooking, the source of fatty acids and its oxidation products may vary and would have a differential influence on the physiological process. Coconut oil (CO) is a medium chain triglyceride-rich edible oil used in South India and other Asia Pacific countries for cooking purposes. The present study evaluated the biological effects of thermally oxidized coconut oil (TCO) as well as its non- polar hexane (TCO H) and polar methanol (TCO-M) sub-fractions in male Wistar rats. Results showed an increase in the thiobarbituric acid reactive substances (TBARs) and conjugated diene levels in TCO, which was extracted to TCO H fraction. The animals consumed TCO and its hexane and methanol fractions had a considerable increase in weight gain. However, serum and hepatic triglycerides were increased only in animals with TCO and TCO H administration. In these animals, the hepatic redox balance was disturbed, with a reduction in GSH and a concomitant increase in thiobarbituric acid reactive substances (TBARs). Increased incidence of microvesicles in hepatic histological observations also supported this assumption. Together, the study shows that TCO consumption is unhealthy, where the nonpolar compounds generated during thermal oxidation may be involved in the toxic insults.
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