Abstract:
Coconut oil meal, a cheap by-product of coconut oil production, is a rich source of phenolic antioxidants. Many age-related
diseases are caused by reactive oxygen species- (ROS-) induced damage to macromolecules such as lipids, proteins, and DNA. In
the present study, the protective effect of the phenolic extract of coconut oil meal (CMPE) against macromolecular oxidative
damage was evaluated using in vitro and in vivo models. Sunflower oil, bovine serum albumin (BSA), and plasmid DNA were used
in the in vitro study, and thiobarbituric acid reactive substances (TBARS), protein carbonyl, and nicked DNA were evaluated as
oxidation products. )e inhibitory effect of CMPE against H2O2-induced macromolecular damage was evaluated using cultured
HEp-2 cells. )e results indicate that CMPE inhibits macromolecular damage both in vitro and in vivo. In addition, CMPE
regulates redox status of HEp-2 cells under oxidative stress conditions by maintaining higher reduced glutathione levels. )ere
was no significant difference in the expression of glutathione peroxidase in stressed and unstressed cells suggesting that CMPE
regulates the cellular oxidative stress responses without affecting the expression of oxidative stress response genes. Oral feeding of
Wistar rats with CMPE improves the serum and plasma antioxidant status without causing any toxic effects.
