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The present study was designed to investigate the effect of glycemic load (GL) on brain and cardiac mitochondrial integrity. The effect of high glycemic load (HGL) and low glycemic load (LGL) diets on the generation of free radicals and its consequent effect on brain and cardiac mitochondrial were assessed. The effect of the reactive oxygen species (ROS) on the activities of electron transport chain (ETC) was examined. A significant decline in enzyme activities of complex I, III and IV were observed, for both brain and cardiac mitochondria ETC. Brain rotenone-sensitive complex I activities decreased by 49.20% (p>0.05) in HGL-fed rats, while antimycin-a sensitive complex III decreased by 19.80% (p>0.05). Same phenomenon was observed in potassium cyanide (KCN)-sensitive complex IV (cytochrome c oxidase), which decreased by 30.17% (p>0.05). For cardiac mitochondrial complexes, Rotenone-sensitive complex I decreased by 25.45% (p>0.05) in HGL fed group, while antimycin-a sensitive complex III activity decreased by 24.78% (p>0.05). Glycemic related changes were also observed in KCN-sensitive complex IV with a decrease of 21.18% (p>0.05). Enzyme activities in both brain and cardiac mitochondrial homogenates decrease minimally in LGL fed rats, compared with the control. Thiol group content, total protein and malondialdehyde (MDA) were found to be significantly elevated in rats fed with HGL diet. Superoxide dismutase (SOD) and catalase (CAT) enzymes activities decreased in both brain and cardiac mitochondria of rats fed with HGL diets. It can be concluded that low glycemic load diet sustains the mitochondrial integrity. Whereas, HGL diets induced oxidative stress and degenerates antioxidant enzymes activities in brain and heart mitochondria; thereby inducing loss of mitochondrial integrity.
Published Date: 2019-02-07; Received Date: 2019-01-20