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Researches have shown the relevance of antioxidants in the management of several diseases. In the present study, the effects of quercetin and vitamin E were investigated on the mitochondrial functions in vivo and in silico.Structures of quercetin and vitamin E were docked against mitochondrial Adenosine triphosphatase (mATPase), and cytochrome c cavity. Activity of liver mATPase and mitochondrial permeability transition pore opening were determined by spectrophotometry and activation of cytochrome c was examined by immunohistochemistry.The binding energy of vitamin E (-9 Kcal/mol) in mATPase cavity compares well with glibenclamide (-9.4 Kcal/mol), while quercetin had a binding energy of -7.1 Kcal/mol. Similarly, vitamin E, quercetin were bound to cytochrome c by -6.4 and - 5.5 Kcal/mol energy, while glibenclamide had -7.0 Kcal/mol binding energy. The results showed that vitamin E was more accessible to the protoporphyrin prosthetic group in cytochrome c than quercetin. In the experimental studies, it was validated that vitamin E inhibited the uncontrolled activity of mATPase in diabetic rat liver. This was also proven and tested on the liver mitochondrial permeability transition pore opening observed in diabetic rats. Further experimental assessment of these on activation of cytochrome c showed that vitamin E reduced the extent of the activation more than quercetin and glibenclamide.There is a favorable protein-ligand interaction between quercetin and vitamin E in certain apoptotic proteins implicated in diabetes complications. |
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