Tocotrienol-rich fraction from palm oil prevents oxidative damage in diabetic rats

This study was carried out to determine the effects of tocotrienol-rich fraction [TRF] [200 mg/Kg] on biomarkers of oxidative stress on erythrocyte membranes and leukocyte deoxyribonucleic acid [DNA] damage in streptozotocin [STZ]-induced diabetic rats. Male rats [n = 40] were divided randomly into four groups of 10: a normal group; a normal group with TRF; a diabetic group, and a diabetic group with TRF. Following four weeks of treatment, fasting blood glucose [FBG] levels, oxidative stress markers and the antioxidant status of the erythrocytes were measured. FBG levels for the STZ-induced diabetic rats were significantly increased [P <0.001] when compared to the normal group and erythrocyte malondialdehyde levels were also significantly higher [P <0.0001] in this group. Decreased levels of reduced glutathione and increased levels of oxidised glutathione [P <0.001] were observed in STZ-induced diabetic rats when compared to the control group and diabetic group with TRF. The results of the superoxide dismutase and glutathione peroxidase activities were significantly lower in the STZ-induced diabetic rats than in the normal group [P <0.001]. The levels of DNA damage, measured by the tail length and tail moment of the leukocyte, were significantly higher in STZ-induced diabetic [P <0.0001]. TRF supplementation managed to normalise the level of DNA damage in diabetic rats treated with TRF. Daily supplementation with 200 mg/Kg of TRF for four weeks was found to reduce levels of oxidative stress markers by inhibiting lipid peroxidation and increasing the levels of antioxidant status in a prevention trial for STZ-induced diabetic rats

role of oxidative stress and antioxidants in diabetic complications

Diabetes is considered to be one of the most common chronic diseases worldwide. There is a growing scientific and public interest in connecting oxidative stress with a variety of pathological conditions including diabetes mellitus [DM] as well as other human diseases. Previous experimental and clinical studies report that oxidative stress plays a major role in the pathogenesis and development of complications of both types of DM. However, the exact mechanism by which oxidative stress could contribute to and accelerate the development of complications in diabetic mellitus is only partly known and remains to be clarified. On the one hand, hyperglycemia induces free radicals; on the other hand, it impairs the endogenous antioxidant defense system in patients with diabetes. Endogenous antioxidant defense mechanisms include both enzymatic and non-enzymatic pathways. Their functions in human cells are to counterbalance toxic reactive oxygen species [ROS]. Common antioxidants include the vitamins A, C, and E, glutathione [GSH], and the enzymes superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GPx], and glutathione reductase [GRx]. This review describes the importance of endogenous antioxidant defense systems, their relationship to several pathophysiological processes and their possible therapeutic implications in vivo