Tocotrienol-Rich Fraction from Palm Oil Prevents Oxidative Damage in Diabetic Rats

• Main Authors: Fatmah A. Matough, Siti B. Budin, Zariyantey A. Hamid, Mariati Abdul-Rahman, Nasar Al-Wahaibi, Jamaludine Mohammed
• Format: Article
• Language: English
• Published: Sultan Qaboos University 2014-02-01
• Series: Sultan Qaboos University Medical Journal
• Subjects: antioxidants; diabetes mellitus; oxidative stress; tocotrienols.
• Online Access: https://journals.squ.edu.om/index.php/squmj/article/view/1889

Objectives: 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. Methods: 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. Results: 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. Conclusion: 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.