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

Fatmah A Matough1, Siti B Budin2, Zariyantey A Hamid2

  • 1Department of Biology, Faculty of Science, Sabha University, Sabha, Libya;

Abstract

Insights

Tocotrienol-rich fraction (TRF) supplementation in diabetic rats significantly reduced oxidative stress markers and DNA damage. TRF also improved antioxidant status, offering a potential therapeutic strategy for diabetes-related complications.

Area of Science:

  • Biochemistry and Molecular Biology
  • Endocrinology and Metabolism
  • Toxicology and Pharmacology

Background:

  • Diabetes mellitus, induced by streptozotocin (STZ), is characterized by hyperglycemia and increased oxidative stress.
  • Oxidative stress contributes to erythrocyte membrane damage and deoxyribonucleic acid (DNA) damage in diabetic individuals.
  • Tocotrienols, components of Vitamin E, possess antioxidant properties that may mitigate oxidative damage.

Purpose of the Study:

  • To investigate the efficacy of tocotrienol-rich fraction (TRF) in ameliorating oxidative stress and DNA damage in STZ-induced diabetic rats.
  • To assess the impact of TRF on key oxidative stress biomarkers and antioxidant status in erythrocytes.
  • To evaluate TRF's effect on leukocyte DNA damage in a diabetic rat model.

Main Methods:

  • Forty male rats were randomly assigned to four groups: normal, normal with TRF, diabetic (STZ-induced), and diabetic with TRF.
  • Animals received daily treatment of 200 mg/Kg TRF for four weeks.
  • Fasting blood glucose, erythrocyte oxidative stress markers (malondialdehyde, reduced/oxidised glutathione, superoxide dismutase, glutathione peroxidase), and leukocyte DNA damage (tail length, tail moment) were measured.

Main Results:

  • STZ-induced diabetic rats exhibited significantly elevated fasting blood glucose and erythrocyte malondialdehyde levels.
  • Diabetic rats showed decreased reduced glutathione and superoxide dismutase/glutathione peroxidase activities, indicating heightened oxidative stress.
  • Leukocyte DNA damage was significantly increased in diabetic rats, while TRF supplementation normalized these markers in treated diabetic rats.

Conclusions:

  • Daily supplementation with 200 mg/Kg TRF for four weeks effectively reduced oxidative stress markers in STZ-induced diabetic rats.
  • TRF demonstrated a significant inhibition of lipid peroxidation and enhanced antioxidant status in the diabetic rat model.
  • These findings suggest TRF holds potential as a preventative agent against oxidative stress and DNA damage associated with diabetes.