DOI: https://doi.org/10.55373/mjchem.v26i1.197

Keywords: Tocotrienol-rich fraction; diabetes; embryo

Abstract

Palm tocotrienol-rich fraction (TRF), a well-known antioxidant, reduces the adverse effects of oxidative stress. Maternal diabetes mellitus is proposed to be responsible for impaired reproductive outcomes by increasing reactive oxygen species production, leading to oxidative stress. However, there is little evidence of whether TRF supplementation can prevent impaired reproductive outcomes in maternal diabetes. Therefore, the aim of this study was to determine the effect of palm-TRF on the quality and development of embryos and blood glucose levels in streptozotocin (STZ)-induced diabetic female mice. Forty, six-week-old female Mus musculus mice were divided into five groups: Group 1: Non-diabetic control, Group 2: STZ-induced diabetic without TRF supplementation, Group 3: Non-diabetic vehicle control, Group 4: Non-diabetic with TRF supplementation and Group 5: STZ-induced diabetic with TRF supplementation. Following induction of diabetes (by a single dose of STZ (40 mg/kg BW) given intraperitoneally for 7 days), mice were administered TRF (150 mg/kg BW) by oral gavage daily for 14 days. At the end of the treatment period, mice from all groups were superovulated, mated, and then euthanized. Embryos were retrieved and cultured. The morphology and in vitro development of embryos were monitored and recorded, and blood glucose level was analyzed. Both the percentage of normal embryos and development to the blastocyst stage was lower (p<0.05) in STZ-induced diabetic mice compared to that of the controls (Group 1). TRF supplementation was able to restore the percentage of normal embryos and their development in diabetic mice. However, two weeks of TRF supplementation was not able to reduce the blood glucose levels in STZ-induced diabetic mice. In conclusion, 150 mg/kg BW TRF supplementation for two weeks was able to overcome the diabetic-induced oxidative stress damage on the embryos and maintain their developmental capacity. However, the mechanism of action of TRF in STZ-induced diabetic mice remains to be elucidated.