Ovarian aging has been associated with oxidative stress and loss of ovarian function. Tocotrienol has been proven to exert beneficial effects on the female reproductive system. However, the role of tocotrienol in affecting metabolism in the ovary and subsequently improving the quality of oocytes in aging mice remains unknown. Therefore, the relationship between metabolic changes in the ovary and the quality of oocytes in aging mice following tocotrienol-rich fraction (TRF) supplementation was investigated. Six-week-old female mice were used as the Young group. Six-month-old aged female mice were divided into four groups; the first group was given tocopherol-stripped corn oil (vehicle control) while the other three groups were supplemented with TRF at the dose of 90, 120, and 150 mg/kg, respectively. The treatment was given orally for two months. At the end of the treatment, mice from all groups were superovulated and then euthanised. Oocyte quality was assessed and non-targeted metabolomic analysis of the ovarian tissues was performed using liquid chromatography-tandem mass spectrometry of quadrupole time-of-flight (LC-MS Q-TOF). Percentages of normal oocytes were higher (p<0.001) while abnormal oocytes were lower (p<0.001) in TRF 150 mg/kg group compared to that of the control. Seventeen metabolites were identified to be significantly different in the ovarian tissue of the aging group when compared to the young group. 14 metabolites were identified to be significantly different in the ovarian tissue between the control and TRF supplemented groups. Pathway analysis revealed significantly altered metabolic pathways for fatty acid and amino acid metabolism that might influence the quality of oocytes. In conclusion, TRF supplementation causes metabolic changes in the ovary that delay the consequences of aging, thus improving the quality of oocytes in aging mice.

Introduction: HbE is the commonest beta haemoglovin (Hb) variant in Southeast Asia. It causes a reduction in synthesis of beta-globin E (βE) chain. Studies indicate HbE coinherited with α-thalassaemia leads to a milder clinical phenotype. This study investigates the concomitant inheritance of α-thalassaemia in Malays with HbE. Methods: Four hundred and fourteen (414) blood samples were screened for haemoglobinopathy using primarily the first 3 steps of the BHES [(B) blood counts, blood film: (H), HPLC; (E),elstrophoresis; (S),stability)] protocol. Complete blood counts were generated on an automated blood cell analyser, HB typing with cation exchange high-performance liquid chromatography (HPLC) and Hb typing with cation exchange high-performance liquid chromatography (HPLC) and Hb electrophoresis at an alkaline pH (pH 8.5). Forty-five (10.9%) were identified as HbE trait and DNA analysis was done for deletional α-thalassaemia using a single-tube multiplex-PCR assay. Results: Among the 45 subjects with HbE trait. 4 (8.9%) were found to have alpha-thalassaemia-2 (α⁺) (α-3.7 kb deletion) and 1 (2.2%) the alpha-thalassaemia-1 (α⁰) (—SEA 20.5kb deletion) defects respectively. Discussion: These findings show that 11.1% of Malays with HbE inherit alpha-thalassaemia concurrently. The most prevalent interaction found was a double heterozygote for HbE/α-thalassaemia 2, followed by HbE/α-thalassaemia 1. Conclusion: Molecular screening of deletional α-thalassaemia identified its concurrent inheritance in 11.1% of Malays who were HbE carriers. This information will guide genetic counseling and the planning of treatment modalities in patients with HbE alpha-thalassaemia.