RESUMO
Long term glucocorticoids administration induces oxidative stress which leads to alteration of bone structure and strength. Palm oil is rich in tocotrienol, an antioxidant. It can be used for the prevention of oxidative stress related diseases. The main objective of this study was to determine the mechanism of palm tocotrienol in maintaining the bone structure and strength in glucocorticoid-induced osteoporosis. Thirty two adult male Sprague-Dawley rats, aged 3 months, weighing 300-320 g rats were used in this study. Sixteen rats undergone adrenalectomy and were administered with 120μg/kg/day intramuscular injection of dexamethasone. Eight rats were supplemented with oral palm tocotrienol 60 mg/kg/day (Adrx+Dex+PTT) and the other eight rats were given oral vehicle palm olein 0.1 ml/kg/day (Adrx+Dex). Eight rats underwent sham procedure and were given vehicle palm olein 0.05 ml/kg/day by intramuscularly and oral 0.1 ml/kg/day (Sham). The rats were euthanized after two months of treatments. Eight rats were euthanized after acclimatic action without receiving any treatment (Baseline). The right femurs were used for bone biomechanical strength and histomorphometry analysis while the left for gene expression and oxidative stress enzymes activities. The results indicated that long-term glucocorticoid treatment significantly increased bone resorption marker, CTX (6060.7 ± 410 pg/ml) and decreased bone structure and strength. Osteoblast and osteoclast related genes expressions indicated an increase in bone turnover. Supplementation of palm tocotrienol had maintained serum resorption (2619.4 + 209 pg/ml) marker level and preserved bone structure and strength. Gene expression analysis showed decrease in bone resorption. The findings suggested that palm tocotrienol has potential benefits against glucocorticoid-induced osteoporosis by regulating osteoblast and osteoclast related gene expression
RESUMO
The occurrence of severe lead (Pb) poisoning has risen in certain countries. There is increasing evidence that chronic lead exposure disturbs the prooxidant: antioxidant balance in the brain tissue and alters brain histology. The present study observed the antioxidant effect of tocotrienol-rich fraction (TRF) on brain tissues of the experimental rats following lead poisoning. Eighteen (n=18) male Sprague-Dawley rats, 6-weeks old, were randomly divided into control (CTRL) group and experimental groups; fed with 0.2% w/v lead acetate, as PB2 group; and fed with 0.2% w/v lead acetate and daily TRF supplementation (200 mg/kg body weight) as PB2T group. The experiment was conducted for 30 days. At the end of the study, the brain tissues were harvested and histopathological changes of the hippocampal region were observed. Biochemical findings such as brain lead, TRF and malondialdehyde (MDA) levels, and erythrocyte superoxide dismutase (SOD) activity were determined. It was observed that atypical apoptotic-like and disorganized neurons were present in the hippocampal region of the untreated PB2 group compared to PB2T group. Biochemical parameters showed a significant decrease (p 0.05) was obtained for MDA level, there was a significant increase (p < 0.05) in the erythrocyte SOD activity in PB2T compared to PB2 and CTRL. Supplementation with TRF improved histopathological changes in the brain tissues caused by lead exposure in drinking water by reducing lead accumulation in the brain of experimental rats.