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 glucocorticoidinduced 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 expressions.
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) in brain lead level in PB2T compared to PB. Even though no
significant difference (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.
Introduction: Tocotrienol exerts neuroprotective effects resulting in an improved circulating oxidative status. However, accumulation of tocotrienol due to longterm intake may exert pro-oxidant effects. Thus the effects of short- and longterm supplementation of vitamin E tocotrienol rich fraction (TRF) on the parameters of oxidative status in rat brains were determined. Methods: Wistar rats aged 3 months were supplemented with TRF for 3 or 8 months. Control groups received equivolume of distilled water. Rats were sacrificed and brains
harvested, weighed and homogenised. Supernatants were analysed for catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities, vitamin E and protein carbonyl. Results: A significant decline in the level of total vitamin E and its isomers with increasing age were found. TRF supplementation increased the level of total vitamin E with alpha-tocotrienol (ATT) being the major isomer raised. Glutathione peroxidase activity was also
significantly increased in the long-term supplemented group compared to the short-term supplemented and control groups. The results also showed significantly higher superoxide dismutase activity (p
Aging is attributed to neuronal loss associated with increased oxidative stress. Vitamin E, and in particular, tocotrienol are potent antioxidants, which have been shown to be neuroprotective. The main aim of the present study was to observe the effect of long term intake of vitamin E in the form of tocotrienol rich fraction (TRF) and refined, bleached, deodorized palm olein (RBDPO) on the brain of experimental rats.