Abstract
Oxidative stress and apoptosis can disrupt the bone formation activity of osteoblasts which can lead to osteoporosis. This study was conducted to investigate the effects of γ-tocotrienol on lipid peroxidation, antioxidant enzymes activities, and apoptosis of osteoblast exposed to hydrogen peroxide (H2O2). Osteoblasts were treated with 1, 10, and 100 μM of γ-tocotrienol for 24 hours before being exposed to 490 μM (IC50) H2O2 for 2 hours. Results showed that γ-tocotrienol prevented the malondialdehyde (MDA) elevation induced by H2O2 in a dose-dependent manner. As for the antioxidant enzymes assays, all doses of γ-tocotrienol were able to prevent the reduction in SOD and CAT activities, but only the dose of 1 μM of GTT was able to prevent the reduction in GPx. As for the apoptosis assays, γ-tocotrienol was able to reduce apoptosis at the dose of 1 and 10 μM. However, the dose of 100 μM of γ-tocotrienol induced an even higher apoptosis than H2O2. In conclusion, low doses of γ-tocotrienol offered protection for osteoblasts against H2O2 toxicity, but itself caused toxicity at the high doses.
Highlights
Bone is a dynamic organ that carries out major functions of the body, which include maintenance of the mechanical integrity, body support, and regulation of mineral homeostasis
This study was conducted to investigate the effects of γ-tocotrienol on lipid peroxidation, antioxidant enzymes activities, and apoptosis of osteoblast exposed to hydrogen peroxide (H2O2)
Exposure of osteoblasts to 490 μM H2O2 for 2 hours significantly increased the MDA levels compared to the control group
Summary
Bone is a dynamic organ that carries out major functions of the body, which include maintenance of the mechanical integrity, body support, and regulation of mineral homeostasis. Bone is continually being resorped by osteoclasts and formed by osteoblasts to maintain bone volume and calcium and phosphorus homeostasis. If the balance is disturbed, the volume and quality of bone will be adversely affected, as in the case of osteoporosis. Many studies and lines of evidence have linked oxidative stress to the pathogenesis of osteoporosis. Basu et al [1] reported that there was a biochemical link between increased oxidative stress and decreased bone mineral density (BMD) in aged men and women. Maggio et al [2] found that there was a significant decrease of plasma antioxidant levels for elderly women who have osteoporosis. Oxidative stress may lead to bone loss by promoting lipid peroxidation [4, 5], lowering antioxidant enzymes [5], and promoting apoptosis of osteoblasts [6]. Several osteoporosis risk factors, such as smoking [7], hypertension [8], and diabetes mellitus [9], were related to oxidative stress
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