ABSTRACT
The pathogenesis of osteoporosis is multifactorial. Oxygen-derived free radicals are involved in the formation and activation of osteoclasts (Garrett et al., 1990), leading to an increase in bone resorption and bone loss. Bone histomorphometric studies have shown that ferric nitrilotriacetate (Fe-NTA), an oxidizing agent, increased osteoclast numbers (Ebina et al., 1991) and impaired mineralization (Takeuchi et al., 1997). Osteoporotic women had signi•cantly higher plasma superoxide dismutase (SOD) enzyme activity and higher malondialdehyde (MDA) levels while glutathione peroxidase (GSH-Px) enzyme activity and nitric oxide (NO) levels were similar when compared to non-osteoporotic controls (Ozgocmen et al., 2007). A negative correlation was found between SOD and lumbar bone mineral density (BMD) levels (r = −0.328; p = 0.021). The same trend was observed between NO and lumbar BMD (r = −0.473; p = 0.001) and femoral neck BMD values (r = −0.540; p = 0.000) (Yalin et al., 2005). Low bone mineral density was associated with increased 8-iso-prostaglandin F2α, an oxidative stress biomarker (Basu et al., 2001). Based on the close association between free radicals and osteoporosis, there is reason to believe that antioxidants, notably the tocotrienols, may be effective in the prevention and treatment of osteoporosis. The most easily available source of tocotrienols in Malaysia is from palm oil. Palm cooking oil contains 178.33 ppm α-tocopherol, 188.50 ppm α-tocotrienol, 260.83 ppm γ-tocotrienol, and 69.83 ppm δ-tocotrienol (Siti Khadijah, 2011). Our studies mainly used tocotrienols extracted from palm oil in the form of tocotrienol mixtures as well as the pure γ-isomer. We used the rat as our animal model since previous studies have shown that their bone anatomy, bone remodeling, and response to treatment are similar to humans (Abe et al., 1993, Mosekilde, 1995).
