Effects of vitamin E on receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG) in rats treated with nicotine.

Vitamin E is found to reverse the effects of nicotine on bone and this study aimed to determine its mechanism. Male Sprague Dawley rats were divided into four groups and treated for 3 months: Group 1 was the control group (RC). Groups 2 (N), 3 (N+TT) and 4 (N+ATF) received nicotine 7 mg/kg throughout the treatment period. In addition, groups 3 and 4 received tocotrienol 60 mg/kg and alpha-tocopherol 60 mg/kg respectively during months 2 and 3. Parameters measured were serum osteoprotegerin (OPG), serum receptor activator of nuclear factor kappa B ligand (RANKL), femoral and lumbar bone calcium content and body weight. Nicotine did not affect OPG or RANKL levels but reduced bone calcium content suggesting the calcium loss is not due to increase osteoclastogenesis. OPG was increased in N+ATF while RANKL was slightly increased in N+TT. Both vitamin E supplements restored bone calcium loss induced by nicotine. Nicotine impaired weight gain in all treatment groups starting week 4 however, N+TT group was comparable to RC from week 6 onwards. Bone protective effects of ATF, but not TT, may be partly due to inhibition of osteoclastogenesis.

Effects of vitamin E supplementation on bone metabolism in nicotine-treated rats.

INTRODUCTION: Nicotine has been shown to exert negative effects on bone. This study determined whether vitamin E supplementation is able to repair the nicotine-induced adverse effects in bone. METHODS: 24 male rats were divided into three groups. The fi rst group was the baseline control and killed untreated at the beginning of the study. Groups 2 and 3 received nicotine at 7 mg per kg for three months but during the second and third months, group 2 was supplemented with alpha-tocopherol (N+ATF) while group 3 was given palm tocotrienol mixture (N+TT). Serum interleukin-1 (IL-1), serum interleukin-6 (IL-6), serum osteocalcin, urine deoxypyridinoline (DPD) and bone calcium content were measured. RESULTS: Palm tocotrienol mixture was able to prevent the increment of IL-1 and IL- 6 due to nicotine treatment. No changes were seen in the osteocalcin levels, but the N+ATF group had lower urine DPD levels after treatment. However, bone-remodelling index revealed no significant changes. No significant differences were seen in the femoral bone calcium content results, although the fourth lumbar bone calcium content was reduced in both groups with 66.5 percent reduction in the N+ATF group and 59.6 percent reduction in the N+TT group. CONCLUSION: Palm tocotrienol mixture was better than alpha-tocopherol in reversing the effects of nicotine on IL-1 and IL-6. Both forms of vitamin E were not able to restore the nicotine-induced bone calcium loss, but the N+ATF group suffered a greater loss. Tocotrienol seemed to be superior to alpha-tocopherol in combating against the adverse effect of nicotine.