Vitamin E reversed nicotine-induced toxic effects on bone biochemical markers in male rats

Abstract

IntroductionVitamin E is beneficial in restoring bone histomorphometric parameters in nicotine-treated rats. This study determined the effectiveness of 3 forms of vitamin E in restoring bone metabolism in nicotine-treated rats.Material and methodsThirty-five male Sprague-Dawley rats were divided into 5 groups: (1) control (C), (2) nicotine cessation (NC), (3) α-tocopherol (ATF), (4) tocotrienol-enhanced fraction (TEF) and (5) γ-tocotrienol (GTT). Treatment was carried out for 4 months. The control group was administered normal saline and olive oil throughout the treatment period while treatment for groups 2-5 was performed in 2 phases. In the first phase, the groups received nicotine 7 mg/kg intraperitoneally for 2 months. The following 2 months, group 2 received normal saline and olive oil while groups 3-5 received ATF, TEF or GTT, 60 mg/kg orally. Pre-treatment and post-treatment serum was collected for bone biochemical marker measurement using the ELISA method.ResultsNicotine increased serum bone-resorbing cytokines (interleukin-1 and interleukin-6) and the bone resorption marker pyridinoline (PYD) while reducing the bone formation marker osteocalcin after 2 months of nicotine treatment. The parameters failed to improve after nicotine was stopped for 2 months. Supplementation with the 3 forms of vitamin E improved the parameters, i.e. reduced the cytokines and pyridinoline as well as increased the osteocalcin. In addition, the TEF and GTT groups had a higher level of osteocalcin than the control group.ConclusionsNicotine impaired bone metabolism and cessation of nicotine treatment did not reverse the effects. Vitamin E, especially the tocotrienols, restored bone metabolism that was impaired due to nicotine.

Effects of nicotine in the presence and absence of vitamin E on morphology, viability and osteogenic gene expression in MG-63 osteoblast-like cells

“…Evidence shows that vitamin E can reverse nicotineinduced toxic effects on bone biochemical markers and osteogenic gene expression [5,6]. These findings were in line with our results, which showed that the negative effects of 5 mM nicotine on ALP/BSP/OC expression significantly decreased in the presence of 5 mM vitamin E to the normal level.…”

“…Furthermore, animal experiments showed that oxidative stress induced by nicotine affected bone metabolism by down-regulating the expression of osteogenic genes [14]. Vitamin E possesses antioxidant properties, and it was shown that it up-regulated osteogenic gene expression in nicotine-treated rats [6] and improved structural, dynamic and cellular histomorphometric parameters of bone [4,5,40,41].…”

“…In addition, vitamin E has been reported to suppress pro-inflammatory cytokines such as interleukins (e.g. IL-1 and IL6) and decrease osteoclastic bone resorption [5]. Vitamin E supplementation in rats increased the biomechanical strength of bone, its degree of mineralization and rate of bone formation [21].…”

“…Nicotine as the main toxic component of cigarette smoke increases oxidative stress due to the formation of free radicals [3]. Animal studies have indicated that oxidative stress due to the effects of nicotine affects bone metabolism and delays bone healing [4][5][6][7]. Reactive oxygen species stimulate osteoclast differentiation [8][9][10] and inhibit the differentiation of osteoblasts [11,12].…”

Vitamin E homologues α- and γ-tocopherol are not associated with bone turnover markers or bone mineral density in peri-menopausal and post-menopausal women

“…Observational studies have found that individuals with lower intakes of dietary vitamin E intake had increased risk of hip fracture [4,5], and osteoporotic, postmenopausal women had lower plasma levels of vitamin E [6,7]. Animal models of nicotine exposure, when given α-tocopherol, had increased bone formation, reversal of bone loss [8] and decreased circulating concentrations of inflammatory cytokines [9]. Dose may be critical, as high concentrations of α-tocopherol in cell media did not support viability of osteoblasts [10] and have been shown to be pro-oxidants [11].…”