Long-Term Nikotine Administration Impairs Blood Parameters and Femoral Bone Tissue Structure in an Osteoporosis Model of Rats (original) (raw)
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Effects of nicotine on markers of bone turnover in ovariectomized rats
Pan African Medical Journal
Introduction: osteoporosis is characterized by low bone mass and density, as well as change in microarchitecture of bone tissue leading to decreased bone strength. In vitro research shows nicotine can increase osteoblast activity and proliferation, also suppress osteoclast activity. Therefore we explore nicotine anti-resorptive property by in vivo true experimental and randomized posttest only controlled group research that was conducted in 18-20 weeks old Rattus norvegicus. Methods: twenty-five female rats were divided into five groups, with 5 rats per group. The first group represented normal rats (Sham), while the second to fifth group underwent bilateral ovariectomy. The second group serves as positive control group (ovariectomy-only/OVX). The third to fifth group serve as dose 1 (P1-0.25mg/kg), dose 2 (P2-0.5 mg/kg), and Dose 3 (P3-0.75 mg/kg) treatment group receiving daily per-oral nicotine for 28 days, started 3 weeks post-ovariectomy. After 28 days treatment, the serum was checked. Results: nicotine has dose-dependent manner on serum osteocalcin and serum DPD level. Level of osteocalcin in P2 group was significantly lower (Mann-Whitney, p = 0.008) compared to OVX group (59.4% lower). Level of DPD in all group was not significantly different (ANOVA, p < 0.05) but shows lowest level in P2 group. For serum calcitonin level, there's no significant different between groups. Conclusion: nicotine at right low-dose might be able to inhibit osteoclast activity, thus open a possibility of anti-resorptive property of nicotine.
Nicotine induced proliferation and cytokine release in osteoblastic cells
International Journal of Molecular Medicine, 2006
Smoking has deleterious effects on osteoporosis and periodontitis both characterized by bone loss. Smoking also interferes with the protective effect that hormone replacement therapy (HRT) has on bone loss. Our study investigated two mechanisms by which smoking may affect bone metabolism: nicotine-induced proliferation and nicotine-induced cytokine secretion in osteoblasts. Two osteoblastic cell models were used: mouse osteoblasts derived from mouse calvaria and human osteoblasts. Thymidine incorporation and immunoassays were used to evaluate proliferation, interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) secretion. Parametric and nonparametric statistical analyses were used for comparisons. The results showed that nicotine induced stimulation and inhibition of proliferation in both osteoblastic cell models. In human osteoblasts, the proliferative and inhibitory effects were also donor dependent. Il-6 secretion showed different patterns in mouse and human osteoblasts. In mouse osteoblasts, nicotine significantly increased IL-6 secretion and estradiol significantly inhibited the nicotine-induced IL-6 release. In human osteoblasts, cells derived from one subject did not respond to nicotine. However, in the second sample, nicotine increased secretion of Il-6 but estradiol did not oppose this effect. In human osteoblasts, nicotine also induced an increase in the TNF-alpha secretion and estradiol opposed this increase. These results suggest that nicotine affects bone metabolism by modulating proliferation, and Il-6 and TNF-alpha secretion. These studies provide a possible explanation for differences in bone loss among subjects who smoke and offer a possible mechanism for the oppositional effect of smoking on HRT in subjects with bone loss.
Effect of Nicotine on RANKL and OPG and Bone Mineral Density
Journal of Investigative Surgery, 2014
Aim: The signaling pathway OPG/RANK/RANKL is a key in maintaining the balance between the activity of osteoblasts and osteoclasts in order to prevent bone loss. In this study, our aim was to assess the effects of longterm nicotine exposure on plasma RANKL and OPG levels, tissue RANKL and OPG immunoreactivities, and bone mineral density (BMD) scores in rats. Materials and Methods: Thirty-six Swiss Albino rats weighing 70 ± 10 g were divided into three groups. While the controls (n = 12) were only given normal drinking water, for lowdose nicotine (LDN) group (n = 12) 0.4 mg/kg/day; for high-dose nicotine (HDN) group (n = 12), 6.0 mg/kg/day nicotine was added to drinking water for a year. At the end of 12th month, BMD scores were measured using an Xray absorptiometry and bone turnover was assessed by measuring plasma RANKL and OPG levels and RANKL and OPG immunoreactivities in tail vertebrae of the rats. Results: There was no statistically significant difference in BMD scores of lumbar spine and femoral regions of the nicotine groups in comparison to controls. Plasma OPG levels were found to be significantly higher in HDN group, in comparison to the controls and LDN groups (p = .001) unlike plasma RANKL levels. Tissue RANKL and OPG immunoreactivities decreased significantly in the LDN and HDN groups (p < .001, p < .01, respectively). Conclusions: The results of this study show that nicotine is not primarily responsible for the decrease in BMD frequently seen in smokers. Measuring plasma RANKL and OPG levels did not reflect tissue immunoreactivities.
Archives of Gynecology and Obstetrics, 2012
Purpose To evaluate the effect of long-term low or high-dose nicotine exposure on bone mass via measuring bone mineral density (BMD) and oxidant-antioxidant status markers. Methods Thirty-five female Swiss Albino rats weighing 70 ± 10 g were divided as the control group (n = 12), low-dose nicotine group (n = 12) and high-dose nicotine group (n = 11). While the control group was given only normal drinking water, the low-dose nicotine group had 0.4 mg/kg per day and the high-dose nicotine group, 6.0 mg/kg per day of nicotine added to their water for the period of 1 year. BMD was determined with X-ray absorptiometry of lumbar vertebra, corpus femoris, proximal and distal femur. To evaluate oxidant-antioxidant status malondialdehyde (MDA) levels, superoxide dismutase (SOD) and catalase (CAT) activities were determined. Results When comparing the nicotine groups and controls, neither BMD nor oxidant-antioxidant status markers showed any statistically significant difference. In comparison to the controls, 12 months of high-dose oral nicotine exposure did not have a significant effect on BMD and low-dose nicotine exposure led to a statistically insignificant increase in BMD. Conclusions Contrary to common belief, the results of this study show that nicotine is not responsible for the decrease in BMD leading to osteoporosis frequently seen in smokers. However, there is a need to explore the other harmful materials in tobacco which may be responsible for the alterations seen in BMD of smokers.
Effect of nicotine on bone healing in rats - A histological study
2014
Background & Objectives: Nicotine is the major alkaloid in tobacco products ( Nicotiona tabacum ) and a psychoactive ingredient responsible for the Central Nervous System (CNS) effects and tobacco addiction. It's been reported to have effects directly on the small blood vessels in producing vasoconstriction and increased vascular resistance that exerts on the microvasculature inhibiting the angioblastic response during re- vascularization and limits the recruitment of cytokines, Bone Morphogenic Proteins (BMPs), Transforming Growth Factor - � (TGF - �), Platelet Derived Growth Factor (PDGF) and the basic Fibroblast Growth Factor (FGF). This leads to inhibition of re-epithelialization, osteogenesis and cellular healing. This study intends to demonstrate histologically the effect of nicotine on bone healing and the healing of bone defects incorporated with autogenous bone graft in an animal model. Methods: 60 female Wistar rats were used in the study. Nicotine hemisulfate at a dos...
Global spine journal, 2012
Previous studies by our group showed that nicotine delivered via a transdermal nicotine patch significantly enhanced posterior spinal fusion rates in rabbits. Nicotine transdermal patches provide a steady serum level; there may be a dose-dependent effect of nicotine on posterior spinal fusion. In an in vitro cell culture model of rabbit bone marrow-derived osteoblast-like cells, cells were exposed to different concentrations of nicotine (0, 20, 40, 80 ng/mL and 10, 100, 250 μg/mL). Wells were stained with an alkaline phosphatase (ALP) staining kit to determine ALP enzyme activity. Cells were stained with Von Kossa for mineralization. A two-way analysis of variance (ANOVA) using dose and time as variables showed significant differences among groups; post hoc analysis showed that the 100-μg/mL dose of nicotine significantly enhanced ALP activity over controls. A one-way ANOVA using dose as the variable showed that the 100- and 250-μg/mL doses had significantly greater mineralization t...