Relationship between Coordination Structure and Biological Activity of Copper(II) Nicotinate

The copper（Ⅱ） complexes of pyridine-3-carboxylic acid （nicotinic acid） and pyridine-2-carboxylic acid （isonicotinic acid） were synthesized, and their structures were characterized by elemental analysis, infrared spectrum, powder X-ray diffraction and so on. The results show that under experimental conditions, the ligands of synthesized copper nicotinate and copper isonicotinate are coordinated simultaneity with copper（Ⅱ） via the nitrogen of pyridine group and an oxygen of carboxylic acid group to form bidentate chelates. The crystal of copper nicotinate with two six-membered chelate rings belongs to monoclinic system, while that of copper isonicotinate having two five-membered chelate rings is of triclinic system. The tests show that the biological activities, such as the improvement of feed utilization, growth, anti-oxidation ability of organism and disease-resistant power, are different when copper nicotinate, copper inicotinate, copper-lysine chelate, copper-methionine chelate and copper sulphate are added in pig＇s feed, respectively. Due to its higher biological activity, less pollution and lower toxicity, copper nicotinate has wide potential applications as a feed additive.

Low-temperature Heat Capacities and Thermodynamic Properties of Solid State Coordination Compound Zn(nicotinate)_2·H_2O(s)

A novel compound-monohydrated zinc nicotinate was prepared via room temperature solid phase synthesis and ball grinding.FTIR,chemical and elemental analyses and X-ray powder diffraction technique were applied to characterizing the structure and composition of the complex.Low-temperature heat capacities of the solid coordination compound were measured by a precision automated adiabatic calorimeter over a temperature range from 77 to 400 K.A solid-solid phase transition process occurred in a temperature range of 321―342 K inferred according to the heat capacity curve,and the peak temperature,molar enthalpy and entropy of the phase transition of monohydrated zinc nicotinate were determined to be Ttrs=（340.584±0.829） K,ΔtrsHm=（12.682±0.041） kJ/mol and ΔtrsSm=（37.235±0.101） KJ/mol）.The experimental values of the molar heat capacities in the temperature regions of 77―321 K and 342―400 K were,respectively,fitted to two polynomial equations.In addition,the polynomial fitted values of the molar heat capacities and fundamental thermodynamic functions of the sample relative to the standard reference temperature 298.15 K were calculated and tabulated at intervals of 5 K.

Sensitive voltammetric determination of xanthinol nicotinate at a carbon nanotubes-ionic liquid gel modified electrode

The electrochemistry of xanthinol nicotinate （Xan） was studied by cyclic voltammetry at a glassy carbon electrode modified by a gel containing multi-walled carbon nanotubes （MWNTs） and room-temperature ionic liquid of 1-butyl-3-methylimidazolium hexafluorophosphate （BMIMPF6）. The modified electrode exhibited good promotion to the electrochemical oxidation of Xan and an ultrasensitive electrochemical method was proposed for the determination of Xan. This method was successfully applied to the determination of Xan in Xan tablets. C 2009 XiaoYu Bao. Published by Elsevier B.V. on behalf of Chinese Chemical Society. All rights reserved.

Synthesis and Characterization of a Silver(Ⅰ)-indium(Ⅲ) Heterometallic Metalorganic Framework Based on Nicotinate

A heterometallic metal-organic framework, Agln（nicotinate）4.1.5DMF, was obtained from the reaction of nicotinic acid, AgNO3 and In（NO3）3 in DMF. The complex was characterized by elemental analysis, infrared spectrum, thermogravimetric analysis, powder X-ray diffraction and single-crystal X-ray diffraction. Crystal data are： C28.5H26.5N55O9.5Agln, orthorhombic space group/222, a = 10.775（15）, b = 11.939（18）, c = 13.93（2） A, V= 1792（5） A3, Z = 2, Dc = 1.521 mg/m3,μ = 1.244 mm1, F（000） = 816, the final R = 0.0672 and wR= 0.1812 for 1912 observed reflections with I 〉 2σ（I）. Single-crystal X-ray structure analysis reveals that nicotinate bridges In（III） and Ag（I） through carboxylate chelating with In（III） and pyridyl nitrogen atom coordinating to Ag（I）, generating a new 2D network consisting of tetrahedral building units of [AgN4]＋ and [In（COO）4]-.

MeNA, Controlled by Reversible Methylation of Nicotinate, Is an NAD Precursor that Undergoes Long-Distance Transport in Arabidopsis

Nicotinamide adenine dinucleotide （NAD） biosynthesis, including synthesis from aspartate via the de novo pathway and from nicotinate （NA） via the Preiss-Handler pathway, is conserved in land plants. Diverse spe-cies of NA conjugates, which are mainly involved in NA detoxification, were also found in all tested land plants. Among these conjugates, MeNA （NA methyl ester） has been widely detected in angiosperm plants, although its physiological function and the underlying mechanism for its production in planta remain largely unknown. Here, we show that MeNA is an NAD precursor undergoing more efficient long-distance trans-port between organs than NA and nicotinamide in Arabidopsis. We found that Arabidopsis has one meth- yltransferase （designated AtNaMT1） capable of catalyzing carboxyl methylation of NA to yield MeNA and one methyl esterase （MES2） predominantly hydrolyzing MeNA back to NA. We further uncovered that the transfer of [^14C]MeNA from the root to leaf was significantly increased in both MES2 knockdown and NaMTl-overexpressing lines, suggesting that both NaMT1 and MES2 fine-tune the long-distance transport of MeNA, which is ultimately utilized for NAD production. Abiotic stress （salt, abscisic acid, and mannitol） treatments, which are known to exacerbate NAD degradation, induce the expression of NaMT1 but sup-press MES2 expression, suggesting that MeNA may play a role in stress adaption. Collectively, our study indicates that reversible methylation of NA controls the biosynthesis of MeNA in Arabidopsis, which pre-sumably functions as a detoxification form of free NA for efficient long-distance transport and eventually NAD production especially under abiotic stress, providing new insights into the relationship between NAD biosynthesis and NA conjugation in plants.

Brain dysfunctions and neurotoxicity induced by psychostimulants in experimental models and humans:an overview of recent findings

Preclinical and clinical studies indicate that psychostimulants,in addition to having abuse potential,may elicit brain dysfunctions and/or neurotoxic effects.Central toxicity induced by psychostimulants may pose serious health risks since the recreational use of these substances is on the rise among young people and adults.The present review provides an overview of recent research,conducted between 2018 and 2023,focusing on brain dysfunctions and neurotoxic effects elicited in experimental models and humans by amphetamine,cocaine,methamphetamine,3,4-methylenedioxymethamphetamine,methylphenidate,caffeine,and nicotine.Detailed elucidation of factors and mechanisms that underlie psychostimulant-induced brain dysfunction and neurotoxicity is crucial for understanding the acute and enduring noxious brain effects that may occur in individuals who use psychostimulants for recreational and/or therapeutic purposes.

Resting-state electroencephalography theta predicts neurofeedback treatment 4-month follow-up response in nicotine addiction

Background The high rate of long-term relapse is a major cause of smoking cessation failure.Recently,neurofeedback training has been widely used in the treatment of nicotine addiction;however,approximately 30%of subjects fail to benefit from this intervention.Our previous randomised clinical trial(RCT)examined cognition-guided neurofeedback and demonstrated a significant decrease in daily cigarette consumption at the 4-month follow-up.However,significant individual differences were observed in the 4-month follow-up effects of decreased cigarette consumption.Therefore,it is critical to identify who will benefit from pre-neurofeedback.Aims We examined whether the resting-state electroencephalography(EEG)characteristics from pre-neurofeedback predicted the 4-month follow-up effects and explored the possible mechanisms.Methods This was a double-blind RCT.A total of 60 participants with nicotine dependence were randomly assigned to either the real-feedback or yoked-feedback group.They underwent 6 min closed-eye resting EEG recordings both before and after two neurofeedback sessions.A follow-up assessment was conducted after 4 months.Results The frontal resting-state theta power spectral density(PSD)was significantly altered in the real-feedback group after two neurofeedback visits.Higher theta PSD in the real-feedback group before neurofeedback was the only predictor of decreased cigarette consumption at the 4-month follow-up.Further reliability analysis revealed a significant positive correlation between theta PSD pre-neurofeedback and post-neurofeedback.A leave-one-out cross-validated linear regression of the theta PSD pre-neurofeedback demonstrated a significant correlation between the predicted and observed reductions in cigarette consumption at the 4-month follow-up.Finally,source analysis revealed that the brain mechanisms of the theta PSD predictor were located in the orbital frontal cortex.Conclusions Our study demonstrated changes in the resting-state theta PSD following neurofeedback training.Moreover,the resting-state theta PSD may serve as a prognostic marker of neurofeedback effects.A higher resting-state theta PSD predicts a better long-term response to neurofeedback treatment,which may facilitate the selection of individualised interventions.

Prenatal and postnatal drug exposure:focus on persistent central effects

Clinical studies indicate significant use of prescription,nonprescription and social/recreational drugs by women during pregnancy;however,limited knowledge exists about the detrimental effects that this practice may have on the developing central nervous system of the fetus.Importantly,few experimental and clinical data are available on how gestational exposure could exacerbate the effects of the same or a different drug consumed by the offspring later in life.The present review summarizes recent findings on the central toxicity elicited by several classes of drugs,administered prenatally and postnatally in experimental animals and humans,focusing on prescription and nonprescription analgesics,anti-inflammatory agents,alcohol and nicotine.

Vagus nerve stimulation protects against cerebral injury after cardiopulmonary resuscitation by inhibiting inflammation through the TLR4/NF-κB and α7nAChR/JAK2 signaling pathways

BACKGROUND: Our previous research proved that vagus nerve stimulation(VNS) improved the neurological outcome after cardiopulmonary resuscitation(CPR) by activating α7 nicotinic acetylcholine receptor(α7nAChR) in a rat model, but the underlying mechanism of VNS in neuroprotection after CPR remains unclear.METHODS: In vivo, we established a mouse model of cardiac arrest(CA)/CPR to observe the survival rate, and the changes in inflammatory factors and brain tissue after VNS treatment. In vitro, we examined the effects of α7nAChR agonist on ischemia/reperfusion(I/R)-induced inflammation in BV2 cells under oxygen-glucose deprivation/reoxygenation(OGD/R) conditions. We observed the changes in cell survival rate, the levels of inflammatory factors, and the expressions of α7nAChR/Janus kinase 2(JAK2) and toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB).RESULTS: In vivo, VNS preconditioning enhanced functional recovery, improved the survival rate, and reduced hippocampal CA1 cell damage, and the levels of inflammatory mediators after CA/CPR. The application of α7nAChR agonists provided similar effects against cerebral injury after the return of spontaneous circulation(ROSC), while α7nAChR antagonists reversed these neuroprotective impacts. The in vitro results mostly matched the findings in vivo. OGD/R increased the expression of tumor necrosis factor-alpha(TNF-α), TLR4 and NF-κB p65. When nicotine was added to the OGD/R model, the expression of TLR4, NF-κB p65, and TNF-α decreased, while the phosphorylation of JAK2 increased, which was prevented by preconditioning with α7nAChR or JAK2 antagonists.CONCLUSION: The neuroprotective effect of VNS correlated with the activation of α7nAChR. VNS may alleviate cerebral IR injury by inhibiting TLR4/NF-κB and activating the α7nAChR/JAK2 signaling pathway.

Vagus nerve stimulation is a potential treatment for ischemic stroke

Microglia are the brain’s primary innate immune cells,and they are activated and affect pro-inflammatory phenotype or regulatory phenotype after ischemic stroke.Vagus nerve stimulation was shown to activate microglial phenotypic changes and exhibit neuroprotective effects in ischemia/reperfusion injury.In this study,we established rat models of ischemic stroke by occlusion of the middle cerebral artery and performed vagus nerve stimulation 30 minutes after modeling.We found that vagus nerve stimulation caused a shift from a pro-inflammatory phenotype to a regulatory phenotype in microglia in the ischemic penumbra.Vagus nerve stimulation decreased the levels of pro-inflammatory phenotype markers inducible nitric oxide synthase and tumor necrosis factorαand increased the expression of regulatory phenotype markers arginase 1 and transforming growth factorβthrough activatingα7 nicotinic acetylcholine receptor expression.Additionally,α7 nicotinic acetylcholine receptor blockade reduced the inhibition of Toll-like receptor 4/nuclear factor kappa-B pathwayassociated proteins,including Toll-like receptor 4,myeloid differentiation factor 88,I kappa B alpha,and phosphorylated-I kappa B alpha,and also weakened the neuroprotective effects of vagus nerve stimulation in ischemic stroke.Vagus nerve stimulation inhibited Toll-like receptor 4/nuclear factor kappa-B expression through activatingα7 nicotinic acetylcholine receptor and regulated microglial polarization after ischemic stroke,thereby playing a role in the treatment of ischemic stroke.Findings from this study confirm the mechanism underlying vagus nerve stimulation against ischemic stroke.

Comparison of protective effects of electroacupuncture and moxibustion at Zusanli(ST 36)on perinatal nicotine exposure-induced lung phenotype in rat offspring

Objective:To compare the effects of electroacupuncture(EA)and moxibustion at Zusanli(ST 36)on the lung phenotype of rat offspring exposed to nicotine during the perinatal period.Methods:Pregnant Sprague-Dawley rats were randomly divided into 4 groups:the control group(saline only),the model group(nicotine only),the EA group(nicotine+EA at ST 36 acupoints bilaterally),and the moxibustion group(nicotine+moxibustion at ST 36 acupoints bilaterally).n=6 rats per group.On postnatal day 21,the body weight,lung weight,and pulmonary function were determined and lung morphometry was performed.Peroxisome proliferator-activated receptor gamma andβ-catenin levels in the lung tissue of offspring were also determined.Results:Perinatal nicotine exposure(PNE)results in decreased body and lung weights of offspring rats,abnormal lung tissue morphology,and significantly altered pulmonary function,showing an increase in total airway resistance and a decrease in tidal volume,minute ventilation,total airway compliance,and peak expiratory flow.Bilateral EA at ST 36 acupoints could block all of these perinatal nicotine-induced effects.Although moxibustion also had protective effects in nicotine-induced offspring lungs,some of these effects did not reach statistical significance,e.g.,protection against the upregulation ofβ-catenin,the downregulation of PPARγsignaling,and the increase in peak expiratory flow.Conclusion:Maternal EA at ST 36 blocked the PNE-induced changes in key developmental signaling pathways,prevented the PNE-induced changes in lung morphology,and protected pulmonary function.Moxibustion at ST 36 showed similar but weaker protective effects against the PNE-induced changes in the exposed offspring.It is important to note that the mechanism underlying the protective effects of moxibustion at ST 36 may be different from those of EA at ST 36,and further research is needed to understand these differences.

Variability and Correlation in Biomarkers of Exposure from Two Randomized Controlled Studies of JUUL Electronic Nicotine Delivery Systems

The data included in this analysis were from two clinical studies (Study A and Study B), which evaluated JUUL electronic nicotine delivery systems (ENDS) against combustible cigarettes. In both studies, biomarkers of exposure including nicotine equivalents, NNAL, 3-HPMA, MHBMA, S-PMA and COHb were measured. Coefficients of variation (CV) of the biomarkers were calculated and compared. Pearson correlation analysis was used to examine the correlation between the biomarkers. Seven out of the nine biomarkers of exposure in Study A were highly variable (CV > 30%). Higher variability was observed in NNAL, MHBMA and S-PMA than in other biomarkers. After adult cigarette smokers switched from combustible cigarettes to JUUL ENDS, the correlation between nicotine equivalents and other biomarkers became weaker. A similar trend was observed between NNAL and other biomarkers. In Study B, the participants in the 5% ENDS group had higher nicotine equivalent levels than those in the 3% ENDS group. The higher nicotine levels did not result in a substantial increase in the levels of other biomarkers (except 1-OHP). The correlations between nicotine equivalents and 3-HPMA, MHBMA, S-PMA, COHb, HMPMA, and 1-OHP were weak in both the 5% and 3% ENDS groups.

Immediate Respiratory Response to Electronic Cigarette Use

Background: Electronic cigarettes were originally designed to reduce adult dependency on normal cigarettes and as a tobacco cessation tool to substitute traditional cigarettes. But it has become the most popular among teenagers. Rationale: To investigate the immediate adverse respiratory effect of short-term electronic cigarette vapor inhalation. Method: Twenty-five subjects were randomly selected and used in this study. The respiratory resistance values were evaluated and used for comparison. The subjects were asked to breathe into the Airflow Perturbation Device (APD) for evaluation of their respiratory resistance before vaping (in triplicate). The same subjects, a minute later, were then asked to use one poke (3 seconds) of the e-Cigarette device to inhale e-Cigarette vapor with nicotine from a pod with 59 mg/ml nicotine. Immediately following the e-Cigarette use, their respiratory resistance was measured again (in triplicate). Results: Comparing the respiratory resistance values before and immediately after exposure to e-Cigarette vapor showed that their respiratory resistance increased almost immediately. Conclusion: Although there are long-term studies showing that the e-Cigarette is as harmful as regular cigarettes, this study showed a nearly immediate effect of using the e-Cigarette that significantly increased the respiratory resistance of the user. Very short exposure time to e-Cigarette vapor (3 seconds only), caused an immediate adverse physiologic effect in respiratory resistance.

EGCG抑制Nicotine诱导肺腺癌H1299细胞JAK2/STAT3 mRNA的表达研究

为探索EGCG对Nicotine诱导肺癌细胞增殖的抑制作用,本研究通过MTT实验筛选出EGCG、Nicotine对肺腺癌细胞H1299的最佳作用浓度,利用实时荧光定量PCR技术检测EGCG、Nicotine对H1299细胞中Bax、Bcl-2、Jak2和Stat3基因mRNA相对表达量的变化。实验结果表明,EGCG对H1299细胞的半抑制浓度IC50值约为32μmol·L-1(24 h)、15μmol·L-1(48 h);1μmol·L-1的Nicotine对H1299细胞促增殖作用明显;以15μmol·L-1的EGCG预处理H1299细胞24 h可显著下调1μmol·L-1 Nicotine的促增殖作用(P<0.05)。1μmol·L-1的Nicotine处理H1299细胞可明显降低JAK2/STAT3信号通路中Bax基因mRNA的表达,增加Bcl-2、Jak2、Stat3基因的mRNA表达;15μmol·L-1 EGCG预处理H1299细胞可反向调控Nicotine诱导所致JAK2/STAT3信号通路中Jak2、Stat3和Bax、Bcl-2基因表达量的变化,结果具有显著性差异(P<0.05)。由此可知,EGCG对Nicotine诱导的肺腺癌H1299细胞增殖及JAK2/STAT3信号通路中促增殖基因mRNA的表达起抑制作用。

尼古丁贴片短期戒烟效果的Meta分析

在烟草的成分当中,尼古丁是烟草中毒性较小的成分之一,它既非致癌物,亦非辅助致癌物,但却是造成烟草成瘾的主要物质。所以,医学戒烟治疗的有效方法为用含有尼古丁的药物替代由吸烟中获取尼古丁,推荐使用尼古丁替代疗法（nicotine replacement therapy,NRT）,使用NRT能使戒烟成功率增加2倍左右。

Comparative Evaluation of the Anti-ulcer Activity of Curcumin and Omeprazole during the Acute Phase of Gastric Ulcer—Efficacy of Curcumin in Gastric Ulcer Prevention against Omeprazole

We have confirmed in our laboratory the antiulcer activity of curcumin during the acute chronic phase of gastric ulcer disease at doses of 20, 40 and 80 mg/kg (dissolved in saline solution). In the previous study, the potent effective dose of curcumin was 80 mg/kg that appears a propitious protective effect against gastric ulcer development. Therefore, the comparison between such recommended dose of curcumin and one of the proton pump inhibitors (PPIs) staff is worth-while. Since, the pharmacological control of gastric acid secretion is the main desired goal for gastro-cytoprotection, particularly, the H+/K+-ATPase (acid proton pump) inhibitors. Nevertheless, several studies have indicated that long-term inhibition of gastric acid secretion results in mucosal hyperplasia and carcinoid tumor development, due to increase circulating gastrin levels. Ulcer and the preventive indexes were scored, mucin, juice volume, total acidity, luminal haemoglobin, total antioxidant and total peroxide were evaluated. The pro-inflammatory cytokine IL-6 and the major angiogenic growth factor VEGF levels were measured. Conclusion, curcumin and omeprazole are potentially preventing gastric lesions development in the gastric wall during the acute phase of gastric ulcer diseases, but curcumin was more potent in its effect. Curcumin promotes gastric ulcer prevention/healing by induction of angiogenesis in the granular tissue of ulcers. That may be via upregulation of VEGF expression as reflected from VEGF level in serum and gastric juice, however, omeprazole might be has no role in this story.

Smoking in schizophrenic patients:A critique of the selfmedication hypothesis

A common remark among laypeople, and notably also among mental health workers, is that individuals with mental illnesses use drugs as self-medication to allay clinical symptoms and the side effects of drug treatments. Roots of the self-medication concept in psychiatry date back at least to the 1980 s. Observations that rates of smokers in schizophrenic patients are multiple times the rates for regular smoking in the general population, as well as those with other disorders, proved particularly tempting for a self-medication explanation. Additional evidence came from experiments with animal models exposed to nicotine and the identification of neurobiological mechanisms suggesting self-medication with smoking is a plausible idea. More recently, results from studies comparing smoking and non-smoking schizophrenic patients have led to the questioning of the self-medication hypothesis. Closer examination of the literature points to the possibility that smoking is less beneficial on schizophrenic symptomology than generally assumed while clearly increasing the risk of cancer and other smoking-related diseases responsible for early mortality. It is a good time to examine the evidence for the self-medication concept as it relates to smoking. Our approach is to focus on data addressing direct or implied predictions of the hypothesis in schizophrenic smokers.

在糖尿病的 nephropathy 吸烟: 在燃料坦克的火花吗？

Diabetic nephropathy is associated with high morbidity and mortality and the prevalence of this disease is continuously increasing worldwide.Long-term diabetes increases the likelihood of developing secondary complications like nephropathy,the most common cause of end stage renal disease.Usually,other factors like hypertension,alcoholism and smoking also partly contribute to the progression of diabetic nephropathy.Among this,cigarette smoking in diabetes has been repeatedly confirmed as an independent risk factor for the onset and progression of diabetic nephropathy.Various studies suggest that smoking is a major fuel in the development of high oxidative stress and subsequently hyperlipidemia,accumulation of advanced glycation end products,activation of the renin angiotensin system and Rho-kinase,which are observed to play a pathogenic role in the progression of diabetic nephropathy.Furthermore,cigarette smoking in diabetic patients with vascular complications produces a variety of pathological changes in the kidney,such as thickening of the glomerular basement membrane and mesangial expansion with progression in glomerulosclerosis and interstitial fibrosis,which ultimately results in end stage renal failure.Strong associations are consistently found between chronic cigarette smoking and diabetic microvascular complications.A diverse group of studies unveil potentialmechanisms that may explain the role of cigarette smoking in the progression of diabetic nephropathy.Tremendous efforts are being made to control smoking mediated progression of diabetic nephropathy,but no promising therapy is yet available.The present review critically discusses the possible detrimental role of chronic cigarette smoking in the progression of diabetic nephropathy and various possible pharmacological interventions to attenuate the exacerbation of diabetic nephropathy.

Regular nicotine intake increased tooth movement velocity,osteoclastogenesis and orthodontically induced dental root resorptions in a rat model

Orthodontic forces have been reported to significantly increase nicotine-induced periodontal bone loss. At present, however, it is unknown, which further （side） effects can be expected during orthodontic treatment at a nicotine exposure corresponding to that of an average European smoker. 63 male Fischer344 rats were randomized in three consecutive experiments of 21 animals each （A/B/C） to 3 experimental groups （7 rats, 112/3）. （A） cone-beam-computed tomography （CBCT）; （B） histology/serology; （C） reverse- transcription quantitative real-time polymerase chain reaction （RT-qPCR）/cotinine serology--（1） control; （2） orthodontic tooth movement （OTM） of the first and second upper left molar （NiTi closed coil spring, 0.25 N）; （3） OTM with 1.89 mg-kg- 1 per day s.c. of L（- ）-nicotine. After 14 days of OTM, serum cotinine and IL-6 concentration as well as orthodontically induced inflammatory root resorption （OIIRR）, osteoclast activity （histology）, orthodontic tooth movement velocity （CBCT, within 14 and 28 days of OTM） and relative gene expression of known inflammatory and osteoclast markers were quantified in the dental-periodontal tissue （RT-qPCR）. Animals exposed to nicotine showed significantly heightened serum cotinine and IL-6 levels corresponding to those of regular European smokers. Both the extent of root resorption, osteoclast activity, orthodontic tooth movement and gene expression of inflammatory and osteoclast markers were significantly increased compared to controls with and without OTM under the influence of nicotine. We conclude that apart from increased periodontal bone loss, a progression of dental root resorption and accelerated orthodontic tooth movement are to be anticipated during orthodontic therapy, if nicotine consumption is present. Thus patients should be informed about these risks and the necessity of nicotine abstinence during treatment.