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.

Flavone improves liver damage in nicotine-exposed rats via the Nrf2/HO-1 pathway

Objective:To assess the hepatoprotective effects of flavone on nicotine-induced liver damage.Methods:Thirty-six rats were allocated into six groups:the control group,the nicotine group,the flavone alone groups(10 and 25 mg/kg/body weight),and the nicotine groups treated with flavone(10 and 25 mg/kg/body weight).Liver function,oxidative stress,Nrf2 pathway(HO-1,Nrf2,and Keap-1),and inflammatory markers(IL-17,TNF-α,and NF-κB)were evaluated.Additionally,a histopathological examination of liver tissues was performed.Results:Nicotine increased liver damage,inflammation,and oxidative stress.However,flavone suppressed nicotine-induced liver enzymes,oxidative stress,and inflammation,as manifested by increased antioxidants and decreased malondialdehyde level,liver enzymatic activities,and inflammatory markers.Flavone(10 and 25 mg/kg/body weight)also reduced the level of Keap-1 and increased HO-1 and Nrf2 levels in the liver of nicotine-exposed rats.Conclusions:Flavone has hepatoprotective properties and may slow the progression of liver injury by reducing oxidative stress,liver enzymes,and inflammation possibly via the Nrf2 pathway.

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。

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。

Cloning and Sequence of Nicotinic Acetylcholine Receptor α Subunit from Chilo suppressalis

Nicotinic acetylcholine receptors (nAChRs) play a significant role in excitatory synaptic transmission in insects and are the target for chloronicotinyl and nereistoxin insecticides.In recent years,Chilo suppressalis,an economically important pest of rice,developed high resistance against monosultap,a nereistoxin insecticide acting on nAChR.In order to reveal the hypothesized target insensitive mechanism,studies on the molecular property of nAChR from Chilo suppressalis are required.In this study,the full length cDNA of nAChR α subunit from this pest was cloned by RT-PCR.Sequence analysis shows that it is a novel nAChR α subunit,which was named as Cs α 1(Genbank accession No.AF418987).It contains 1?997?bp nucleotides and involves an open reading frame (ORF) encoding a mature protein of 509 amino acids excluding a signal peptide of 24 amino acids.The deduced amino acid sequence was 52%-94% identical to the reported insect nAChR genes.

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.

Variation Dynamics of Total Nitrogen and Nicotine of Burley Tobacco at Various Growing Stages under Different Nitrogen Nutrition Levels

[Objective] This study aimed to investigate the variation dynamics of total nitrogen and nicotine of burtey tobacco at various growing stages under different ni- trogen nutrition levels to provide reference for optimizing fertilization technologies for burley tobacco. [Method] Fresh burley tobacco leaves were collected at various growing stages and dried to measure the content of total nitrogen, protein and nico- tine by using INTEGRAL automated chemical analyzer and analyze the correlation with nitrogen application level. [Result] Regardless of the nitrogen application level, the content of total nitrogen and protein showed a downward trend since root ex- tending stage and reached the minimum at mature stage; the content of nicotine showed an upward trend since early vigorous growing stage and increased to the maximum at mature stage; the content of total nitrogen, protein and nicotine all in- creased after air curing; the content of total nitrogen, protein and nicotine showed positive correlation with nitrogen application level, while total nitrogen/nicotine was negatively correlated. The results indicate that nitrogen level is closely related to the total nitrogen and nicotine of burley tobacco at growing period and post-air curing, rational application of nitrogen is an important measure to regulate the content of total nitrogen and nicotine of tobacco. [Conclusion] This study provides scientific ba- sis for rational fertilization of burley tobacco.

A Preliminary Study on Control Efficiency of New Nicotine Biopesticides against Pomegranate Aphids

In this study, toxicity and control efficiency of three nicotine biopesticides against pomegranate aphids were determined via indoor toxicity test and field effica- cy test, aiming at screening the appropriate reagent for prevention and control of pomegranate aphids. The results of indoor toxicity test showed that LC^o of reagent 1, reagent 2 and reagent 3 reached 10 270, 12 810 and 13 040 mg/L, respectively. The results of field efficacy test showed that control efficacy of reagent 1, reagent 2 and reagent 3 reached 60.52%, 34.60% and 46.99%, respectively. Overall, reagent 1 （91% ultrafine powder of tobacco leaves, 3% silicone oil, 2% sasangua cake, 2% emulsifier, 2% ascorbic acid） exhibited the highest control efficiency against pomegranate aphids, which can be further popularized and utilized.

Yield and Nicotine Content of Flue-Cured Tobacco as Affected by Soil Nitrogen Mineralization

Nitrogen(N)supply is the most important factor affecting yield and quality of flue-cured tobacco(FCT).A field experiment and an in situ incubation method were used to study the effects of soil N mineralization in the later stages of growth on yield and nicotine content of FCT in Fenggang and Jinsha,Guizhou Province.The yield and market value of FCT at Fenggang were much lower than those at Jinsha.However,the nicotine content of middle and upper leaves was much higher at Fenggang than at Jinsha when the same rate of fertilizer N was applied,which might be due to a higher N supply capacity at the Fenggang site.At later stages of growth(7-16 weeks after transplanting),the soil net N mineralization at Fenggang(56 kg N ha^(-1))was almost double that at Jinsha(30 kg N ha^(-1)).While soil NH_4-N and NO_3-N were almost exhausted by the plants or leached 5 weeks after transplanting,the N taken up at the later growth stages at Fenggang were mainly derived from soil N mineralization,which contributed to a high nicotine content in the upper leaves.The order of soil N contribution to N buildup in different leaves was:upper leaves>middle leaves>lower leaves.Thus,soil N mineralization at late growth stages was an important factor affecting N accumulation and therefore the nicotine content in the upper leaves.

Ulcerative colitis in smokers,non-smokers and ex-smokers

Smoking is a major environmental factor that interferes in the establishment and clinical course of ulcerative colitis (UC). Firstly, the risk of smoking status impact in the development of UC is reviewed, showing that current smoking has a protective association with UC. Similarly, being a former smoker is associated with an increased risk of UC. The concept that smoking could have a role in determining the inflammatory bowel disease phenotype is also discussed. Gender may also be considered, as current smoking delays disease onset in men but not in women. No clear conclusions can be driven from the studies trying to clarify whether childhood passive smoking or prenatal smoke exposure have an influence on the development of UC, mainly due to methodology flaws. The influence of smoking on disease course is the second aspect analysed. Some studies show a disease course more benign in smokers that in non-smokers, with lower hospitalizations rates, less flare-ups, lower use of oral steroids and even less risk of proximal extension. This is not verified by some other studies. Similarly, the rate of colectomy does not seem to be determined by the smoking status of the patient. The third issue reviewed is the use of nicotine as a therapeutic agent. The place of nicotine in the treatment of UC is unclear, although it could be useful in selected cases, particularly in recent ex-smokers with moderate but refractory attacks of UC. Finally, the effect of smoking cessation in UC patients is summarised. Given that smoking represents a major worldwide cause of death, for inpatients with UC the risks of smoking far outweigh any possible benefit. Thus, physicians should advise, encourage and assist UC patients who smoke to quit.

Exploitation of the nicotinic anti-inflammatory pathway for the treatment of epithelial inflammatory diseases

Discoveries in the first few years of the 21st century have led to an understanding of important interactions between the nervous system and the inflammatory response at the molecular level, most notably the acetylcholine （ACh）- triggered,α7-nicotinic acetylcholine receptor （α7nAChR）- dependent nicotinic antinflammatory pathway. Studies using the α7nAChR agonist, nicotine, for the treatment of mucosal inflammation have been undertaken but the efficacy of nicotine as a treatment for inflammatory bowel diseases remains debatable. Further understanding of the nicotinic anti-inflammatory pathway and other endogenous anti-inflammatory mechanisms is required in order to develop refined and specific therapeutic strategies for the treatment of a number of inflammatory diseases and conditions, including periodontitis, psoriasis, sarcoidosis, and ulcerative colitis.

The genetics of nicotine dependence:Relationship to Pancreatic cancer

Smoking of tobacco products continues to be a major cause of worldwide health problems. Epidemiological studies have shown that tobacco smoking is the greatest risk factor for the development of pancreatic cancer. Smokers who are able to quit smoking can reduce their risk of pancreatic cancer by nearly 50% within two years, however, their risk of developing pancreatic cancer remains higher than that of non-smokers for 10 years. Nicotine is the major psychoactive substance in tobacco, and is responsible for tobacco dependence and addiction. Recent evidence suggests that individuals have genetically based differences in their ability to metabolize nicotine, as well as genetic differences in the psychological reward pathways that may influence individual response to smoking initiation, dependence, addiction and cessation. Numerous associations have been reported between smoking behavior and genetic polymorphisms in genes that are responsible for nicotine metabolism. In addition, polymorphisms in genes that encode neurotransmitters and transporters that function in psychological reward pathways have been implicated in differences in smoking behavior. However, there is a large degree of between-study variability that demonstrates the need for larger, well-controlled casecontrol studies to identify target genes and deduce mechanisms that account for the genetic basis of interindividual differences in smoking behavior. Understanding the genetic factors that increase susceptibility to tobacco addiction may result in more effective tobacco cessation programs which will, in turn, reduce the incidence of tobacco related disease, including pancreatic cancer.

Effect of areca on contraction of colonic muscle strips in rats

AIM: To investigate the effects of areca on the contractile activity of isolated colonic muscle strips in rats and mechanism involved. METHODS: Each strip (LMPC, longitudinal muscle of proximal colon; CMPC, circular muscle of proximal colon; LMDC, longitudinal muscle of distal colon; CMDC, circular muscle of distal colon.) was suspended in a tissue chamber containing 5 mL Krebs solution (37 degrees C), bubbled continuously with 950 mL.L(-1) O(2) and 50 mL.L(-1) CO(2). The mean contractile amplitude (A), the resting tension (T), and the contractile frequency (F) were simultaneously recorded on recorders. RESULTS: Areca dose dependently increased the mean contractile amplitude, the resting tension of proximal and distal colonic smooth muscle strips in rats (P【0.05). It also partly increased the contractile frequency of colonic smooth muscle strips in rats (P【0.05). The effects were partly inhibited by atropine (the resting tension of LMPC decreased from 0.44 +/- 0.12 to 0.17 +/- 0.03; the resting tension of LMDC decreased from 0.71 +/- 0.14 to 0.03 +/- 0.01; the mean contractile amplitude of LMPC increased from -45.8 +/- 7.2 to -30.5 +/- 2.9; the motility index of CMDC decreased from 86.6 +/- 17.3 to 32.8 +/- 9.3; P【0.05 vs areca), but the effects were not inhibited by hexamethonium (P】0.05). CONCLUSION: Areca stimulated the motility of isolated colonic smooth muscle strips in rats. The stimulation of areca might be relevant with M receptor partly.

Effect of smoking on inflammatory bowel disease: Is it disease or organ specific?

Smoking is an important environmental factor in inflammatory bowel disease （IBD） with differing effects in ulcerative colitis （UC） and Crohn＇s disease （CD）. Never smoking and formerly smoking increase the risk of UC, whereas smoking exacerbates the course of CD. The potential mechanisms involved in this dual relationship are yet unknown. A reasonable assumption is that smoking has different effects on the small and large intestine. This assumption is based on animal and human studies that show that the effects of smoking/nicotine on CD and UC depend on the site of inflammation and not on the type of disease.