Nicotine is a potent parasympathomimetic stimulant and alkaloids found in the nightshade plant family. Nicotine acts as the nicotinic acetylcholine receptor agonist (nAChRs), except in two nicotinic receptor subunits (nAChR 9 and nAChR 10) in which it acts as a receptor antagonist. Nicotine is found in leaf Nicotiana rustica , in concentrations of 2-14%; at the tobacco factory, Nicotiana tabacum ; at Duboisia hopwoodii ; and in Asclepias syriaca .
Nicotine is about 0.6-3.0% of the dry weight of tobacco. This also occurs in edible plants, such as those in the Solanaceae family, which include eggplants, potatoes, and tomatoes, for example, but at a generally under 200 nanogram per gram trace rate, dry weight (less than 0.00002%). Nicotine acts as an antiherbivorous chemical; consequently, nicotine is widely used as an insecticide in the past, and neonicotinoids, such as imidacloprid, are widely used.
Nicotine is highly addictive. The average cigarette yield is about 2 mg of nicotine absorbed; in lower doses of the order, the substance acts as a stimulant in mammals, while high numbers (50-100 mg) can be harmful. This stimulant effect is a contributing factor to the addictive nature of smoking tobacco. Nicotine's addictive properties include psychoactive effects, drug reinforced behavior, compulsive usage, relapse after abstinence, physical dependence and tolerance.
In addition to addiction, both short-term and long-term nicotine exposure has not been established as dangerous for adults, except among certain susceptible groups. At fairly high doses, nicotine is associated with poisoning and potentially deadly. Nicotine as a tool to stop smoking has a good security history. There is insufficient research to show that nicotine itself is associated with cancer in humans. Nicotine in the form of nicotine replacement products has a lower cancer risk than smoking. Nicotine is associated with the possibility of birth defects. During pregnancy, there is a risk for later childhood for type 2 diabetes, obesity, hypertension, neurobehavioral defects, respiratory dysfunction, and infertility. The use of electronic cigarettes, designed to be replenished with nicotine-containing e-liquids, has raised concerns over nicotine overdose, especially with regard to the possibility of children ingesting fluids.
The FDA recommends that adults with children in their homes be careful to keep the e-fluid up and away from curious children as well as pets. The ideal time to explain to children is when they are ready to understand that these products are only for adults to handle and they can be dangerous.
Video Nicotine
Psychoactive effects
The effects that change Nicotine's mood differ from reports: in particular, they are stimulants and relaxants. First cause the release of glucose from the liver and epinephrine (adrenaline) from the adrenal medulla, causing stimulation. Users report feelings of relaxation, sharpness, tranquility, and alertness.
When cigarettes are smoked, nicotine-rich blood travels from lungs to brain within seven seconds and immediately stimulates nicotinic acetylcholine receptors; this indirectly promotes the release of many chemical messengers such as acetylcholine, norepinephrine, epinephrine, arginine vasopressin, serotonin, dopamine, and beta-endorphin in the brain. Nicotine also extends the duration of the positive effects of dopamine and increases the sensitivity of the brain reward system to useful stimuli. Most cigarettes contain 1-3 milligrams of nicotine that can be inhaled. Studies show that when smokers want to achieve stimulation effects, they take short quick puffs, which results in low levels of nicotine blood.
Nicotine is unusual compared to most drugs, as its profile changes from a stimulant to a sedative with increased doses, a phenomenon known as the "Nesbitt Paradox" after the doctor first described it in 1969. At very high doses it inhibits neuronal activity.
Maps Nicotine
Usage
Medical
The main therapeutic use of nicotine is in treating nicotine dependence to eliminate cigarettes with the resulting damage to health. Controlled nicotine levels are administered to patients through gums, skin plasters, suction tablets, electronic cigarettes/substitutes or nasal sprays in an attempt to stop their dependence. Research has found that these therapies increase the chances of successful stopping by 50 to 70%, although reductions in the overall population have not been proven.
Improved performance
Nicotine is often used for the effect of improving performance on cognition, alertness, and focus. A meta-analysis of 41 double-blind, placebo-controlled studies concluded that nicotine or smoking had a significant positive effect on aspects of fine motor skills, reminiscent and attention-oriented, and episodic memory and work. Review 2015 notes that stimulation of nicotinic receptors? 2? 2 is responsible for certain improvements in attention performance; among the nicotinic receptor subtypes, nicotine has the highest binding affinity in receptor 4? 2 (k i = 1Ã, nM ), which is also a biological target that mediates the addictive nature of nicotine. Nicotine has a potential beneficial effect, but it also has a paradoxical effect, which may be due to its inverted U-shape or pharmacokinetic features.
Recreation
Nicotine is generally consumed as a recreational drug for its stimulant effect. Recreational nicotine products include chewing tobacco, cigars, cigarettes, e-cigarettes, tobacco, pipe tobacco, and snus.
Adverse effects
Limitations of the data are on the health effects of long-term pure nicotine use, because nicotine is usually consumed through tobacco products. The use of long-term nicotine in the form of snus causes a slight risk of cardiovascular disease compared to tobacco smoking. Nicotine is one of the most thoroughly studied drugs. The complex effects of nicotine are not fully understood. Studies of continuous use of nicotine replacement products in those who quit smoking found no side effects from months to years, and that people with cardiovascular disease were able to tolerate them for 12 weeks. The general medical position is the nicotine itself, in small doses , poses some health risks, except among certain susceptible groups. The Royal College of Physicians 2016 report found "nicotine alone in doses used by smokers represents little if any harm to users". The American Heart Association 2014 policy statement finds that some health problems are related to nicotine. Experimental studies have shown that adolescent nicotine use can harm brain development. Children exposed to nicotine may have lifelong health problems. Administration of nicotine for guinea pigs has been shown to cause damage to the inner ear cells. As a drug, nicotine is used to help quit smoking and has good security in this form.
Metabolism and weight
By reducing appetite and increasing metabolism, some smokers can lose weight as a consequence. By increasing the rate of metabolism and inhibiting the usual increase in appetite compensation, the weight of smokers is lower than the average non-smoker. When smokers quit, they get an average weight of 5-6Ã, kg, returning to the average weight of nonsmokers.
Vascular system
A review of 2014 found that nicotine use is not a significant cause of cardiovascular disease, but a 2015 review found that nicotine is associated with cardiovascular disease. The 2016 review suggests that "the risk of nicotine without tobacco-burning products is low compared to smoking, but is still a concern for people with cardiovascular disease." Some studies in people suggest the possibility that nicotine contributes to acute cardiovascular events in smokers with existing cardiovascular disease, and induces pharmacological effects that may contribute to increased atherosclerosis. The old use of nicotine does not seem to increase atherosclerosis. The use of nicotine briefly, such as nicotine, seems to pose a mild cardiovascular risk, even in people with existing cardiovascular disease. 2015's review of "in vitro nicotine and in animal models may inhibit apoptosis and improve angiogenesis, an effect that raises concerns about the role of nicotine in promoting the acceleration of atherosclerotic disease." The Cochrane Review 2012 found no evidence of increased risk of cardiovascular disease with nicotine replacement products. A 1996 randomized controlled trial using a nicotine patch found that serious side effects were not more frequent among smokers with cardiovascular disease. A meta-analysis shows that snus consumption, which delivers nicotine at a dose equivalent to cigarettes, is not associated with a heart attack. Therefore, it is not nicotine, but another component of tobacco smoke that seems to be involved in ischemic heart disease. Nicotine increases heart rate and blood pressure and induces abnormal heart rhythms. Nicotine can also induce potential atherogenic genes in human coronary artery endothelial cells. Microvascular injury can occur by acting on nicotinic acetylcholine receptors (nAChRs). Nicotine does not affect serum cholesterol levels, but the 2015 review found it may increase serum cholesterol levels. Many studies stop smoking using nicotine drugs reported decreased dyslipidemia with considerable benefits in HDL/LDL ratios. Nicotine supports clot formation and helps the formation of plaque by increasing the smooth muscle of the blood vessels. Cancer
Although there is not sufficient evidence to classify nicotine as a carcinogen, there is still debate as to whether it functions as a tumor promoter. In vitro studies have linked it to cancer, but carcinogenicity has not been shown in vivo. There is insufficient research to show that nicotine is associated with cancer in humans, but there is evidence to suggest a possible risk of oral, esophageal or pancreatic cancer. Nicotine in the form of nicotine replacement products less risk of cancer than smoking. Nicotine replacement products have not been shown to be linked to cancer in the real world.
Although there is no epidemiological evidence that directly supports the idea that nicotine acts as a carcinogen in human cancer formation, studies have identified indirect nicotine involvement in cancer formation in animal models and cell cultures. Nicotine increases cholinergic and adrenergic signaling in colon cancer cases, inhibiting apoptosis, promoting tumor growth, and activating growth factors and cell mitogen factors such as 5-lipoxygenase (5-LOX), and epidermal growth factor. (EGF). Nicotine also promotes cancer growth by stimulating angiogenesis and neovascularization. In one study, nicotine was administered to mice with tumors causing an increase in tumor size (doubling), metastasis (nine-fold increase), and tumor recurrence (threefold increase). N -Nitrosonornicotine (NNN), classified by the International Agency for Research on Cancer (IARC) as group 1 carcinogen, has been shown to form in vitro from nornicotine in humans. saliva, indicating nornicotine is a carcinogen precursor. The IARC has not evaluated pure nicotine or assigned it to an official carcinogenic classification.
In cancer cells, nicotine increases the epithelial-mesencalal transition that makes cancer cells more resistant to drugs that treat cancer.
Fetal development
In pregnancy, the 2013 review notes that "nicotine is only one of more than 4000 compounds infected by the fetus through mothers who smoke • Of these, 30 compounds have been linked to poor health outcomes.Although the exact mechanism by which nicotine produces harmful fetal effects is not known, the possibility of hypoxia, malnutrition of the fetus, and direct vasoconstrictor effect on the placental and umbilical vessels all play a role.7 Nicotine has also been shown to have significant adverse effects on brain development, including changes in the brain, metabolic systems and neurotransmitters and abnormal brain development. It also notes that "newborn neurobehavior disorders, including disorders of orientation and autonomic regulation and muscle tone abnormalities, have been identified in a number of studies of prenatal nicotine exposure" and that there is weak data linking fetal nicotine exposure to newborn facial clefts, and that there is no good evidence for the baby yes Newborns suffer from nicotine withdrawal from fetal exposure to nicotine.
Effective April 1, 1990, the Environmental Health Hazards (OEHHA) Office of the California Environmental Protection Agency added nicotine to a list of chemicals known to cause developmental toxicity.
Nicotine is not safe to use in any amount during pregnancy. There are questions about the use of nicotine during pregnancy and their potential consequences for fetal growth and death. Nicotine negatively affects pregnancy outcomes and fetal brain development. Risks to children later in life through exposure to nicotine during pregnancy include type 2 diabetes, obesity, hypertension, neurobehavioral defects, respiratory dysfunction, and infertility. Nicotine crosses the placenta and is found in the mother's mother who smokes and the mother breathes passive smoke.
Stronger disturbance
Nicotine dependence involves aspects of psychological dependence and physical dependence, since the cessation of extended use has been shown to produce affective (eg anxiety, irritability, addiction, anhedonia) and somatic (mild motor dysfunction such as tremor) withdrawal symptoms. The symptoms of peak withdrawal on the first or second day and can last for several weeks. Nicotine has a clinically significant cognitive enhancement effect at low doses, especially in fine motor skills, attention, and memory. This beneficial cognitive effect can play a role in the maintenance of tobacco dependence.
Nicotine is highly addictive, comparable to heroin or cocaine. Nicotine activates the mesolimbic pathway and induces the expression of Fosb in the long-term nucleus accumbens when inhaled or injected at a sufficiently high dose, but not necessarily when ingested. As a result, repeated daily exposure (may not include the oral route) to nicotine can lead to accumbal? FosB overexpression, in turn causes nicotine addiction.
In dependent smokers, smoking during withdrawal restores cognitive ability to pre-withdrawal levels, but chronic use may not offer cognitive benefits rather than non-smoking.
Use of other drugs
In animals, it is relatively easy to determine whether the consumption of certain drugs increases the subsequent attractiveness of other drugs. In humans, where such direct experiments are not possible, longitudinal research can show whether the probability of using a substance is related to the prior use of another substance.
In nicotine mice increase the likelihood of later cocaine consumption and experiments allow concrete conclusions about changes in underlying molecular biology in the brain. Biological changes in rats correspond to epidemiological observations in humans that nicotine consumption is matched by an increased chance of marijuana and cocaine use later in life.
In marijuana consumption of rats - early in life - increase the administration of nicotine in the future. A study of drug use from 14,577 US 12th grade students showed that alcohol consumption was associated with an increased chance of tobacco, marijuana, and other illegal drugs.
Overdose
Nicotine is considered a potentially lethal poison. LD 50 of nicotine is 50 mg/kg for mice and 3 mg/kg for mice. 30-60 mg (0.5-1.0 mg/kg) can be a lethal dose for adult humans. However, the widely used predicted LD 50 0,5-1,0 mg/kg is questioned in the 2013 review, as some documented human cases survive at much higher doses; The 2013 review shows that the lower limit that causes fatal outcomes is 500-1000 mg of ingested nicotine, corresponding to 6.5-13 mg/kg orally. However, nicotine has relatively high toxicity compared with many other alkaloids such as caffeine, which has LD 50 of 127 mg/kg when administered to mice.
At a fairly high dose, it is associated with nicotine intoxication. Today nicotine is used less frequently in agricultural insecticides, which are the main source of poisoning. Newer cases of poisoning usually appear in the form of Green Tobacco Disease or due to the unintentional consumption of tobacco or tobacco products or the consumption of plants containing nicotine. People who harvest or cultivate tobacco can experience Green Tobacco Sickness (GTS), a type of nicotine intoxication caused by exposure to wet tobacco leaf. This is most common in young inexperienced tobacco harvesters who do not consume tobacco. People can be exposed to nicotine at work by inhaling, absorption of the skin, swallowing, or eye contact. Occupational Safety and Health Administration (OSHA) has established a legal limit (allowable exposure limits) for nicotine exposure in the workplace as 0.5 mg/m 3 skin exposure for 8 hours. The US National Institute for Occupational Safety and Health (NIOSH) has set the recommended exposure limits (REL) of skin exposure 0.5/mg/m 3 for 8 hours. At an environmental level of 5 mg/m 3 , nicotine is immediately harmful to life and health.
There's no way a person will overdose on nicotine through smoking alone. The US Food and Drug Administration (FDA) stated in 2013 that "There are no significant safety issues associated with the use of more than one NRT OTC at the same time, or using NRT OTC at the same time as other products containing nicotine - including a cigarette. "
Increased use of electronic cigarettes, many forms that are designed to be replenished with e-liquids containing nicotine supplied in small plastic bottles, have raised concerns over nicotine overdose, especially in the possibility of young children ingesting fluids. The UK Public Health 2015 report notes "unconfirmed newspaper reports of fatal childhood poisoning of two-year-olds" and two case reports published about children of the same age who have recovered after ingestion of e-liquid and vomiting. They also recorded reports of suicide cases by nicotine. When adults drink fluids containing up to 1,500 mg of nicotine, they are recovered (aided by vomiting), but an apparent consumption of about 10,000 mg is fatal, such as injections. They commented that "Serious nicotine intoxication seems to be typically prevented by the fact that a relatively low dose of nicotine causes nausea and vomiting, which stops users from further intake."
Pharmacology
Pharmacodynamics
Nicotine acts as a receptor agonist in most nicotinic acetylcholine receptors (nAChRs), except in two nicotinic receptor subunits (nAChR 9 and nAChR 10) in which it acts as a receptor antagonist.
Central nervous system
By binding nicotinic acetylcholine receptors in the brain, nicotine has a psychoactive effect and increases the level of some neurotransmitters in various brain structures - acting as a kind of "volume control." Nicotine has a higher affinity for the nicotinic receptors in the brain than in the skeletal muscle, although at toxic doses it can induce contractions and respiratory paralysis. The selectivity of nicotine is thought to be caused by a certain amino acid difference in this receptor subtype.
Nicotine activates nicotinic receptors (especially? 4? 2 nicotinic receptors) in neurons that infect ventral ventral areas and in mesolimbic pathways that appear to cause dopamine release. This release of nicotine-induced dopamine occurs at least in part through the activation of the dopaminergic cholinergic-reward chain in the ventral tegmental area. Nicotine also appears to trigger the release of endogenous opioids that activate opioid pathways in the reward system, because naltrexone - the opioid receptor antagonist - blocks nicotine administration. This action is largely responsible for the highly potent effect of nicotine, which often occurs in the absence of euphoria; However, mild euphoria of nicotine use can occur in some individuals. The use of chronic nicotine inhibits class I and II histone deacetylases in the striatum, where this effect plays a role in nicotine addiction.
Sympathetic nervous system
Nicotine also activates the sympathetic nervous system, acting through the splanchnic nerve to the adrenal medulla, stimulating epinephrine release. Acetylcholine released by preganglionic nerve fibers from this nerve acts on nicotinic acetylcholine receptors, causing the release of epinephrine (and norepinephrine) into the bloodstream.
Medulla adrenal
By binding to ganglion type nicotinic receptors in the adrenal medulla, nicotine increases the flow of adrenaline (epinephrine), stimulating hormones and neurotransmitters. By binding to the receptor, it causes cellular depolarization and the inclusion of calcium through a voltage-gated calcium channel. Calcium triggers the exocytosis of chromaffin granules and thus the release of epinephrine (and norepinephrine) into the bloodstream. The release of epinephrine (adrenaline) causes increased heart rate, blood pressure and respiration, as well as higher blood glucose levels.
Pharmacokinetics
When nicotine enters the body, it is distributed rapidly through the bloodstream and across the blood-brain barrier that reaches the brain in 10-20 seconds after inhalation. The half-life of nicotine elimination in the body is about two hours.
The amount of nicotine absorbed by the body from cigarettes can depend on many factors, including tobacco types, whether smoke is inhaled, and whether filters are used. However, it has been found that the nicotine yield of individual products has only a small effect (4.4%) on the concentration of nicotine in the blood, suggesting "the assumed health benefits of switching to lower-tar cigarettes and lower nicotine may be largely offset by the tendency of smokers to compensate by increasing inhalation ".
Nicotine has a half-life of 1-2 hours. Cotinine is the active nicotine metabolite remaining in the blood with an half-life of 18-20 hours, making it easier to analyze.
Nicotine is metabolized in the liver by the cytochrome P450 enzyme (mostly CYP2A6, and also by CYP2B6) and FMO3, which selectively metabolize ( S ) - nicotine. The main metabolite is cotinine. Other primary metabolites include nicotine N ' -oxide, nornicotine, nicotine isomethonium ions, 2-hydroxynicotine and nicotine glucuronide. In some conditions, other substances may be formed such as miosmine.
Glucuronidation and oxidative nicotine metabolism for cotinine are both inhibited by menthol, an additive for menthol cigarettes, thereby increasing the nicotine half in vivo.
Chemistry
Nicotine is a hygroscopic fluid, colorless to brownish yellow, oily, soluble in alcohol, ether or light oil. It can be mixed with water in its basic form between 60 Ã, Â ° C and 210 Ã, Â ° C. As a base nitrogen, nicotine forms salts with an acid that is usually solid and soluble in water. The flash point is 95 Â ° C and its automatic ignition temperature is 244 Â ° C.
Easy to evaporate (steam pressure 5.5 Pa at 25?) And dibasic (K b1 = 1ÃÆ'â € "10 ??, K b2 = 1ÃÆ'â €" 10 ? Ã,¹Ã,¹).
Nicotine is optically active, has two forms of enantiomers. The naturally occurring form of nicotine is levorotatory with a specific rotation [?] D = -166,4Ã, Â ° ((-) - nicotine). The dextrorotatory, () - nicotine form is physiologically less active than (-) - nicotine. (-) - nicotine is more toxic than () - nicotine. Salt () - nicotine is usually dextrorotatory. The hydrochloride and sulphate salts become optically inactive when heated in a closed vessel above 180 ° C.
In exposure to ultraviolet light or various oxidizers, nicotine is converted to nicotine oxide, nicotinic acid (vitamin B3), and methylamine.
Genesis and biosynthesis
Nicotine is a natural tobacco product, which occurs in leaves in the range of 0.5 to 7.5% depending on the variety. Nicotine also occurs naturally in smaller amounts in plants from the Solanaceae family (such as potatoes, tomatoes, and eggplants).
The nicotine biosynthesis pathway involves the coupling reaction between two cyclic structures that make up nicotine. Metabolic studies show that nicotine pyridine ring is derived from niacin (nicotinic acid) whereas pyridine is derived from N -methyl -? 1 -pyrrollidium cation. The biosynthesis of the two component structures takes place through two independent syntheses, the NAD path for niacin and the tropane pathway for N -methyl -? 1 -pyrrollidium cation.
The path of NAD in the genus Nicotiana begins with the oxidation of aspartic acid into? -imino succinate by aspartate oxidase (AO). This is followed by condensation with glyceraldehyde-3-phosphate and cyclization catalyzed by quinolinate synthase (QS) to produce quinolinic acid. Quinolinic acid then reacts with phosphoriboxyl pyrophosphate which is catalyzed by quinolinic acid phosphoribosyl transferase (QPT) to form niacin mononucleotide (NaMN). The reaction now takes place through the NAD rescue cycle to produce niacin through the conversion of nicotinamide by the nicotinamidase enzyme.
The N -methyl -? 1 -pyrrollidium cation used in the synthesis of nicotine is an intermediate in the synthesis of the inherited tropane alkaloids. Biosynthesis begins with ornithine decarboxylation by ornithine decarboxylase (ODC) to produce putrescine. Putrescine is then converted to N -methyl putrescine by methylation by SAM catalyzed by putrescine N -methyltransferase (PMT). N -methylputrescine then undergoes deamination to 4-methylaminobutanal by enzyme N -methyl-putrescine oxidase (MPO), 4-methylaminobutanal then spontaneously cyclizes to N -methyl -? 1 -pyrrollidium cation.
The final step in nicotine synthesis is coupling between N -methyl -? 1 -proleration and niacin. Although the study concludes some form of coupling between two component structures, the exact processes and mechanisms remain undetermined. The current agreed theory involves converting niacin to 2,5-dihydropyridine via 3,6-dihydronotinic acid. The 2.5-dihydropyridine intermediates will then react with N -methyl -? 1 -pirrrolidium cation to form pure (-) - nicotine enantiomer.
Detection in body fluids
Nicotine can be quantified in blood, plasma, or urine to confirm the diagnosis of poisoning or to facilitate forensic autopsy. The concentration of urine or salivary cotinine is often measured for both pre-employment and health insurance screening programs. Careful interpretation of results is important, since passive exposure to cigarette smoke can result in significant accumulation of nicotine, followed by the emergence of its metabolites in various body fluids. The use of nicotine is not regulated in competitive sports programs.
History
Nicotine is named after the tobacco plant Nicotiana tabacum, which in turn is named after the French ambassador in Portugal, Jean Nicot de Villemain, who sent tobacco and beans to Paris in 1560, was handed over to the King of France, and who promoted the use of their medicine. Smoking is believed to protect against disease, especially outbreaks.
Tobacco was introduced to Europe in 1559, and by the end of the 17th century, it was used not only for smoking but also as an insecticide. After World War II, more than 2,500 tons of nicotine insecticides were used worldwide, but by the 1980s the use of nicotine insecticides had dropped below 200 tons. This is due to the availability of other insecticides that are less expensive and less harmful to mammals.
Currently, nicotine, even in the form of tobacco dust, is banned as a pesticide for organic farming in the United States.
In 2008, the EPA received a request, from the registrant, to cancel the registration of the latest nicotine pesticide registered in the United States. This request was granted, and as of 1 January 2014, this pesticide is not yet available for sale.
Chemical identification
Nicotine was first isolated from tobacco plants in 1828 by doctor Christian Wilhelm Posselt and chemist Karl Ludwig Reimann of Germany, who regarded it as poison. The empirical chemical formula was described by Melsens in 1843, its structure invented by Adolf Pinner and Richard Wolffenstein in 1893, and was first synthesized by AmÃÆ' Â © Pictet and A. Rotschy in 1904.
Society and culture
The nicotine content of popular American brand cigarettes has increased over time, and one study found that there was an average increase of 1.78% per year between 1998 and 2005.
Research
While acute/early nicotine intake leads to activation of nicotine receptors, the use of low-dose nicotine causes the desensitization of nicotine receptors (due to tolerance development) and produces antidepressant effects, with early studies suggesting low doses of nicotine may be an effective treatment of major depressive disorders in non-smokers. However, the original study concluded that: "Nicotine patches result in short-term depression improvements with small side effects.Because of the high risk of nicotine on health, nicotine patches are not recommended for clinical use in depression."
Although tobacco smoking is associated with an increased risk of Alzheimer's disease, there is evidence that nicotine itself has the potential to prevent and treat Alzheimer's disease.
Studies of the most dominant nicotine metabolite, cotinine, show that some of the nicotine-negative effects of nicotine are mediated by cotinine.
Small studies are available in humans but animal studies show there is a potential benefit of nicotine in Parkinson's disease.
See also
References
Further reading
External links
- Description of the nicotine mechanism
- Erowid Nicotine Vault: Nicotine Material Safety Data Sheet
- Thomas, Gareth AO; Rhodes, John; Ingram, John R (2005). "Disease Mechanism: Nicotine - a review of its actions in the context of gastrointestinal disease". Clinical Practice of Gastroenterology & amp; Hepatology . 2 (11): 536-544. doi: 10.1038/ncpgasthep0316. PMIDÃ, 35 16355159.
- CDC - NIOSH A Pocket Guide for Chemical Hazards
Source of the article : Wikipedia
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