Selasa, 09 Oktober 2012
NICOTINE
Nicotine is an alkaloid found in the nightshade family of plants (Solanaceae) that acts as a nicotinic acetylcholine agonist and a monoamine oxidase inhibitor. The biosynthesis takes place in the roots and accumulation occurs in the leaves of the Solanaceae. It constitutes approximately 0.6–3.0% of the dry weight of tobacco and is present in the range of 2–7 µg/kg of various edible plants. It functions as an antiherbivore chemical; therefore, nicotine was widely used as an insecticide in the past and nicotine analogs such as imidacloprid are currently widely used.
In low doses (an average cigarette yields about 1 mg of absorbed nicotine), the substance acts as a stimulant in mammals, while high amounts (30–60 mg can be fatal. This stimulant effect is the main factor responsible for the dependence-forming properties of tobacco smoking. According to the American Heart Association, nicotine addiction has historically been one of the hardest addictions to break, while the pharmacological and behavioral characteristics that determine tobacco addiction are similar to those determining addiction to heroin and cocaine. The nicotine content of popular American-brand cigarettes has slowly increased over the years, and one study found that there was an average increase of 1.6% per year between the years of 1998 and 2005. This was found for all major market categories of cigarettes. Research in 2011 has found that nicotine inhibits chromatin-modifying enzymes (class I and II histone deacetylases) which increases the ability of cocaine to cause an addiction.
History and name
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 seeds to Paris in 1560,and who promoted their medicinal use. The tobacco and seeds were brought to ambassador Nicot from Brazil by Luis de Gois, a Portuguese colonist in São Paulo. Nicotine was first isolated from the tobacco plant in 1828 by physician Wilhelm Heinrich Posselt and chemist Karl Ludwig Reimann of Germany, who considered it a poison. Its chemical empirical formula was described by Melsens in 1843, its structure was discovered by Adolf Pinner and Richard Wolffenstein in 1893, and it was first synthesized by Amé Pictet and A. Rotschy in 1904.
Chemistry
Nicotine is a hygroscopic, oily liquid that is miscible with water in its base form. As a nitrogenous base, nicotine forms salts with acids that are usually solid and water soluble. Nicotine easily penetrates the skin. As shown by the physical data, free base nicotine will burn at a temperature below its boiling point, and its vapors will combust at 308 K (35 °C; 95 °F) in air despite a low vapor pressure. Because of this, most of the nicotine is burned when a cigarette is smoked; however, enough is inhaled to cause pharmacological effects.
Optical activity
Nicotine is optically active, having two enantiomeric forms. The naturally occurring form of nicotine is levorotatory with a specific rotation of [α]D = –166.4° ((−)-nicotine). The dextrorotatory form, (+)-nicotine is physiologically less active than (–)-nicotine. (−)-nicotine is more toxic than (+)-nicotine. The salts of (+)-nicotine are usually dextrorotatory.
Biosynthesis
Nicotine biosynthesis
The biosynthetic pathway of nicotine involves a coupling reaction between the two cyclic structures that compose nicotine. Metabolic studies show that the pyridine ring of nicotine is derived from nicotinic acid while the pyrrolidone is derived from N-methyl-Δ1-pyrrollidium cation. Biosynthesis of the two component structures proceeds via two independent syntheses, the NAD pathway for nicotinic acid and the tropane pathway for N-methyl-Δ1-pyrrollidium cation.
The NAD pathway in the genus nicotiana begins with the oxidation of aspartic acid into α-imino succinate by aspartate oxidase (AO). This is followed by a condensation with glyceraldehyde-3-phosphate and a cyclization catalyzed by quinolinate synthase (QS) to give quinolinic acid. Quinolinic acid then reacts with phosphoriboxyl pyrophosphate catalyzed by quinolinic acid phosphoribosyl transferase (QPT) to form nicotinic acid mononucleotide (NaMN). The reaction now proceeds via the NAD salvage cycle to produce nicotinic acid via the conversion of nicotinamide by the enzyme nicotinamidase.
The N-methyl-Δ1-pyrrollidium cation used in the synthesis of nicotine is an intermediate in the synthesis of tropane-derived alkaloids. Biosynthesis begins with decarboxylation of ornithine by ornithine decarboxylase (ODC) to produce putrescine. Putrescine is then converted into N-methyl putrescine via methylation by SAM catalyzed by putrescine N-methyltransferase (PMT). N-methylputrescine then undergoes deamination into 4-methylaminobutanal by the N-methylputrescine oxidase (MPO) enzyme, 4-methylaminobutanal then spontaneously cyclize into N-methyl-Δ1-pyrrollidium cation.
The final step in the synthesis of nicotine is the coupling between N-methyl-Δ1-pyrrollidium cation and nicotinic acid. Although studies conclude some form of coupling between the two component structures, the definite process and mechanism remains undetermined. The current agreed theory involves the conversion of nicotinic acid into 2,5-dihydropyridine through 3,6-dihydronicotinic acid. The 2,5-dihydropyridine intermediate would then react with N-methyl-Δ1-pyrrollidium cation to form enantiomerically pure (–)-nicotine.
Pharmacology
Pharmacokinetics
Side effects of nicotine.
As nicotine enters the body, it is distributed quickly through the bloodstream and crosses the blood–brain barrier reaching the brain within 10–20 seconds after inhalation. The elimination half-life of nicotine in the body is around two hours.
The amount of nicotine absorbed by the body from smoking depends on many factors, including the types of tobacco, whether the smoke is inhaled, and whether a filter is used. For chewing tobacco, dipping tobacco, snus and snuff, which are held in the mouth between the lip and gum, or taken in the nose, the amount released into the body tends to be much greater than smoked tobacco] Nicotine is metabolized in the liver by cytochrome P450 enzymes (mostly CYP2A6, and also by CYP2B6). A major metabolite is cotinine.
Other primary metabolites include nicotine N'-oxide, nornicotine, nicotine isomethonium ion, 2-hydroxynicotine and nicotine glucuronide. Under some conditions, other substances may be formed such as myosmine.
Glucuronidation and oxidative metabolism of nicotine to cotinine are both inhibited by menthol, an additive to mentholated cigarettes, thus increasing the half-life of nicotine in vivo.
Detection of use
Medical detection
Nicotine can be quantified in blood, plasma, or urine to confirm a diagnosis of poisoning or to facilitate a medicolegal death investigation. Urinary or salivary cotinine concentrations are frequently measured for the purposes of pre-employment and health insurance medical screening programs. Careful interpretation of results is important, since passive exposure to cigarette smoke can result in significant accumulation of nicotine, followed by the appearance of its metabolites in various body fluids. Nicotine use is not regulated in competitive sports programs, yet the drug has been shown to have a significant beneficial effect on athletic endurance in subjects who have not used nicotine before.
Pharmacodynamics
Nicotine acts on the nicotinic acetylcholine receptors, specifically the ganglion type nicotinic receptor and one CNS nicotinic receptor. The former is present in the adrenal medulla and elsewhere, while the latter is present in the central nervous system (CNS). In small concentrations, nicotine increases the activity of these receptors. Nicotine also has effects on a variety of other neurotransmitters through less direct mechanisms.
In the central nervous system
Effect of nicotine on dopaminergic neurons.
By binding to nicotinic acetylcholine receptors, nicotine increases the levels of several neurotransmitters – acting as a sort of "volume control". It is thought that increased levels of dopamine in the reward circuits of the brain are responsible for the apparent euphoria and relaxation, and addiction caused by nicotine consumption. Nicotine has a higher affinity for acetylcholine receptors in the brain than those in skeletal muscle, though at toxic doses it can induce contractions and respiratory paralysis. Nicotine's selectivity is thought to be due to a particular amino acid difference on these receptor subtypes.
Tobacco smoke contains anabasine, anatabine, and nornicotine.[citation needed] It also contains the monoamine oxidase inhibitors harman and norharman. These beta-carboline compounds significantly decrease MAO activity in smokers. MAO enzymes break down monoaminergic neurotransmitters such as dopamine, norepinephrine, and serotonin. It is thought that the powerful interaction between the MAOI's and the nicotine is responsible for most of the addictive properties of tobacco smoking. The addition of five minor tobacco alkaloids increases nicotine-induced hyperactivity, sensitization and intravenous self-administration in rats. Chronic nicotine exposure via tobacco smoking up-regulates alpha4beta2* nAChR in cerebellum and brainstem regions but not habenulopeduncular structures. Alpha4beta2 and alpha6beta2 receptors, present in the ventral tegmental area, play a crucial role in mediating the reinforcement effects of nicotine.
In the sympathetic nervous system
Nicotine also activates the sympathetic nervous system, acting via splanchnic nerves to the adrenal medulla, stimulates the release of epinephrine. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing the release of epinephrine (and norepinephrine) into the bloodstream. Nicotine also has an affinity for melanin-containing tissues due to its precursor function in melanin synthesis or due to the irreversible binding of melanin and nicotine. This has been suggested to underlie the increased nicotine dependence and lower smoking cessation rates in darker pigmented individuals. However, further research is warranted before a definite conclusive link can be inferred.
Effect of nicotine on chromaffin cells.
In adrenal medulla
By binding to ganglion type nicotinic receptors in the adrenal medulla nicotine increases flow of adrenaline (epinephrine), a stimulating hormone and neurotransmitter. By binding to the receptors, it causes cell depolarization and an influx of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of chromaffin granules and thus the release of epinephrine (and norepinephrine) into the bloodstream. The release of epinephrine (adrenaline) causes an increase in heart rate, blood pressure and respiration, as well as higher blood glucose levels. Nicotine is the natural product of tobacco, having a half-life of 1 to 2 hours. Cotinine is an active metabolite of nicotine that remains in the blood for 18 to 20 hours, making it easier to analyze due to its longer half-life.
Psychoactive effects
Nicotine's mood-altering effects are different by report: in particular it is both a stimulant and a relaxant.[44] First causing a release of glucose from the liver and epinephrine (adrenaline) from the adrenal medulla, it causes stimulation. Users report feelings of relaxation, sharpness, calmness, and alertness.[45] Like any stimulant, it may very rarely cause the often catastrophically uncomfortable neuropsychiatric effect of akathisia. By reducing the appetite and raising the metabolism, some smokers may lose weight as a consequence.
When a cigarette is smoked, nicotine-rich blood passes from the lungs to the brain within seven seconds and immediately stimulates the release of many chemical messengers such as acetylcholine, norepinephrine, epinephrine, vasopressin, histamine, arginine, serotonin, dopamine, autocrine agents, and beta-endorphin. This release of neurotransmitters and hormones is responsible for most of nicotine's effects. Nicotine appears to enhance concentration and memory due to the increase of acetylcholine. It also appears to enhance alertness due to the increases of acetylcholine and norepinephrine. Arousal is increased by the increase of norepinephrine. Pain is reduced by the increases of acetylcholine and beta-endorphin. Anxiety is reduced by the increase of beta-endorphin. Nicotine also extends the duration of positive effects of dopamine and increases sensitivity in brain reward systems. Most cigarettes (in the smoke inhaled) contain 1 to 3 milligrams of nicotine.
Research suggests that, when smokers wish to achieve a stimulating effect, they take short quick puffs, which produce a low level of blood nicotine. This stimulates nerve transmission. When they wish to relax, they take deep puffs, which produce a high level of blood nicotine, which depresses the passage of nerve impulses, producing a mild sedative effect. At low doses, nicotine potently enhances the actions of norepinephrine and dopamine in the brain, causing a drug effect typical of those of psychostimulants. At higher doses, nicotine enhances the effect of serotonin and opiate activity, producing a calming, pain-killing effect. Nicotine is unique in comparison to most drugs, as its profile changes from stimulant to sedative/pain killer in increasing dosages and use.
Technically, nicotine is not significantly addictive, as nicotine administered alone does not produce significant reinforcing properties. However, after coadministration with an MAOI, such as those found in tobacco, nicotine produces significant behavioral sensitization, a measure of addiction potential. This is similar in effect to amphetamine. Nicotine gum, usually in 2-mg or 4-mg doses, and nicotine patches are available, as well as smokeless tobacco, nicotine lozenges and electronic cigarettes.
A 21 mg patch applied to the left arm. The Cochrane Collaboration finds that NRT increases a quitter's chance of success by 50 to 70%. But in 1990, researchers found that 93% of users returned to smoking within six months.
Side Effects
Nicotine not only increases blood pressure and heart rate in humans, but it also mimics the venous endothelial dysfunction caused by smoking. Nicotine can stimulate abnormal proliferation of vascular endothelial cells, similar to that seen in atherosclerosis. Nicotine induces potentially atherogenic genes in human coronary artery endothelial cells. Nicotine could cause microvascular injury through its action on nicotinic acetylcholine receptors (nAChRs), however other mechanisms are also likely at play.
A study on rats showed that nicotine exposure abolishes the beneficial and protective effects of estrogen on the hippocampus, an estrogen-sensitive region of the brain involved in memory formation and retention.
Dependence and withdrawal
Modern research shows that nicotine acts on the brain to produce a number of effects. Specifically, research examining its addictive nature has been found to show that nicotine activates the mesolimbic pathway ("reward system") – the circuitry within the brain that regulates feelings of pleasure and euphoria.
Dopamine is one of the key neurotransmitters actively involved in the brain. Research shows that by increasing the levels of dopamine within the reward circuits in the brain, nicotine acts as a chemical with intense addictive qualities. In many studies it has been shown to be more addictive than cocaine and heroin. Like other physically addictive drugs, nicotine withdrawal causes down-regulation of the production of dopamine and other stimulatory neurotransmitters as the brain attempts to compensate for artificial stimulation. As dopamine regulates the sensitivity of nicotinic acetylcholine receptors decreases. To compensate for this compensatory mechanism, the brain in turn upregulates the number of receptors, convoluting its regulatory effects with compensatory mechanisms meant to counteract other compensatory mechanisms. An example is the increase in norepinephrine, one of the successors to dopamine, which inhibit reuptake of the glutamate receptors, in charge of memory and cognition. The net effect is an increase in reward pathway sensitivity, the opposite of other addictive drugs such as cocaine and heroin, which reduce reward pathway sensitivity. This neuronal brain alteration can persist for months after administration ceases.
A study found that nicotine exposure in adolescent mice retards the growth of the dopamine system, thus increasing the risk of substance abuse during adolescence.
Immunology prevention
Because of the severe addictions and the harmful effects of smoking, vaccination protocols have been developed. The principle is under the premise that if an antibody is attached to a nicotine molecule, it will be prevented from diffusing through the capillaries, thus making it less likely that it ever affects the brain by binding to nicotinic acetylcholine receptors.
These include attaching the nicotine molecule as a hapten to a protein carrier such as Keyhole limpet hemocyanin or a safe modified bacterial toxin to elicit an active immune response. Often it is added with bovine serum albumin.
Additionally, because of concerns with the unique immune systems of individuals being liable to produce antibodies against endogenous hormones and over the counter drugs, monoclonal antibodies have been developed for short term passive immune protection. They have half-lives varying from hours to weeks. Their half-lives depend on their ability to resist degradation from pinocytosis by epithelial cells.
Toxicology
Nicotine poisoning
NFPA 704
1
4
0
The LD of nicotine is 50 mg/kg for rats and 3 mg/kg for mice. 30–60 mg (0.5–1.0 mg/kg) can be a lethal dosage for adult humans. Nicotine therefore has a high toxicity in comparison to many other alkaloids such as cocaine, which has an LD50 of 95.1 mg/kg when administered to mice. It is unlikely that a person would overdose on nicotine through smoking alone, although overdose can occur through combined use of nicotine patches or nicotine gum and cigarettes at the same time. Spilling a high concentration of nicotine onto the skin can cause intoxication or even death, since nicotine readily passes into the bloodstream following dermal contact.
Historically, nicotine has not been regarded as a carcinogen and the IARC has not evaluated nicotine in its standalone form and assigned it to an official carcinogen group. While no epidemiological evidence supports that nicotine alone acts as a carcinogen in the formation of human cancer, research over the last decade has identified nicotine's carcinogenic potential in animal models and cell culture. Nicotine has been noted to directly cause cancer through a number of different mechanisms such as the activation of MAP Kinases. Indirectly, nicotine increases cholinergic signalling (and adrenergic signalling in the case of colon cancer), thereby impeding apoptosis (programmed cell death), promoting tumor growth, and activating growth factors and cellular mitogenic factors such as 5-LOX, and EGF. Nicotine also promotes cancer growth by stimulating angiogenesis and neovascularization. In one study, nicotine administered to mice with tumors caused increases in tumor size (twofold increase), metastasis (nine-fold increase), and tumor recurrence (threefold increase).
Though the teratogenic properties of nicotine may or may not yet have been adequately researched, women who use nicotine gum and patches during the early stages of pregnancy face an increased risk of having babies with birth defects, according to a study of around 77,000 pregnant women in Denmark. The study found that women who use nicotine-replacement therapy in the first 12 weeks of pregnancy have a 60% greater risk of having babies with birth defects, compared to women who are non-smokers.
Effective April 1, 1990, the Office of Environmental Health Hazard Assessment (OEHHA) of the California Environmental Protection Agency added nicotine to the list of chemicals known to the state to cause developmental toxicity, for the purposes of Proposition 65.
Nicotine reduces the chance of breast cancer among women carrying the very high risk BRCA gene, preeclampsia, and atopic disorders such as allergic asthma. A plausible mechanism of action in these cases may be nicotine acting as an anti-inflammatory agent, and interfering with the inflammation-related disease process, as nicotine has vasoconstrictive effects.
Tobacco smoke has been shown to contain compounds capable of inhibiting monoamine oxidase, which is responsible for the degradation of dopamine in the human brain. When dopamine is broken down by MAO-B, neurotoxic by-products are formed, possibly contributing to Parkinson's and Alzheimers disease. Many such papers regarding Alzheimer's diseaseand Parkinson's Disease have been published. While 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. Nicotine has been shown to delay the onset of Parkinson's disease in studies involving monkeys and humans. A study has shown a protective effect of nicotine itself on neurons due to nicotine activation of α7-nAChR and the PI3K/Akt pathway which inhibits apoptosis-inducing factor release and mitochondrial translocation, cytochrome c release and caspase 3 activation. Recent studies have indicated that nicotine can be used to help adults suffering from autosomal dominant nocturnal frontal lobe epilepsy. The same areas that cause seizures in that form of epilepsy are responsible for processing nicotine in the brain.
Studies suggest a correlation between smoking and schizophrenia, with estimates near 75% for the proportion of schizophrenic patients who smoke. Although the nature of this association remains unclear, it was recently argued that the increased level of smoking in schizophrenia may be due to a desire to self-medicate with nicotine. More recent research has found that mildly dependent users got some benefit from nicotine, but not those who were highly dependent. There are very few research done on this subject, including the research by Duke University Medical Centre which found that nicotine may improve the symptoms of depression in people. Nicotine appears to improve ADHD symptoms. Some studies are focusing on benefits of nicotine therapy in adults with ADHD.
While acute/initial nicotine intake causes activation of nicotine receptors, chronic low doses of nicotine use leads to desensitisation of nicotine receptors (due to the development of tolerance) and results in an antidepressant effect, with research showing low dose nicotine patches being an effective treatment of major depressive disorder in non-smokers. Nicotine (in the form of chewing gum or a transdermal patch) is being explored as an experimental treatment for OCD. Small studies show some success, even in otherwise treatment-refractory cases. The relationship between smoking and inflammatory bowel disease is now firmly established but remains a source of confusion among both patients and doctors. It is negatively associated with ulcerative colitis but positively associated with Crohn's disease. In addition, it has opposite influences on the clinical course of the two conditions with benefit in ulcerative colitis but a detrimental effect in Crohn's disease
Langganan:
Posting Komentar (Atom)
i have some problems lin,,
BalasHapushow to work in inhibiting nicotine and chromatin modifying enzymes (class I and II histone deacetylases) that enhances the ability of cocaine to cause addiction??
and described in your article that the dextrorotatory form, (+)-nicotine is physiologically less active than (-)-nicotine (-).-nicotine is more toxic than the (+)-nicotine, why?
please explain to me,,
whether The biosynthesis just takes place in the roots and accumulation Occurs in the leaves of the Solanaceae? and please explain that mecanism
BalasHapusthanks for your question vebria
Hapusi will try to answer Biosynthesis of Nicotine
the biosynthetic pathway of nicotine involves a coupling reaction between the two cyclic structures that compose nicotine. Metabolic studies show that the pyridine ring of nicotine is derived from nicotinic acid while the pyrrolidone is derived from N-methyl-Δ1-pyrrollidium cation.[18][19] Biosynthesis of the two component structures proceeds via two independent syntheses, the NAD pathway for nicotinic acid and the tropane pathway for N-methyl-Δ1-pyrrollidium cation.
The NAD pathway in the genus nicotiana begins with the oxidation of aspartic acid into α-imino succinate by aspartate oxidase (AO). This is followed by a condensation with glyceraldehyde-3-phosphate and a cyclization catalyzed by quinolinate synthase (QS) to give quinolinic acid. Quinolinic acid then reacts with phosphoriboxyl pyrophosphate catalyzed by quinolinic acid phosphoribosyl transferase (QPT) to form nicotinic acid mononucleotide (NaMN). The reaction now proceeds via the NAD salvage cycle to produce nicotinic acid via the conversion of nicotinamide by the enzyme nicotinamidase.
The N-methyl-Δ1-pyrrollidium cation used in the synthesis of nicotine is an intermediate in the synthesis of tropane-derived alkaloids. Biosynthesis begins with decarboxylation of ornithine by ornithine decarboxylase (ODC) to produce putrescine. Putrescine is then converted into N-methyl putrescine via methylation by SAM catalyzed by putrescine N-methyltransferase (PMT). N-methylputrescine then undergoes deamination into 4-methylaminobutanal by the N-methylputrescine oxidase (MPO) enzyme, 4-methylaminobutanal then spontaneously cyclize into N-methyl-Δ1-pyrrollidium cation.
The final step in the synthesis of nicotine is the coupling between N-methyl-Δ1-pyrrollidium cation and nicotinic acid. Although studies conclude some form of coupling between the two component structures, the definite process and mechanism remains undetermined. The current agreed theory involves the conversion of nicotinic acid into 2,5-dihydropyridine through 3,6-dihydronicotinic acid. The 2,5-dihydropyridine intermediate would then react with N-methyl-Δ1-pyrrollidium cation to form enantiomerically pure (–)-nicotine
PROBLEMS
BalasHapus1. we know that the nicotine contained in cigarettes, if there is someone smoking in a place and no one else d place, how the effect of smoke inhaled by others who were there (passive smokers), whether efeknhya more dangerous than active smokers?
2. why the (-)-nicotine is more toxic than (+)-nicotine? what is the difference of IT?
3. why nicotine can cause addiction? asnd how it process?
please give your opinion guys,thanks
passive smoke (also called environmental tobacco smoke, involuntary smoke,and secondhand smoke) is people that inhaler cigarette smoke from people who were smoking. A non-smoker is subjected to both the "sidestream" smoke from the burning tip of the cigarette and the "mainstream" smoke that has been inhaled and then is exhaled into their environment by the smoker. Nearly four-fifths of the smoke that builds up in a room containing a smoker is of the more harmful "sidestream" type.
HapusIt is not too much of a conceptual leap to understand that the smoke from cigarettes, which is so bad for the smoker, is also damaging to everyone else. Tobacco smoke contains over 4000 chemical compounds, including at least 40 cancer-causing carcinogenic agents. Tobacco smoke also contains carbon monoxide, a poisonous gas, which inhibits the transportation of oxygen to the body's vital organs via the blood. The smoke emitted from the tip of a cigarette has about double the concentration of nicotine and tar as the smoke being directly inhaled by the smoker. It also contains about three times the amount of the carcinogen benzo(a)pyrene, five times the level of carbon monoxide and about 50 times the amount of ammonia. Add to these the other chemicals in the smoke like arsenic, formaldehyde, vinyl chloride, and hydrogen cyanide and you have a very unappetizing toxic gas cocktail. Remember that the passive smoker receives all of this and gets none of the enjoyment that you get out of smoking in return. Many of the potentially toxic gasses in the smoke are present in higher concentrations in the "sidestream" smoke than in the "mainstream" smoke. In tests tobacco specific carcinogens have been found in samples of blood or urine provided by non-smokers who have been exposed to passive smoking.
Any person exposed to passive smoking may experience short-term symptoms such as a headache, a cough, wheezing, an eye irritation, a sore throat, nausea or dizziness. Adults with asthma may also experience a significant decline in lung function when exposed to secondhand smoke. Under these conditions it can take as little as half an hour for an individual's coronary blood flow to become reduced.It was estimated that prolonged exposure to secondhand tobacco smoke, increases the risk of lung cancer by approximately 20 to 25%. Studies have shown that the risk of experiencing a heart attack is believed to be almost doubled by regular exposure to secondhand smoke.
As a result, passive smoking is more dangerous than active smokers. Even the dangers of passive smoking to be borne triple jeopardy active smokers.
hi lina, I read an article on nicotine as well, I was confused because the article says that If smoking is stopped, the concentration of nicotine in the blood showed a rapid decrease reflecting the spread into the tissues of the body and the elimination phase with a half-life of 2 hours. Nicotine destroyed through oxidation reactions. please explain , how the oxidation reactions that occur so that the nicotine is destroyed?.
BalasHapussource:(http://cingdoland.blogspot.com/2010/10/kafein-vs-nikotin.html)
i read an article that "Nicotine is a powerful addictive than heroin or cocaine", can you explain about that? thank's
BalasHapusHy elsa I will try to answer
HapusNicotine is a substance contained in tobacco leaves. Every time someone inhaling nicotine-containing materials the substance will enter the body and the brain bersemayan. Every single cigarette contains at least 10 milligrams of nicotine. Nicotine is what will make a person addicted to smoking.
Although that is contained in one cigarette about 10 milligrams, but that is really absorbed into the body is as much as 1 to 2 milligrams of course, the rest is lost to the air. Nicotine in large numbers are highly fatal and is often used as pesticides in agriculture.
Each smoke cigarettes, nicotine will go into the lungs and then absorbed into the bloodstream. In just 8 seconds, nicotine is going up to the brain and alter brain works. This process goes quickly because its shape is similar to the nicotine acetylcholine present in the normal brain.
Nicotine will further increase the heart rate and respiratory frequency. Nicotine also increases blood sugar levels. This causes a smoker will feel more refreshed after smoking.
Nicotine present in the brain nerve cells will also stimulate dopamine expenditure. This substance is a substance that can improve satisfaction, comfortable and fun. In normal people, the effect of dopamine is usually triggered by food, comfort and affection with loved ones. That's why smokers feel pleasure when smoking cigarettes.
In 40 minutes, half of the dopamine effect will disappear. Well, at times like this that the desire to smoke a cigarette again. This is why smokers will continue to smoke without end for they want the concentration of dopamine in the brain.
Nicotine dependence will lead to a similar dependence on narcotic drugs as nicotine can change some brain function as described above.
By Barbara M. Dossey and Lynn Keegan, author of Holistic Nursing, nicotine is a major cause of the increasing impotence in men in the United States (2009).
Nicotine can make blood vessels constrict, decreased levels of oxygen that is needed by the skin causing premature aging, reduce blood flow to the penis, and can weaken even inhibit erections in men, as reported by LIVESTRONG.
Nicotine affects the nerve pathways associated with erection, causing difficulties for men to achieve and maintain an erection. In addition, nicotine can also release acetylcholine and epinephrine in the body, a substance in the body that modulate erection and ejaculation.
elsa I will try to answer your questions. for example, nicotine in cigarettes,
HapusNicotine cigarettes, just seconds after the first puff, begin to affect the central nervous system and the rest of your body. In certain parts of the brain, after being exposed to nicotine stimulation, you will be able to think more lightly. Another part of the brain, which is the center of "pleasure", when stimulated nicotine can make you feel more relaxed and comfortable, free from tension.
Cigarette Nicotine also affects the hormones produced by the body. This is done by hormones to make the chemical balance of the nicotine addiction and the accompanying. Heavy smokers will become dependent on the hormone levels are very high, caused by nicotine, which can be a very powerful addictive substance. They need to smoke a cigarette with a certain time interval. After the stimulation of hormones decreases, they will need another cigarette to smoke in order to feel good / better.
Cigarette Nicotine creates a biochemical reaction in your body, which quickly gives effect to the 'mood', your body's metabolism and ability to act. The more smoke you breathe, the more your body's chemical dependency. Smokers can also become addicted to cigarettes are always dependent on the psychological effects caused by induced nicotine. If this happens, smoking will be able to influence the attitudes and feelings in certain situations.
Nicotine cigarettes can respond to brain to the body makes substances more endorphins. Endorphins are protein compounds or rather the body's natural pain killer. Endorphins chemical structure similar to morphine which is a painkiller upscale. Endorphins can make a person feel relaxed and euphoric. thank's
i'll try to answer..
BalasHapusAmong the properties of a psychoactive drug - how much craving it can cause, how severe is the withdrawal, how intense a high it brings - each addicting drug has its own profile.
Heroin has a painful, powerful withdrawal, as does alcohol. But cocaine has little or no withdrawal. On the other hand, cocaine is more habit-forming in some respects, it is more reinforcing in the scientific terminology, meaning that animals and humans will seek to use it frequently in short periods of time, even over food and water.
Drugs rank differently on the scale of how difficult they are to quit as well, with nicotine rated by most experts as the most difficult to quit. A central property of addiction is the user's control over the substance. With all drugs. including heroin, many are occasional users. The addictive property of the substance can be measured by how many users maintain a casual habit and how many are persistent, regular users.
According to large Government surveys of alcohol users, only about 15 percent are regular. dependent drinkers. Among cocaine users, about 8 percent become dependent. For cigarettes, the percentage is reversed. About 90 percent of smokers are persistent daily users, and 55 percent become dependent Only 10 percent are occasional users.