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Nicotine and cigarette smoke both induce the expression of liver enzymes (e.g., certain cytochrome P450 proteins) which metabolize drugs, leading to the potential for alterations in drug metabolism. [77] Smoking cessation may decrease the metabolism of acetaminophen, beta-blockers, caffeine, oxazepam, pentazocine, propoxyphene, theophylline ...
Cytochrome P450 2A6 (abbreviated CYP2A6) is a member of the cytochrome P450 mixed-function oxidase system, which is involved in the metabolism of xenobiotics in the body. CYP2A6 is the primary enzyme responsible for the oxidation of nicotine and cotinine. It is also involved in the metabolism of several pharmaceuticals, carcinogens, and a ...
In cellular metabolism, NAD is involved in redox reactions, carrying electrons from one reaction to another, so it is found in two forms: NAD + is an oxidizing agent, accepting electrons from other molecules and becoming reduced; with H +, this reaction forms NADH, which can be used as a reducing agent to donate electrons.
Cotinine has an in vivo half-life of approximately 20 hours, and is typically detectable for several days (up to one week) after the use of tobacco. The level of cotinine in the blood, saliva, and urine is proportionate to the amount of exposure to tobacco smoke, so it is a valuable indicator of tobacco smoke exposure, including secondary (passive) smoke. [14]
As nicotine is an appetite suppressant and smokers expend more energy, weight gain due to smoking cessation is generally attributed to increased calorific intake and a slowed metabolic rate. Weight gain can be a deterrent in the smoking cessation process, even if many smokers did not smoke for weight control purposes. [ 31 ]
Nicotine has been known for centuries for its intoxicating effect. It was first isolated in 1828 from the tobacco plant by German chemists Posselt and Reimann. [2] The discovery of positive effects from nicotine on animal memory was discovered by in vivo researches in the mid 1980s. Those researches led to a new era in studies of nicotinic ...
How does the nicotine in e-cigarettes affect the brain? [6] Until about age 25, the brain is still growing. [6] Each time a new memory is created or a new skill is learned, stronger connections – or synapses – are built between brain cells. [6] Young people's brains build synapses faster than adult brains. [6]
Nicotine may result in adverse effects to the neurological growth of the fetus. [65] Nicotine can lead to vasoconstriction of uteroplacental vessels, which reduces the delivery of both nutrients and oxygen to the fetus. As a result, nutrition is re-distributed to prioritize vital organs, such as the heart and the brain, at the cost of less ...