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Ethanol[1]
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Commonly referred to simply as alcohol or spirits, ethanol is also called ethyl alcohol, and drinking alcohol. It is the principal type of alcohol found in alcoholic beverages, produced by the fermentation of sugars by yeasts. It is a neurotoxic[6][7] psychoactive drug and one of the oldest recreational drugs used by humans. It can cause alcohol intoxication when consumed in sufficient quantity. Ethanol is used as a solvent, an antiseptic, a fuel and the active fluid in modern (post-mercury) thermometers. It is a volatile, flammable, colorless liquid with a strong chemical odor. Its structural formula CH 3CH 2OH, is often abbreviated as C 2H 5OH, C 2H 6O or EtOH.
Ethanol is the International Union of Pure and Applied Chemistry (IUPAC) for a molecule with two carbon atoms (prefix "eth-"), having a single bond between them (suffix "-ane"), and an attached functional group-OH group (suffix "-ol").[1]
The prefix ethyl was coined in 1834 by the German chemist Justus Liebig.[8] Ethyl is a contraction of the French word ether (any substance that evaporated or sublimated readily at room temperature) and the Greek word ύλη (hyle, substance).[9]
The name ethanol was coined as a result of a resolution that was adopted at the International Conference on Chemical Nomenclature that was held in April 1892 in Geneva, Switzerland.[10]
The term "alcohol" now refers to a wider class of substances in chemistry nomenclature, but in common parlance it remains the name of ethanol. Ultimately a medieval loan from Arabic al-kuḥl,[11] use of alcohol in this sense is modern, introduced in the mid 18th century. Before that time, Middle Latin alcohol referred to "powdered ore of antimony; powdered cosmetic", by the later 17th century "any sublimated substance; distilled spirit" use for "the spirit of wine" (shortened from a full expression alcohol of wine) recorded 1753. The systematic use in chemistry dates to 1850.
Ethanol is a 2-carbon alcohol. Its molecular formula is CH3CH2OH. An alternative notation is CH3–CH2–OH, which indicates that the carbon of a methyl group (CH3–) is attached to the carbon of a methylene group (–CH2–), which is attached to the oxygen of a hydroxyl group (–OH). It is a constitutional isomer of dimethyl ether. Ethanol is sometimes abbreviated as EtOH, using the common organic chemistry notation of representing the ethyl group (C2H5) with Et.
Ethanol is a byproduct of the metabolic process of yeast. As such, ethanol will be present in any yeast habitat. Ethanol can commonly be found in overripe fruit.[12] Ethanol produced by symbiotic yeast can be found in Bertam Palm blossoms. Although some animal species such as the Pentailed Treeshrew exhibit ethanol-seeking behaviors, most show no interest or avoidance of food sources containing ethanol.[13] Ethanol is also produced during the germination of many plants as a result of natural anerobiosis.[14] Ethanol has been detected in outer space, forming an icy coating around dust grains in interstellar clouds.[15] Minute quantity amounts (244 ppb) of endogenous ethanol and acetaldehyde were found in the exhaled breath of healthy volunteers.[16]
Ethanol is known to possess the following direct pharmacodynamic actions (most important actions are bolded):[17]
Some of its actions on ligand-gated ion channels, specifically the nACh receptors and the glycine receptor, are dose-dependent, with potentiation or inhibition occurring dependent on ethanol concentration. This is because ethanol's effects on these channels are a summation of positive and negative allosteric modulatory actions.[17]
The removal of ethanol from the human body, through oxidation by alcohol dehydrogenase in the liver, is limited. Hence, the removal of a large concentration of alcohol from blood may follow zero-order kinetics. This means that alcohol leaves the body at a constant rate, rather than having an elimination half-life.[21]
The rate-limiting steps for one substance may be in common with other substances. As a result, the blood alcohol concentration can be used to modify the rate of metabolism of methanol and ethylene glycol. Methanol itself is not highly toxic, but its metabolites formaldehyde and formic acid are; therefore, to reduce the rate of production and concentration of these harmful metabolites, ethanol can be ingested.[22] Ethylene glycol poisoning can be treated in the same way.
Pure ethanol will irritate the skin and eyes.[23] Nausea, vomiting and intoxication are symptoms of ingestion. Long-term use by ingestion can result in serious liver damage.[24] Atmospheric concentrations above one in a thousand are above the European Union Occupational exposure limits.[24]
Ethanol is a central nervous system depressant and has significant psychoactive effects in sublethal doses; for specifics, see "Effects of alcohol on the body by dose". Based on its abilities to change the human consciousness, ethanol is considered a psychoactive drug.[26] Death from ethanol consumption is possible when blood alcohol level reaches 0.4%. A blood level of 0.5% or more is commonly fatal. Levels of even less than 0.1% can cause intoxication, with unconsciousness often occurring at 0.3–0.4%.[27]
The amount of ethanol in the body is typically quantified by blood alcohol content (BAC), which is here taken as weight of ethanol per unit volume of blood. The table at the right summarizes the symptoms of ethanol consumption. Small doses of ethanol, in general, produce euphoria and relaxation; people experiencing these symptoms tend to become talkative and less inhibited, and may exhibit poor judgment. At higher dosages (BAC > 1 g/L), ethanol acts as a central nervous system depressant, producing at progressively higher dosages, impaired sensory and motor function, slowed cognition, stupefaction, unconsciousness, and possible death.
Ethanol acts in the central nervous system primarily by binding to the GABAA receptor, increasing the effects of the inhibitory neurotransmitter GABA (i.e., it is a positive allosteric modulator).[28]
Prolonged heavy consumption of alcohol can cause significant permanent damage to the brain and other organs. See Alcohol consumption and health.
According to the US National Highway Traffic Safety Administration, in 2002 about "41% of people fatally injured in traffic crashes were in alcohol related crashes".[29] The risk of a fatal car accident increases exponentially with the level of alcohol in the driver's blood.[30] Most drunk driving laws governing the acceptable levels in the blood while driving or operating heavy machinery set typical upper limits of blood alcohol content (BAC) between 0.02% and 0.08%.
Discontinuing consumption of alcohol after several years of heavy drinking can also be fatal. Alcohol withdrawal can cause anxiety, autonomic dysfunction, seizures, and hallucinations. Delirium tremens is a condition that requires people with a long history of heavy drinking to undertake an alcohol detoxification regimen.
The reinforcing effects of alcohol consumption are also mediated by acetaldehyde generated by catalase and other oxidizing enzymes such as cytochrome P-4502E1 in the brain.[31] Although acetaldehyde has been associated with some of the adverse and toxic effects of ethanol, it appears to play a central role in the activation of the mesolimbic dopamine system.[32]
Ethanol within the human body is converted into acetaldehyde by alcohol dehydrogenase and then into the acetyl in acetyl CoA by acetaldehyde dehydrogenase. Acetyl CoA is the final product of both carbohydrate and fat metabolism, where the acetyl can be further used to produce energy or for biosynthesis. As such, ethanol can be compared to an energy-bearing macronutrient, yielding approximately 7 kcal per gram consumed.[33] However, the product of the first step of this breakdown, acetaldehyde,[34] is more toxic than ethanol. Acetaldehyde is linked to most of the clinical effects of alcohol. It has been shown to increase the risk of developing cirrhosis of the liver[35] and multiple forms of cancer.
During the metabolism of alcohol via the respective dehydrogenases, NAD (Nicotinamide adenine dinucleotide) is converted into reduced NAD. Normally, NAD is used to metabolise fats in the liver, and as such alcohol competes with these fats for the use of NAD. Prolonged exposure to alcohol means that fats accumulate in the liver, leading to the term 'fatty liver'. Continued consumption (such as in alcoholism) then leads to cell death in the hepatocytes as the fat stores reduce the function of the cell to the point of death. These cells are then replaced with scar tissue, leading to the condition called cirrhosis.
Ethanol can intensify the sedation caused by other central nervous system depressant drugs such as barbiturates, benzodiazepines, opioids, non-benzodiazepines (such as Zolpidem and Zopiclone), antipsychotics, sedative antihistamines, and antidepressants.[27] It interacts with cocaine in vivo to produce cocaethylene, another psychoactive substance.[36] Ethanol enhances the bioavailability of methylphenidate (elevated plasma d-MPH).[37] In combination with cannabis, ethanol increases plasma THC levels, which suggets that ethanol may increase the absorption of THC.[38]
Alcohol and metronidazole
One of the most important drug/food interactions that should be noted is between alcohol and metronidazole.
Metronidazole is an antibacterial agent that kills bacteria by damaging cellular DNA and hence cellular function.[39] Metronidazole is usually given to people who have diarrhea caused by Clostridium difficile bacteria. C. difficile is one of the most common microorganisms that cause diarrhea and can lead to complications such as colon inflammation and even more severely, death.
Patients who are taking metronidazole are strongly advised to avoid alcohol, even after 1 hour after the last dose. The reason is that alcohol and metronidazole can lead to side effects such as flushing, headache, nausea, vomiting, abdominal cramps, and sweating.[40][41][41] These symptoms are often called the disulfiram-like reaction. The proposed mechanism of action for this interaction is that metronidazole can bind to an enzyme that normally metabolizes alcohol. Binding to this enzyme may impair the liver's ability to process alcohol for proper excretion.[42]
A part of ethyl alcohol is hydrophobic. This hydrophobic or lipophilic end can diffuse across cells that line the stomach wall. In fact, alcohol is one of the rare substances that can be absorbed in the stomach. Most food substances are absorbed in the small intestine. However, even though alcohol can be absorbed in the stomach, it is mostly absorbed in the small intestine because the small intestine has a large surface area that promotes absorption. Once alcohol is absorbed in the small intestine, it delays the release of stomach contents from emptying into the small intestine. Thus, alcohol can delay the rate of absorption of nutrients.[43] After absorption, alcohol reaches the liver where it is metabolized.
Breathalyzers Alcohol that is not processed by the liver goes to the heart. The liver can process only a certain amount of alcohol per unit time. Thus, when a person drinks too much alcohol, more alcohol can reach the heart. In the heart, alcohol reduces the force of heart contractions. Consequently, the heart will pump less blood, lowering overall body blood pressure.[44] Also, blood that reaches the heart goes to the lungs to replenish blood's oxygen concentration. It is at this stage that a person can breathe out traces of alcohol.[44] This is the underlying principle of the alcohol breath testing (or breathalyzers) to determine if a driver has been drinking and driving.[45]
From the lungs, blood returns to the heart and will be distributed throughout the body. Interestingly, alcohol increases levels of high-density lipoproteins(HDLs), which carry cholesterol.[44] Alcohol is known to make blood less likely to clot, reducing risk of heart attack and stroke. This could be the reason why alcohol could produce health benefits when consumed in moderate amounts.[46] Also, alcohol dilates blood vessels. Consequently, a person will feel warmer, and their face turns flush and pink.[44]
Loss of balance When alcohol reaches the brain, it has the ability to delay signals that are sent between nerve cells that control balance, thinking and movement.[44]
Frequent urination Moreover, alcohol can affect the brain's ability to produce antidiuretic hormones. These hormones are responsible for controlling the amount of urine that is produced. Alcohol prevents the body from reabsorbing water, and consequently a person who recently drank alcohol will urinate frequently.[44]
Alcohol stimulates gastric juice production, even when food is not present. In other words, when a person drinks alcohol, the alcohol will stimulate stomach's acidic secretions that are intended to digest protein molecules. Consequently, the acidity has potential to harm the inner lining of the stomach. Normally, the stomach lining is protected by a mucus layer that prevents any acids from reaching the stomach cells.
However, in patients who have a peptic ulcer disease (PUD), this mucus layer is broken down. PUD is commonly associated with a bacteria H. pylori. H. pylori secretes a toxin that weakens the mucosal wall. As a result, acid and protein enzymes penetrate the weakened barrier. Because alcohol stimulates a person's stomach to secrete acid, a person with PUD should avoid drinking alcohol on an empty stomach. Drinking alcohol would cause more acid release to damage the weakened stomach wall.[47] Complications of this disease could include a burning pain in the abdomen, bloating and in severe cases, the presence of dark black stools indicate internal bleeding.[48] A person who drinks alcohol regularly is strongly advised to reduce their intake to prevent PUD aggravation.[48]
Some individuals have less effective forms of one or both of the metabolizing enzymes, and can experience more severe symptoms from ethanol consumption than others. However, those having acquired alcohol tolerance have a greater quantity of these enzymes, and metabolize ethanol more rapidly.[49]
Ethanol is classified as a teratogen. See fetal alcohol syndrome and fetal alcohol spectrum disorder.
IARC list ethanol in alcoholic beverages as Group 1 carcinogens and arguments "There is sufficient evidence for the carcinogenicity of acetaldehyde (the major metabolite of ethanol) in experimental animals.".[50]
Frequent drinking of alcoholic beverages has been shown to be a major contributing factor in cases of elevated blood levels of triglycerides.[51]
Ethanol is also widely used, clinically and over the counter, as an antitussive agent.[52]
The fermentation of sugar into ethanol is one of the earliest biotechnologies employed by humans. The intoxicating effects of ethanol consumption have been known since ancient times. Ethanol has been used by humans since prehistory as the intoxicating ingredient of alcoholic beverages. Dried residue on 9,000-year-old pottery found in China suggests that Neolithic people consumed alcoholic beverages.[53]
Although distillation was well known by the early Greeks and Arabs, the first recorded production of alcohol from distilled wine was by the School of Salerno alchemists in the 12th century.[54] The first to mention absolute alcohol, in contrast with alcohol-water mixtures, was Raymond Lull.[54]
In 1796, German-Russian chemist Johann Tobias Lowitz obtained pure ethanol by mixing partially purified ethanol (the alcohol-water azeotrope) with an excess of anhydrous alkali and then distilling the mixture over low heat.[55] French chemist Antoine Lavoisier described ethanol as a compound of carbon, hydrogen, and oxygen, and in 1807 Nicolas-Théodore de Saussure determined ethanol's chemical formula.[56][57] Fifty years later, Archibald Scott Couper published the structural formula of ethanol. It was one of the first structural formulas determined.[58]
Ethanol was first prepared synthetically in 1825 by
Note: Many of the AChE inhibitors listed above also act as BChE inhibitors.
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The alcohols and the phenols will be called after the name of the hydrocarbon from which they are derived, terminated with the suffix ol (ex. pentanol, pentenol, etc.).