771 Ethanol Ethanol is a clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. Indeed, ethanol has widespread use as a solvent of substances intended for human contact or consumption, including scents, flavorings, colorings, and medicines. Ethanol has a depressive effect on the central nervous system and because of its psychoactive effects, it is considered a drug. Ethanol has a complex mode of action and affects multiple systems in the brain, most notably it acts as an agonist to the GABA receptors. 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 %. Ethanol is metabolized by the body as an energy-providing carbohydrate nutrient, as it metabolizes into acetyl CoA, an intermediate common with glucose metabolism, that can be used for energy in the citric acid cycle or for biosynthesis. Ethanol within the human body is converted into acetaldehyde by alcohol dehydrogenase and then into acetic acid by acetaldehyde dehydrogenase. The product of the first step of this breakdown, acetaldehyde, 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,[77] multiple forms of cancer, and alcoholism. Industrially, ethanol is produced both as a petrochemical, through the hydration of ethylene, and biologically, by fermenting sugars with yeast. Small amounts of ethanol are endogenously produced by gut microflora through anaerobic fermentation. However most ethanol detected in biofluids and tissues likely comes from consumption of alcoholic beverages. Absolute ethanol or anhydrous alcohol generally refers to purified ethanol, containing no more than one percent water. Absolute alcohol is not intended for human consumption. It often contains trace amounts of toxic benzene (used to remove water by azeotropic distillation). Consumption of this form of ethanol can be fatal over a short time period. Generally absolute or pure ethanol is used as a solvent for lab and industrial settings where water will disrupt a desired reaction. Pure ethanol is classed as 200 proof in the USA and Canada, equivalent to 175 degrees proof in the UK system. 64-17-5 702 C2H6O 46.041870 -114.1°C 78.2°C 1E+006 mg/L (at 25°C) Oral, rapidly absorbed. Blood alcohol level and the time necessary to achieve it are controlled largely by the rapidity and extent of ethanol consumption. (T10) Alcohol binds to the GABA(A) receptors (delta subunit), NMDA receptors, Glycine receptors, Serotonin receptors, Acetylcholine receptors, L-channel calcium channels and GIRK channels. Ethanol acts in the central nervous system primarily by binding to the GABAA receptor, increasing the effects of the inhibitory neurotransmitter GABA. Ethanol within the human body is converted into acetaldehyde by alcohol dehydrogenase. 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 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 is metabolized to acetaldehyde by three enzymes: 1. Alcohol dehydrogenase metabolized methanol to acetaldehyde, which is oxidized by acetaldehyde dehydrogenase to acetate. 2. Catalase metabolizes ethanol by utilizing H2O2 supplied by the actionhs of NADPH oxidase and xanthine oxidase. This normally accounts for more than 10% of ethanol metabolism. 3. CYP2E1, is the principal component of the hepatic microsomal ethanol oxidizing system, MEOS) (T10) LD50: 5628 mg/kg (Oral, rat) The fatal dose of ethanol is 300-400 mL of pure ethanol (600-800 mL of 50% spirits), for the average adult if consumed in less than one hour. More specifically, the lethal dose of alcohol is 5-8g/kg (3g/kg for children). Ethanol in alcoholic beverages is carcinogenic to humans (Group 1). (L135) Ethanol is used as a solvent in industry, in many household products and pharmaceuticals, and in intoxicating beverages. It is also used for therapeutic neurolysis of nerves or ganglia for the relief of intractable chronic pain in such conditions as inoperable cancer and trigeminal neuralgia (tic douloureux), in patients for whom neurosurgical procedures are contraindicated. Acute: At 0.1% blood alcohol levels individuals experience CNS depression, nausea, possible vomiting, impaired cognition and impaired motor and sensory function. Accidents or injury can also occur due to the side effects of loss of coordination, slowed reaction time, sleepiness and impaired judgment. At >0.14% blood alcohol levels there is decreased blood flow to the brain. At greater than 0.3% blood alcohol there is a marked degree of stupefaction and possible unconsciousness. At levels greater than 0.4% there is a risk of death. Acute consumption leading to blood alcohol levels greater than 0.5% is almost universally fatal. Chronic: high levels of alcohol consumption are associated with an increased risk of alcoholism, malnutrition, chronic pancreatitis, alcoholic (fatty) liver disease, and cancer. Frequent drinking of alcoholic beverages has been shown to be a major contributing factor in cases of elevated blood levels of triglycerides. In addition, damage to the central nervous system and peripheral nervous system can occur from chronic alcohol abuse. The long-term use of alcohol is capable of damaging nearly every organ and system in the body. The developing adolescent brain is particularly vulnerable to the toxic effects of alcohol. In addition, the developing fetal brain is also vulnerable, and fetal alcohol syndrome (FAS) may result if pregnant mothers consume alcohol. The net effect of alcohol consumption on global human health is quite detrimental, with an estimated 3.8% of all global deaths and 4.6% of global disability-adjusted life-years attributable to alcohol. Ethanol is considered a teratogen (causing fetal alcohol syndrome) and a Group 1 carcinogen because of the carcinogenicity of acetaldehyde (a major metabolite of alcohol). Symptoms and effects of overdose include nausea, vomiting, CNS depression, acute respiratory failure or death and with chronic use, severe health problems, such as liver and brain damage. At >0.14% blood alcohol levels there is decreased blood flow to the brain. At greater than 0.3% blood alcohol there is a marked degree of stupefaction and possible unconsciousness. At levels greater than 0.4% there is a risk of death. Acute consumption leading to blood alcohol levels greater than 0.5% is almost universally fatal. With chronic alcohol abuse, severe health problems, such as liver and brain damage can be present. If you suspect someone has alcohol poisoning, call for an ambulance to take them to a hospital. While you're waiting: try to keep them sitting up and awake, give them water if they can drink it. If they've passed out, lie them on their side in the recovery position and check they're breathing properly, keep them warm and stay with them and monitor their symptoms. Acute alcohol poisoning is a medical emergency due to the risk of death from respiratory depression and/or inhalation of vomit if emesis occurs while the patient is unconscious and unresponsive. Emergency treatment for acute alcohol poisoning strives to stabilize the patient and maintain a patent airway and respiration, while waiting for the alcohol to metabolize. Emergency treatment in a hospital can involve: 1) treating hypoglycaemia (low blood sugar) with 50 ml of 50% dextrose solution and saline flush, as ethanol induced hypoglycaemia is unresponsive to glucagon; 2) Administration of the vitamin thiamine to prevent Wernicke-Korsakoff syndrome, which can cause a seizure; 3) application of haemodialysis if the blood concentration is dangerously high (>400 mg%), and especially if there is metabolic acidosis and 4) Providing oxygen therapy as needed via nasal cannula or non-rebreather mask. 2009-05-06T21:37:51Z 2014-12-24T20:22:48Z Alcohol dehydrogenase 1A (P07327), Alcohol dehydrogenase 1B (P00325), Alcohol dehydrogenase 1C (P00326), Alcohol dehydrogenase 4 (P08319), Alcohol dehydrogenase 6 (P28332), Alcohol dehydrogenase class 4 mu/sigma chain (P40394), Alcohol dehydrogenase class-3 (P11766), Catalase (P04040) Ethanol C00469 16236 ETOH D000431 Ethanol DB00898 EOH 594 true Alcohol dehydrogenase 1A (P07327) Alcohol dehydrogenase 1B (P00325) Alcohol dehydrogenase 1C (P00326) Alcohol dehydrogenase 4 (P08319) Alcohol dehydrogenase 6 (P28332) Alcohol dehydrogenase class 4 mu/sigma chain (P40394) Alcohol dehydrogenase class-3 (P11766) Catalase (P04040) (T10) CCO C2H6O InChI=1S/C2H6O/c1-2-3/h3H,2H2,1H3 InChIKey=LFQSCWFLJHTTHZ-UHFFFAOYSA-N 46.0684 46.041864814 Endogenous Liquid -0.31 HMDB00108 CHEMBL545 682 <p>William S. Hedrick, &#8220;Process for ethanol production from cellulosic materials.&#8221; U.S. Patent US4650689, issued June, 1917.</p>