Ethanol toxicity

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  • As a research scientist in the area of human nutrition, I have observed a sea change in emphasis within my field over the past 10–15 years. There have always been dynamics within the subject: During the first half of the twentieth century, scientists grappled with discovering the essential micronutrients and with characterizing the biological effects of their deficiency. This interest in “too little” was supplanted in the mid-1980s by a preoccu- pation with too much—too much fat, too much sugar, and too much obesity.

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  • Ethanol hoặc "rượu" vì nó là tốt hơn được biết đến, được sử dụng trong y học như một chất khử trùng, dung môi, và chất bảo quản. Nó hiện diện trong nhiều over-the-chuẩn bị ở nồng độ khác nhau,

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  • Tuyển tập các báo cáo nghiên cứu khoa học quốc tế về bệnh thú y đề tài: Protective and therapeutic effects of an extract mixture of alder tree, labiate herb, milk thistle green bean-rice bran fermentation, and turnip against ethanol-induced toxicity in the rat

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  • A compound consisting of an alkyl group and the functional group -OH is an alcohol. The identity of an individual alcohol depends on the identity of R, the alkyl group. For example, when R is the methyl group, we have CH30H. This is methyl alcohol or methanol, also known as wood alcohol. It is highly toxic and can cause blindness or even death in relatively small doses. When R is the ethyl group, we have CH3CH20H. This is ethyl alcohol or ethanol. Ethanol is the alcohol in alcoholic beverages. When R is the isopropyl group, we have (CH3)2CHOH. This is isopropyl alcohol.

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  • Introduction: Methanol (methyl alcohol) poisoning accidents take place most frequently by drinking it in mistake for ethanol. Methanol poisoning is not due to the effect of methanol itself, but due to toxicity of its metabolites. Methanol is rapidly absorbed into human body through the airway mucous membranes, digestive tract mucous membranes or the skin; it is metabolized into formaldehyde (formalin, HCHO) and then formic acid (HCOOH) by the actions of alcohol dehydrogenase and aldehyde dehydrogenase, respectively.

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  • Lactic Acidosis An increase in plasma L-lactate may be secondary to poor tissue perfusion (type A)—circulatory insufficiency (shock, cardiac failure), severe anemia, mitochondrial enzyme defects, and inhibitors (carbon monoxide, cyanide)—or to aerobic disorders (type B)—malignancies, nucleoside analogue reverse transcriptase inhibitors in HIV, diabetes mellitus, renal or hepatic failure, thiamine deficiency, severe infections (cholera, malaria), seizures, or drugs/toxins (biguanides, ethanol, methanol, propylene glycol, isoniazid, and fructose).

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