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[1] [2] These effects are caused by accumulation of acetaldehyde, a major but toxic metabolite of alcohol formed by the enzyme alcohol dehydrogenase. [1] [2] The reaction has been variously termed a disulfiram-like reaction, alcohol intolerance, and acetaldehyde syndrome. [3]
Disulfiram-alcohol reaction (DAR) is the effect of the interaction in the human body of alcohol drunk with disulfiram or some types of mushrooms. [ 1 ] [ 2 ] The DAR is key to disulfiram therapy that is widely used for alcohol-aversive treatment and management of other addictions (e.g. cocaine [ 3 ] [ 4 ] use).
[34] [35] [36] On the other hand, the more uncommon alcohol allergy is an immune system reaction to alcohol (specifically ethanol) that causes symptoms such as rashes, difficulty breathing, and anaphylaxis in severe cases. [37] [38] Nausea is a symptom common to both alcohol intolerance and alcohol allergy. [35]
Disulfiram is a medication used to support the treatment of chronic alcoholism by producing an acute sensitivity to ethanol (drinking alcohol). Disulfiram works by inhibiting the enzyme aldehyde dehydrogenase (specifically the ALDH2 enzyme [3]), causing many of the effects of a hangover to be felt immediately following alcohol consumption.
Beryllium poisoning is poisoning by the toxic effects of beryllium, or more usually its compounds. It takes two forms: It takes two forms: Acute beryllium poisoning , usually as a result of exposure to soluble beryllium salts
The most obvious symptom of alcohol flush reaction is flushing on a person's face and body after drinking alcohol. [4] Other effects include "nausea, headache and general physical discomfort". [9] People affected by this condition show greater reduction in psychomotor functions on alcohol consumption than those without. [10] Many cases of ...
In a related case, the Rosenmund reduction of acyl halides to aldehydes, the palladium catalyst (over barium sulfate or calcium carbonate) is intentionally poisoned by the addition of sulfur or quinoline in order to lower the catalyst activity and thereby prevent over-reduction of the aldehyde product to the primary alcohol.
The lipid accumulates in the human body and competes at agonists sites of lipid-gated ion channels contributing to alcohol intoxication. [3] The chemical similarity of PEth to phosphatidic acid (PA) and phosphatidylinositol 4,5-bisphosphate (PIP2) suggest a likely broad perturbation to lipid signaling; the exact role of PEth as a competitive lipid ligand has not been studied extensively.