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Alcohol-related brain damage [1] [2] alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe , [ 3 ] limbic system , and cerebellum , [ 4 ] with widespread ...
Drug-induced liver injury (DILI) is a cause of acute and chronic liver disease caused specifically by medications and the most common reason for a drug to be withdrawn from the market after approval. The liver plays a central role in transforming and clearing chemicals and is susceptible to the toxicity from these agents.
Excessive alcohol intake (binge drinking) causes a decrease in hippocampal neurogenesis, via decreases in neural stem cell proliferation and newborn cell survival. [19] [20] Alcohol decreases the number of cells in S-phase of the cell cycle, and may arrest cells in the G1 phase, thus inhibiting their proliferation. [19]
Neurotoxicity can result from organ transplants, radiation treatment, certain drug therapies, recreational drug use, exposure to heavy metals, bites from certain species of venomous snakes, pesticides, [2] [3] certain industrial cleaning solvents, [4] fuels [5] and certain naturally occurring substances. Symptoms may appear immediately after ...
Drugs which cause disulfiram-like reactions upon ingestion of alcohol as an unintended effect include: [6] [1] [7] Abacavir Cephalosporins , but only these with a methylthiotetrazole side chain or a methylthiodioxotriazine ring; thought to be due to common N -methylthiotetrazole metabolite , which is similar in structure to disulfiram. [ 8 ]
Ammonia toxicity is often seen through two routes of administration, either through consumption or through endogenous ailments such as liver failure. [89] [90] One notable case in which ammonia toxicity is common is in response to cirrhosis of the liver which results in hepatic encephalopathy, and can result in cerebral edema (Haussinger 2006 ...