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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cause of acute and chronic liver disease caused specifically by medications and the most common reason for a drug to be withdrawn from the market after approval.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.
A potential cause of chronic alcoholic cerebellar dysfunction is an alteration of GABA-A receptor. This dysfunction causes an increase in the neurotransmitter GABA in cerebellar Purkinje cells, granule cells, and interneurons leading to a disruption in normal cell signaling. [8] GABA-A receptor embedded in cell membrane
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 ...
Benzodiazepines, like many other sedative hypnotic drugs, cause apoptotic neuronal cell death. However, benzodiazepines do not cause as severe apoptosis to the developing brain as alcohol does. [105] [106] [107] The prenatal toxicity of benzodiazepines is most likely due to their effects on neurotransmitter systems, cell membranes and protein ...
Exposure to these chemicals can occur at public buildings, schools, residential areas, and in agricultural areas. Chlorpyrifos and Malathion have been linked to reproductive effects, neurotoxicity, kidney/liver damage, and birth defects. Dichlorvos has also been linked to reproductive effects, neurotoxicity, and kidney/liver damage.
Excessive glutamate release is a known major cause of neuronal cell death. Glutamate causes neurotoxicity due to excitotoxicity and oxidative glutamate toxicity. Evidence from animal studies suggests that some people may be more genetically sensitive to the neurotoxic and brain damage associated with binge drinking regimes.
Toxic encephalopathy is a neurologic disorder caused by exposure to neurotoxic organic solvents such as toluene, following exposure to heavy metals such as manganese, as a side effect of melarsoprol treatment for African trypanosomiasis, adverse effects to prescription drugs, or exposure to extreme concentrations of any natural toxin such as cyanotoxins found in shellfish or freshwater ...
Local pathology of neurotoxin exposure often includes neuron excitotoxicity or apoptosis [14] but can also include glial cell damage. [15] Macroscopic manifestations of neurotoxin exposure can include widespread central nervous system damage such as intellectual disability, [5] persistent memory impairments, [16] epilepsy, and dementia. [17]