| Term 
 
        | Functional range of neurotoxicities |  | Definition 
 
        | Cognitive, Motor, Sensory, Mood/Personality, General |  | 
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        | Term 
 
        | Classes of neurotoxicants |  | Definition 
 
        | Pharmaceuticals, Chemicals, Neurotoxins |  | 
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        | Term 
 
        | REMEMBER THIS PHONE NUMBER FOR POISON CONTROL |  | Definition 
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        | Term 
 
        | produced by living organisms |  | Definition 
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        | Term 
 | Definition 
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        | we make within our own bodies |  | Definition 
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        | the most lethal toxin of any known animal (exogenous) |  | Definition 
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 | Definition 
 
        | opens neuronal sodium channels so cell membrane is no longer polarized and can no longer transmit impulses |  | 
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        | Term 
 | Definition 
 
        | blocks sodium channels from passing sodium --> paralysis and respiratory arrest within minutes --> cardiac arrest due to lack of oxygen |  | 
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        | Term 
 | Definition 
 
        | Batrachotoxin, Tetrodotoxin |  | 
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 | Definition 
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        | Term 
 
        | Glutamate-induced excitotoxicity |  | Definition 
 
        | overactivation of receptors for excitatory amino acid transmitters lead to cell damage and death |  | 
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        | Term 
 
        | Normal conditions: role of glutamate |  | Definition 
 
        | activates NMDA and AMPA receptors resulting in an influx of both Na and Ca ions, depolarization --> action potential |  | 
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        | Term 
 
        | Excitotoxicity: role of glutamate |  | Definition 
 
        | results in high intracellular levels of calcium ions resulting in neuronal death |  | 
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        | Term 
 
        | Massive activation of NMDA receptors |  | Definition 
 
        | dramatic increase in cytosolic calcium, which is taken up by the mitochondria |  | 
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        | Term 
 
        | Mitochondrial calcium overload |  | Definition 
 
        | leads to explosion of oxygen production and the subsequent release of cytochrome C |  | 
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        | Term 
 
        | High cystolic calcium activates nNOS and increases NO production |  | Definition 
 
        | oxygen and NO react to produce ONOO-, which then diffuses into the nucleus to cause DNA damage |  | 
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        | Term 
 
        | results in release of glutamate, eating away at neurons |  | Definition 
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        | Term 
 
        | when certain parts of brain are deprived of oxygen, results in excessive release of glutamate |  | Definition 
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        | Term 
 
        | have implicated glutamate in the pathophysiology |  | Definition 
 
        | ALS, MS, Alzheimers, Parkinsons, Huntingtons, Alcohol withdrawal |  | 
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        | Term 
 
        | Transmission, Axonopathy, Myelinopathy, Neuronopathy |  | Definition 
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        | Term 
 
        | drug-induced transmission toxicity |  | Definition 
 
        | organophosphate poisoning; cocaine intoxication; nicotine-induced brain damage |  | 
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        | Term 
 
        | inhibits AChE so buildup of unhydrolyzed ACh continues transmitting nervous signals to muscles |  | Definition 
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        | Term 
 
        | inhibition of DA and NE transporters; overactivation of DA and alpha adrenergic receptors centrally and peripherally |  | Definition 
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        | induces ROS levels in a dose-dependent manner and activates a NF-kb involved in biological processes (inflammation, innate immunity, development, apoptosis) |  | Definition 
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        | Term 
 
        | Nicotine activates a mitogen-activated protein kinase (MAPK) which is involved in the cellular apoptosis pathway |  | Definition 
 
        | c-Jun terminal kinase (JNK) |  | 
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        | Term 
 
        | Significantly smaller grey matter and lower grey matter density in front regions, occipital lob and temporal lobe |  | Definition 
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        | Term 
 | Definition 
 
        | organophosphates, cisplatin, vincristine |  | 
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        | Term 
 
        | similar to ALS; usually starting distally and progression towards the neuron |  | Definition 
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        | Term 
 
        | occurs 1-5 weeks following severe intoxication |  | Definition 
 
        | Organophosphates-induced delayed neuropathy (OPIDN) |  | 
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        | Term 
 
        | organophosphates inhibit this to cause symmetrical sensory-motor degeneration of peripheral nerves and spinal cord |  | Definition 
 
        | neuropathy target esterase (NTE) |  | 
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        | Term 
 
        | symmetrical sensory-motor degeneration of peripheral nerves and spinal cord |  | Definition 
 
        | --> muscle weakness, ataxia and subsequent paralysis of the limbs |  | 
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        | Term 
 | Definition 
 
        | deacylates the major neuronal membrane phospholipid, phosphatidylcholine |  | 
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        | produces  damage to the organ of Corti,including the destruction of auditory sensory cells |  | Definition 
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        | begins 3-4 days after Cisplatin toxicity; |  | Definition 
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        | symmetrical peripheral axonal sensorimotor neuropathy early in therapy |  | Definition 
 
        | --> paresthesia and severe motor weakness |  | 
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        | interferenece with microtubule, affecting axonal transport |  | Definition 
 
        | vincristine-induced sensorimotor neuropathy |  | 
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        | interference with salutatory conduction or the facilitated propagation of action potentials along myelinated axons |  | Definition 
 
        | drug-induced myelinopathy |  | 
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        | Term 
 | Definition 
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        | drug-induced myelinopathy |  | Definition 
 
        | may progress to axonopathy |  | 
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        | Term 
 
        | Lead-induced neurotoxicity, hexachlorophene-induced spongiform encephalopathy, nitrous oxide-induced myelinopathy, carbon monoxide-induced encephalopathy |  | Definition 
 
        | drug-induced myelinopathy |  | 
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        | Term 
 
        | primary target is the CNS; diff. mechanisms include oxidative stress, intensification of apoptosis of neurons, interfering with Ca-dependent enzyme like nitric oxide synthase |  | Definition 
 
        | Lead-induced neurotoxicity |  | 
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        | Term 
 
        | inhibit respiratory D-lactate dehydrogenase and interfere with the electron transport chain |  | Definition 
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        | Term 
 | Definition 
 
        | mitochondrial neurotoxin especially toxic to developing oligodendrocytes |  | 
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        | myelin with water-filled spaces or vacuoles (spongiform encephalopathy) |  | Definition 
 
        | biomarker for hexachlorophene effects |  | 
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        | irreversibly oxidizes cobalt ion in methylcobalamin and inhibits the synthesis of methionine |  | Definition 
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        | Lack of S-adenosylmetionine |  | Definition 
 
        | impairs methylation of myelin sheath phospholipids --> reduction in myelin formation |  | 
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        | causes endothelial and platelet release of NO and formation of oxygen free radiccals including peroxynitrite |  | Definition 
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        | causes delayed but reversible demyelination of white matter, which can lead to edema and necrosis |  | Definition 
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        | Irreversible neuronal loss peripherally or centrally |  | Definition 
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        | neuronopathy clinical disease state |  | Definition 
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        | twisted fragments of protein |  | Definition 
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 | Definition 
 
        | abnormal clusters of amyloid and tau protein remnants |  | 
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        | drug-induced neuronopathy |  | Definition 
 
        | MPTP-induced parkinsonism, Methylmercury-induced neuropathy, Arsenic-induced neurotoxicit, Streptomycin-induced ototoxicity |  | 
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        | a by product of MPP synthesis |  | Definition 
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        | Term 
 | Definition 
 
        | taken up into dopamine neurons |  | 
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        | attacks the mitochondrion and inhibits energy production, causing neuronopathy and a syndrome resembling advanced parkinsonism |  | Definition 
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        | organic form of mercy and the form of mercury that is most easily bioaccumulated |  | Definition 
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        | major source of human exposure to MeHg in the U.S. |  | Definition 
 
        | consumption of contaminated fish |  | 
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        | Term 
 
        | cerebral palsy, blindness, deafness, growth problems, mental retardation, microcephaly |  | Definition 
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        | reacts with the thiol groups of proteins and enzymes and inhibits their catalytic activity |  | Definition 
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        | causes changes in the cytoskeletal protein composition and hyper-phosphorylation |  | Definition 
 
        | Arsenic-induced Neurotoxicity |  | 
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        | key mechanism of As-induced neuronopathy |  | Definition 
 
        | disorganization of the cytoskeletal framework |  | 
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        | disruption of mitochondrial protein synthesis and the formation of free oxygen radicals |  | Definition 
 
        | Aminoglycoside ototoxicity |  | 
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        | Term 
 
        | out of the all ototoxic drugs, these are the most vestibulotoxic |  | Definition 
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