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In some cases the level or exposure-time may be critical, with some substances only becoming neurotoxic in certain doses or time periods. Some of the most common naturally occurring brain toxins that lead to neurotoxicity as a result of long term drug use are amyloid beta (Aβ), glutamate, dopamine, and oxygen radicals.
Properties leading to the susceptibility of nervous tissue include a high surface area of neurons, a high lipid content which retains lipophilic toxins, high blood flow to the brain inducing increased effective toxin exposure, and the persistence of neurons through an individual's lifetime, leading to compounding of damages. [21]
Excitotoxicity can occur from substances produced within the body (endogenous excitotoxins).Glutamate is a prime example of an excitotoxin in the brain, and it is also the major excitatory neurotransmitter in the central nervous system of mammals. [14]
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 ...
It has no known function for clostridia in the soil environment where they are normally encountered. It is also called spasmogenic toxin , tentoxilysin , tetanospasmin , or tetanus neurotoxin . The LD 50 of this toxin has been measured to be approximately 2.5–3 ng/kg, [ 2 ] [ 3 ] making it second only to the related botulinum toxin (LD 50 2 ...
It may be initiated in response to a variety of cues, including infection, traumatic brain injury, [1] toxic metabolites, or autoimmunity. [2] In the central nervous system (CNS), including the brain and spinal cord , microglia are the resident innate immune cells that are activated in response to these cues. [ 2 ]
Botulinum toxin, or botulinum neurotoxin (commonly called botox), is a neurotoxic protein produced by the bacterium Clostridium botulinum and related species. [24] It prevents the release of the neurotransmitter acetylcholine from axon endings at the neuromuscular junction, thus causing flaccid paralysis. [25]
Oxidative stress mechanisms in tissue injury. Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).. Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. [1]