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Acute ammonia neurotoxicity in vivo involves increase in cytoplasmic protein P53 without alterations in other markers of apoptosis.

2007

Acute intoxication with large ammonia doses leads to activation of NMDA receptors in the brain, resulting in oxidative stress and disturbance of mitochondrial function. Altered mitochondrial function is a crucial step in some mechanisms of cellular apoptosis. This study assesses whether ammonia intoxication in vivo leads to induction of apoptotic markers such as permeability transition pore (PTP) formation, caspase-3, and caspase-9 activation, changes in p53 protein, or cytochrome c release. Acute ammonia intoxication did not affect caspase-9 or caspase-3 activities. The mitochondrial membrane potential also remained unaltered in non-synaptic brain mitochondria after injection of ammonia, i…

MaleCytoplasmApoptosisMitochondrionmedicine.disease_causeCellular and Molecular NeuroscienceIn vivoAmmoniamedicineAnimalsRats WistarbiologyCaspase 3brain mitochondriaCytochrome capoptosisNeurotoxicityBrainCytochromes cammonia toxicitybrain nucleimedicine.diseaseCaspase 9Cell biologyMitochondriaRatsEnzyme ActivationCytosolcytochrome cCytoplasmApoptosisbiology.proteinTumor Suppressor Protein p53Oxidative stressJournal of neuroscience research
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