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Previous reports have shown that ketamine triggered apoptosis in immature developing brain involving mitochondrial mediated pathways. However, no data for ketamine effects on hippocampal and cortical mitochondrial function are available in pre-pubertal rats. Twenty-one days-old Sprague-Dawley rats received ketamine (40 mg/Kg i.p.) for 3 days and were sacrificed 24 hours after last injection. Hippocampal mitochondria from ketamine-treated rats showed decreased malate-glutamate state 4 and 3 respiratory rates and an inhibition in Complex I and IV activities. Hippocampal mitochondrial membrane depolarization and mitochondrial permeability transition induction were observed. This was not reflected in an increment of H O production probably due to increased Mn-SOD and catalase activities, 24 hours after treatment. Interestingly, increased H O production rates and cardiolipin oxidation were found in hippocampal mitochondria shortly after ketamine treatment (45 min). Unlike hippocampus, ketamine did not affect mitochondrial parameters in brain cortex, being this area less vulnerable to suffer ketamine-induced oxidative damage. Results provide evidences that exposure of pre-pubertal rats to ketamine leads to an induction of mitochondrial ROS generation at early stages of treatment, that was normalized by the triggering of antioxidant systems. Although hippocampal mitochondria from pre-pubertal rats were capable of respond to the oxidative stress, they remain partially dysfunctional.
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A cyclohexanone derivative used for induction of anesthesia. Its mechanism of action is not well understood, but ketamine can block NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE) and may interact with sigma receptors.
A hallucinogen formerly used as a veterinary anesthetic, and briefly as a general anesthetic for humans. Phencyclidine is similar to KETAMINE in structure and in many of its effects. Like ketamine, it can produce a dissociative state. It exerts its pharmacological action through inhibition of NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE). As a drug of abuse, it is known as PCP and Angel Dust.
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Mitochondrial anion carrier proteins that function as dimers and form proton channels in the INNER MITOCHONDRIAL MEMBRANE which creates proton leaks and uncouples OXIDATIVE PHOSPHORYLATION from ATP synthesis, resulting in the generation of heat instead of ATP.
Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.
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