Increased Rat Brain Cytochrome C Correlates with Degree of Perinatal Copper Deficiency Rather than Apoptosis

摘要: Reductions in copper due to dietary restriction or transporter deficiency brindled mice humans with Menkes disease lead reduced cuproenzyme activities, mitochondrial abnormalities, neurodegeneration and early mortality. The mechanisms for observed neuropathology remain unknown. Some researchers studying mutant suggest brain apoptosis as a possible factor based on changes transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining increased cytosolic cytochrome c decreased Bcl-2 levels. Perinatal was induced Holtzman rats during late gestation lactation investigate the role of developing brain. Analysis 13- 24-d-old (P13 P24) brains from male copper-deficient copper-adequate revealed no difference total Cerebellar TUNEL caspase-3 activity were higher P12 than pups. However, not detected at P24 even though pups more deficient cortex copper, Cu, Zn-superoxide dismutase oxidase activities. This suggests that neuronal is enhanced by Lower levels rat hearts, consistent apoptotic processes reported others. A robust enhancement extracts purified mitochondria Higher appeared be correlated degree seemed associated mass, because voltage-dependent anion channel complex I also detected. biochemical elevated are known nor physiological consequences.