Pro-Apoptotic Changes in Brain Mitochondria After Toxin Exposure
Abstract
Mitochondria normally function to provide sources of energy for vital cellular functions. However, under stressful conditions these organelles may trigger events that lead eventually to cell death. Thus, mitochondria have been implicated as major contributors to neuronal death in a variety of neurodegenerative disorders. In this report we provide evidence that certain mitochondrial toxins cause selective cell death in hippocampal subfield CA1 that has previously been shown to be selectively vulnerable to hypoxia/ischemia. We show also that selective changes in the redox activity of mitochondrial pyridine nucleotides (NADH) may occur in subfield CA1 and show preliminary data of a new method designed to measure the activity of mitochondrial dehydrogenases in intact cells. These dehydrogenases are responsible for mitochondrial NADH production. Data provided here provides no evidence that mitochondrial permeability transition occurs in hippocampal subfield CA1 following inhibition of mitochondrial function although we show pronounced elevation of intracellular calcium activity. Western blot analysis showed evidence of cytochrome c release from mitochondria suggesting that permeability transition is not required for release of this pro-paoptotic factor following toxin exposure.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2004
- Accession Number
- ADA434079
Entities
People
- Thomas J. Sick
Organizations
- University of Miami