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 CAl that has previously been shown to be selectively vulnerable to hypoxia/ischemia. We have also measured changes in mitochondrial membrane potential following toxin exposure. Respiratory chain Complex I inhibitors caused mitochondrial depolarization by the degree of depolarization, although significant, was not dramatic. No mitochondrial depolarization was observed after excitotoxin or Complex II inhibition. All toxins tested produced an increase in reactive oxygen species. Our data show no evidence for mitochondrial permeability transition after toxin exposure.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2002
- Accession Number
- ADA407627
Entities
People
- Thomas J. Sick
Organizations
- University of Miami