Accession Number:

ADA383069

Title:

Pro-Apoptotic Changes in Brain Mitochondria After Toxin Exposure

Descriptive Note:

Annual rept. 1 Jul 1999-30 Jun 2000

Corporate Author:

MIAMI UNIV FL

Personal Author(s):

Report Date:

2000-07-01

Pagination or Media Count:

22.0

Abstract:

Nitochondria 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 describe functional changes in mitochondria measured in living brain tissue as a result of exposure to toxins thought to contribute to neurodegeneration. Mitochondrial NADH levels were shown to increase following treatment with l-methyl-4-phenylpyridium MPP at times when neuronal electrophysiology was impaired. In addition, NPP appeared to cause oxidation of cytochrome b, providing further Support that this toxin inhibits Mitochondrial complex I. 3-nitropropionic acid 3-NP also resulted in blockade of neuronal electrical activity but had minimal effects on mitochondrial NADH and redox activity of respiratory chain cytochromes. Both toxins produced delayed and selective cell death in hippocampal subfield CAl. Neurons in this subfield have been shown previously to be selectively vulnerable to hypoxiaischemia. The data reported here suggest that these neurons may also be selectively vulnerable to mitochondrial toxins.

Subject Categories:

  • Anatomy and Physiology
  • Stress Physiology
  • Toxicology

Distribution Statement:

APPROVED FOR PUBLIC RELEASE