Accession Number:

ADA434079

Title:

Pro-Apoptotic Changes in Brain Mitochondria After Toxin Exposure

Descriptive Note:

Final addendum rept. 1 Jul 2003-30 Sep 2004

Corporate Author:

MIAMI UNIV FL SCHOOL OF MEDICINE

Personal Author(s):

Report Date:

2004-10-01

Pagination or Media Count:

15.0

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 hypoxiaischemia. 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.

Subject Categories:

  • Anatomy and Physiology
  • Stress Physiology
  • Toxicology

Distribution Statement:

APPROVED FOR PUBLIC RELEASE