CELLULAR BASIS OF ANOXIC DAMAGE.

Abstract

Guinea pigs have been exposed to an atme of nitrogen for periods up to 60 minutes and polarographic studies of capacity for respira tion and oxidative phosphorylation made on homo genates of liver, kidney cortex and brain. The earliest sign of anoxic damage was a failure of the tissue homogenates to increase their oxygen consumption in response to the addition of ADP; this was seen after 10 minutes in liver and kid ney but not until later in brain. Basal oxygen consumption and capacity for oxidative phos phorylation were well maintained in all 3 tissues after at least 20 minutes exposure to nitrogen. In studies to begin shortly, tissue pO2 and pH will be monitored continuously during graded hypoxia and recovery, together with biochemical assays of free and total acid hydrolase activ ities. The effects of tissue buffering (IV THAM) and of inhibition of anaerobic glycolysis with iodoacetate will also be observed. It is hoped that these studies will provide information on (a) the relative roles of intracellular hypoxia and acidity in producing cell damage and (b) the role of anaerobic glycolysis in compensating for the deficit in oxidative energy production. (Author)

Document Details

Document Type
Technical Report
Publication Date
Sep 30, 1963
Accession Number
AD0418576

Entities

People

  • A.t. Miller

Organizations

  • University of North Carolina at Chapel Hill

Tags

DTIC Thesaurus Topics

  • Cells
  • Energy Production
  • Glycolysis
  • Hydrolases
  • Inhibition
  • Kidneys
  • Nitrogen
  • Phosphorylation
  • Production
  • Recovery
  • Rodents

Fields of Study

  • Biology

Readers

  • Aquatic Ecology
  • Molecular and Cellular Biochemistry
  • Toxicology/Environmental Toxicology