Studies on the pathogenesis of ischemic cell injury. VI. Accumulation of calcium by isolated mitochondria of ischemic rat kidney cortex.
Mitochondria isolated from rat kidney subject to in vitro ischemia at various time intervals demonstrated a continuous decline of the ability to accumulate calcium following a high initial stable phase of accumulation of calcium which is dependent both on ATP and respiration. This decline occurs during the reversible phase of cell injury and appears to be a sensitive indicator of membrane changes in a binding and/or transport protein or of other membrane permeability characteristics. The morphology of mitochondrial densities related to calcium accumulation in mitochondria varied. Any form of calcium accumulation, resulted in marked swelling of mitochondria. Control renal mitochondria in sucrose were highly condensed. Partially inhibited calcium accumulation in the presence of phosphate was also associated with numerous small spheric or punctate deposits in close relationship to the inner membrane. Uninhibited calcium accumulation resulted in the formation of needle-like structures radiating from such inner membrane associated sites.
D000255:Adenosine Triphosphate; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D007511:Ischemia / Q000473:pathology*; D007672:Kidney Cortex / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D008933:Mitochondrial Swelling; D010539:Permeability; D051381:Rats; D012119:Respiration
D000255:Adenosine Triphosphate; D002118:Calcium