Metabolic and electron microscopic studies post mortem in brain mitochondria.
The RCR of malate+glutamate oxidation of isolated rat brain mitochondria decreased with increasing duration of anoxia and it ceased completely in the 12 hour ischemic group. After one hour of ischemic anoxia neither the respiration of mitochondria nor their morphology altered irreversibly. There is a strong correlation between the ultrastructural changes and RCR value of mitochondria, namely the RCR decreased proportionally with increasing number of light type of mitochondria. From our results we can conclude that the dense form seems to be the functional form, while the light mitochondrial structure is a transition to the non functioning homogenous type of brain mitochondria.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000378:metabolism / Q000648:ultrastructure; D004140:Dinitrophenols / Q000494:pharmacology; D005971:Glutamates / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology; D007511:Ischemia / Q000378:metabolism* / Q000473:pathology; D008293:Malates / Q000378:metabolism; D008854:Microscopy, Electron; D008928:Mitochondria / Q000378:metabolism* / Q000648:ultrastructure; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D012709:Serum Albumin / Q000494:pharmacology; D013997:Time Factors
D004140:Dinitrophenols; D005971:Glutamates; D008293:Malates; D012709:Serum Albumin; D000244:Adenosine Diphosphate