Acute and chronic effects of carbon monoxide on mitochondrial function.
The purpose of the present study was to examine whether there were some differences between metabolic responses induced by carbon monoxide (CO) poisoning and those by hypoxic hypoxia. Significant decrease in cytochrome oxidase (COX) activity in heart and liver was observed during acute exposure, while no change was observed in brain. When the control of respiration was investigated, cerebral energy homeostasis was maintained even after severe exposure. In order to document this phenomenon we measured blood flow in liver and brain, but increase in cerebral blood flow was not observed and the experiments failed to show a relationship between cerebral homeostasis and blood flow. The prolonged exposure to CO and hypoxia resulted in an increase in COX and these responses were obviously considered to be adaptive to chronic exposure. From the results of acute and chronic exposure it is considered to be difficult to determine if CO has the direct effect on the respiratory chain. Further studies of the mechanism of the CO toxicity may be necessary.
Shigezane
J
J
Kita
T
T
Furuya
Y
Y
D000208:Acute Disease; D000818:Animals; D002249:Carbon Monoxide Poisoning / Q000378:metabolism / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D002908:Chronic Disease; D003576:Electron Transport Complex IV / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology; D008102:Liver Circulation / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012119:Respiration / Q000187:drug effects
D003576:Electron Transport Complex IV