[Deamination of adenosine monophosphate in the rat brain in hyperoxia, hypoxia, and cold stress].
The causes of the adenosine monophosphate (AMP) deamination increase in rat brain mitochondria under conditions of hyperoxia, hypoxia and cold stress were studied. Data from the inhibitory analysis suggest that the increased intensity of AMP deamination under hypoxia is conditioned by the alterations in the substrate specificity of type A monoamine oxidase which acquires the ability to deaminate AMP. The enhancement of AMP deamination under hyperoxia and cold stress is due to the activation of true AMP deaminase in the mitochondrial fraction. The cytoplasmic AMP deaminase activity remains unchanged thereby. The effects of the AMP deaminase specific effectors, ATP and inorganic phosphate, were investigated.
Goroshinskaia
I A
IA
D000659:AMP Deaminase / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D003080:Cold Temperature; D003593:Cytoplasm / Q000201:enzymology; D003641:Deamination; D000860:Hypoxia / Q000378:metabolism*; D008297:Male; D008928:Mitochondria / Q000201:enzymology; D008995:Monoamine Oxidase / Q000378:metabolism; D008996:Monoamine Oxidase Inhibitors / Q000494:pharmacology; D010100:Oxygen / Q000494:pharmacology*; D051381:Rats; D013312:Stress, Physiological / Q000378:metabolism*
D008996:Monoamine Oxidase Inhibitors; D000249:Adenosine Monophosphate; D008995:Monoamine Oxidase; D000659:AMP Deaminase; D010100:Oxygen
Dezaminirovanie adenozinmonofosfata v mozge krys pri giperoksii, gipoksii i kholodovom stresse.