Augmented conversion of aspartate and glutamate to succinate during anoxia in rabbit heart

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Abstract
Alterations in the metabolism of aspartate and glutamate induced by anaerobiosis were investigated using the isolated rabbit right ventricular papillary muscle. [14C]Glutamate oxidation to 14CO2 was studied by incubating oxygenated and anoxic muscles in Krebs-Ringer buffer containing either [1-14C]glutamate or [U-14C]glutamate. 14CO2 release was identical in both muscle groups with [1-14C]glutamate tracer but 5 times greater in oxygenated muscles with [U-14C] glutamate tracer. Although the 1-C position of glutamate is oxidized at equal rates in anoxic and oxygenated muscles, oxidation of carbons 2-5 is inhibited during anoxia. Because this is consistent with the hypothesized role of glutamate as a succinate precursor, the rates of conversion of aspartate and glutamate to fumarate and succinate in anoxic and oxygenated muscles were directly measured. Papillary muscles were incubated with either [U-14C]glutamate or [U-14C]aspartate for periods of 5-60 min. Perchlorate extracts of the muscles were prepared and succinate and fumarate isolated by 2-dimensional thin-layer chromatography. The conversion of aspartate and glutamate to succinate were stimulated 10-20 times (P < 0.01) by anoxia. Conversion of aspartate but not of glutamate, to fumarate was stimulated 3-5 times (P < 0.01) by anoxia, indicating aspartate is converted to succinate via a reductive mechanism involving the reduction of fumarate to succinate. Alterations of the specific radioactivity of the intracellular glutamate or aspartate pool were not responsible for the data because direct measurements of the specific radioactivity of these pools in anoxic and oxygenated muscles revealed no alteration was induced by anoxia.

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