In the reoxygenated hypoxic heart, hypoxanthine is either oxidized by xanthine oxidase with production of toxic oxygen species or salvaged for the ATP pool by hypoxanthine-guanine phosphoribosyl transferase. To characterize the repartition of hypoxanthine between the two pathways, we have subjected rat hearts to 20 min hypoxia and monitored the recovery (ventricular, end-diastolic and coronary pressures, and the contraction rate) during the reoxygenation (30 min) in the presence of either hypoxanthine or guanine alone, or both. The rate-pressure product recovered 78% of the pre-hypoxia values in hearts reoxygenated with 100 μm hypoxanthine and 80% in hearts recoxygenated with 100 μm guanine, in contrast to 49% in the presence of both hypoxanthine and guanine (100 μm each). Thus, it is likely that hypoxanthine is salvaged when present alone and is oxidized generating the reperfusion injury when the salvage is prevented by guanine that competes with hypoxanthine from the same site of hypoxanthine-guanine phosphoribosyl transferase. The functional impairment was slower when hypoxanthine was replaced by xanthine, and was eliminated by superoxide dismutase and catalase, indicating that the injury is caused by toxic oxygen species generated from hypoxanthine and xanthine oxidase. These data suggest that the salvage pathway may be critical in preventing the reperfusion injury in hypoxic hearts.

DUAL ROLE OF HYPOXANTHINE IN THE REOXYGENATION OF HYPOXIC ISOLATED RAT HEARTS / M. TARANTOLA, R. MOTTERLINI, M. BERETTA, M. SAMAJA. - In: JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY. - ISSN 0022-2828. - 23:1(1991), pp. 77-82.

DUAL ROLE OF HYPOXANTHINE IN THE REOXYGENATION OF HYPOXIC ISOLATED RAT HEARTS

M. SAMAJA
Ultimo
1991

Abstract

In the reoxygenated hypoxic heart, hypoxanthine is either oxidized by xanthine oxidase with production of toxic oxygen species or salvaged for the ATP pool by hypoxanthine-guanine phosphoribosyl transferase. To characterize the repartition of hypoxanthine between the two pathways, we have subjected rat hearts to 20 min hypoxia and monitored the recovery (ventricular, end-diastolic and coronary pressures, and the contraction rate) during the reoxygenation (30 min) in the presence of either hypoxanthine or guanine alone, or both. The rate-pressure product recovered 78% of the pre-hypoxia values in hearts reoxygenated with 100 μm hypoxanthine and 80% in hearts recoxygenated with 100 μm guanine, in contrast to 49% in the presence of both hypoxanthine and guanine (100 μm each). Thus, it is likely that hypoxanthine is salvaged when present alone and is oxidized generating the reperfusion injury when the salvage is prevented by guanine that competes with hypoxanthine from the same site of hypoxanthine-guanine phosphoribosyl transferase. The functional impairment was slower when hypoxanthine was replaced by xanthine, and was eliminated by superoxide dismutase and catalase, indicating that the injury is caused by toxic oxygen species generated from hypoxanthine and xanthine oxidase. These data suggest that the salvage pathway may be critical in preventing the reperfusion injury in hypoxic hearts.
ATP catabolism; Heart recovery; Hypoxanthine; Oxygen-derived free radicals; Purine salvage; Reoxygenation injury; Reperfusion injury; Xanthine oxidase
Settore BIO/10 - Biochimica
1991
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/181151
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