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Hyperoxia and xanthine dehydrogenase/oxidase activities in rat lung and heart.
Arch Biochem Biophys. 1989 Sep; 273(2):281-6.AB

Abstract

Cell injury from hyperoxia is associated with increased formation of superoxide radicals (O2-). One potential source for O2- radicals is the reduction of molecular O2 catalyzed by xanthine oxidase (XO). Physiologically, this reaction occurs at a relatively low rate, because the native form of the enzyme is xanthine dehydrogenase (XD) which produces NADH instead of O2-. Reports of accelerated conversion of XD to XO, and increased formation of O2- formation in ischemia-reperfusion injury, led us to examine whether hyperoxia, which is known to increase O2- radical formation, is associated with increased lung XO activity, and accelerated conversion of XD to XO. We exposed 3-month-old rats either to greater than 98% O2 or room air. After 48 h, we sacrificed the rats and measured XD and XO activities and uric acid contents of the lungs. We also measured the activities of the two enzymes in the heart as a control organ. We found that the activity of XD was not altered significantly by hyperoxia in rat lungs or hearts, but XO activity was markedly lower in the lung, whether expressed per whole organ or per milligram protein, and remained unchanged in the heart. Lung uric acid content was also significantly lower with hyperoxia. The decrease in lung XO activity may reflect inactivation of the enzyme by reactive O2 metabolites, possibly as a negative feedback mechanism. The concomitant decrease in uric acid content suggests either decreased production mediated by XO due to its inactivation or greater utilization of uric acid as an antioxidant. We examined these postulates in vitro using a xanthine/xanthine oxidase system and found that H2O2, but not uric acid, has an inhibitory effect on O2- formation in the system. We therefore conclude that hyperoxia is not associated with increased conversion of XD to XO, and that the exact contribution of XO to hyperoxic lung injury in vivo remains unclear.

Authors+Show Affiliations

Department of Medicine, School of Public Health, University of California, Los Angeles 90024.No affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

2549869

Citation

Elsayed, N M., and D F. Tierney. "Hyperoxia and Xanthine Dehydrogenase/oxidase Activities in Rat Lung and Heart." Archives of Biochemistry and Biophysics, vol. 273, no. 2, 1989, pp. 281-6.
Elsayed NM, Tierney DF. Hyperoxia and xanthine dehydrogenase/oxidase activities in rat lung and heart. Arch Biochem Biophys. 1989;273(2):281-6.
Elsayed, N. M., & Tierney, D. F. (1989). Hyperoxia and xanthine dehydrogenase/oxidase activities in rat lung and heart. Archives of Biochemistry and Biophysics, 273(2), 281-6.
Elsayed NM, Tierney DF. Hyperoxia and Xanthine Dehydrogenase/oxidase Activities in Rat Lung and Heart. Arch Biochem Biophys. 1989;273(2):281-6. PubMed PMID: 2549869.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hyperoxia and xanthine dehydrogenase/oxidase activities in rat lung and heart. AU - Elsayed,N M, AU - Tierney,D F, PY - 1989/9/1/pubmed PY - 1989/9/1/medline PY - 1989/9/1/entrez SP - 281 EP - 6 JF - Archives of biochemistry and biophysics JO - Arch Biochem Biophys VL - 273 IS - 2 N2 - Cell injury from hyperoxia is associated with increased formation of superoxide radicals (O2-). One potential source for O2- radicals is the reduction of molecular O2 catalyzed by xanthine oxidase (XO). Physiologically, this reaction occurs at a relatively low rate, because the native form of the enzyme is xanthine dehydrogenase (XD) which produces NADH instead of O2-. Reports of accelerated conversion of XD to XO, and increased formation of O2- formation in ischemia-reperfusion injury, led us to examine whether hyperoxia, which is known to increase O2- radical formation, is associated with increased lung XO activity, and accelerated conversion of XD to XO. We exposed 3-month-old rats either to greater than 98% O2 or room air. After 48 h, we sacrificed the rats and measured XD and XO activities and uric acid contents of the lungs. We also measured the activities of the two enzymes in the heart as a control organ. We found that the activity of XD was not altered significantly by hyperoxia in rat lungs or hearts, but XO activity was markedly lower in the lung, whether expressed per whole organ or per milligram protein, and remained unchanged in the heart. Lung uric acid content was also significantly lower with hyperoxia. The decrease in lung XO activity may reflect inactivation of the enzyme by reactive O2 metabolites, possibly as a negative feedback mechanism. The concomitant decrease in uric acid content suggests either decreased production mediated by XO due to its inactivation or greater utilization of uric acid as an antioxidant. We examined these postulates in vitro using a xanthine/xanthine oxidase system and found that H2O2, but not uric acid, has an inhibitory effect on O2- formation in the system. We therefore conclude that hyperoxia is not associated with increased conversion of XD to XO, and that the exact contribution of XO to hyperoxic lung injury in vivo remains unclear. SN - 0003-9861 UR - https://www.unboundmedicine.com/medline/citation/2549869/Hyperoxia_and_xanthine_dehydrogenase/oxidase_activities_in_rat_lung_and_heart_ L2 - https://linkinghub.elsevier.com/retrieve/pii/0003-9861(89)90485-2 DB - PRIME DP - Unbound Medicine ER -