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Mechanisms of conversion of xanthine dehydrogenase to xanthine oxidase in ischemic rat liver and kidney.
Am J Physiol. 1988 May; 254(5 Pt 1):G753-60.AJ

Abstract

Previous studies have proposed and supported a role for the proteolytic, irreversible conversion of xanthine dehydrogenase to xanthine oxidase (XO) in postischemic injury in a wide variety of organs. A second mechanism of conversion, due to sulfhydryl modification and reversible with dithiothreitol (DTT), is potentially important but has not been well investigated. In this study rat liver and kidney were found to produce significant amounts of DTT-reversible XO during normothermic global ischemia. Formation of reversible XO precedes that of irreversible XO by approximately 0.5 h with a strong correlation (r = 0.92) existing between the rate of irreversible XO formation and the concentration of reversible XO. The formation of reversible XO is preceded by a depletion of glutathione with concentrations of glutathione during ischemia correlating (r = 0.85) with the observed concentration of reversible XO. While a large increase in the extent of liver damage occurs concurrently with conversion in an in vivo liver model of liver ischemia, an ischemia-reperfusion regimen (1 h of ischemia plus 0.5 h of reperfusion) that resulted in no conversion caused significant elevations in serum glutamic pyruvic transaminase and serum glutamic-oxaloacetic transaminase. Rats depleted of XO by tungsten dieting release 65% less enzyme after the same insult, suggesting that endogenous XO may also participate in the damage process independent of any conversion.

Authors+Show Affiliations

Department of Biochemistry, University of South Alabama, Mobile 36688.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

3163235

Citation

McKelvey, T G., et al. "Mechanisms of Conversion of Xanthine Dehydrogenase to Xanthine Oxidase in Ischemic Rat Liver and Kidney." The American Journal of Physiology, vol. 254, no. 5 Pt 1, 1988, pp. G753-60.
McKelvey TG, Höllwarth ME, Granger DN, et al. Mechanisms of conversion of xanthine dehydrogenase to xanthine oxidase in ischemic rat liver and kidney. Am J Physiol. 1988;254(5 Pt 1):G753-60.
McKelvey, T. G., Höllwarth, M. E., Granger, D. N., Engerson, T. D., Landler, U., & Jones, H. P. (1988). Mechanisms of conversion of xanthine dehydrogenase to xanthine oxidase in ischemic rat liver and kidney. The American Journal of Physiology, 254(5 Pt 1), G753-60.
McKelvey TG, et al. Mechanisms of Conversion of Xanthine Dehydrogenase to Xanthine Oxidase in Ischemic Rat Liver and Kidney. Am J Physiol. 1988;254(5 Pt 1):G753-60. PubMed PMID: 3163235.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanisms of conversion of xanthine dehydrogenase to xanthine oxidase in ischemic rat liver and kidney. AU - McKelvey,T G, AU - Höllwarth,M E, AU - Granger,D N, AU - Engerson,T D, AU - Landler,U, AU - Jones,H P, PY - 1988/5/1/pubmed PY - 1988/5/1/medline PY - 1988/5/1/entrez SP - G753 EP - 60 JF - The American journal of physiology JO - Am J Physiol VL - 254 IS - 5 Pt 1 N2 - Previous studies have proposed and supported a role for the proteolytic, irreversible conversion of xanthine dehydrogenase to xanthine oxidase (XO) in postischemic injury in a wide variety of organs. A second mechanism of conversion, due to sulfhydryl modification and reversible with dithiothreitol (DTT), is potentially important but has not been well investigated. In this study rat liver and kidney were found to produce significant amounts of DTT-reversible XO during normothermic global ischemia. Formation of reversible XO precedes that of irreversible XO by approximately 0.5 h with a strong correlation (r = 0.92) existing between the rate of irreversible XO formation and the concentration of reversible XO. The formation of reversible XO is preceded by a depletion of glutathione with concentrations of glutathione during ischemia correlating (r = 0.85) with the observed concentration of reversible XO. While a large increase in the extent of liver damage occurs concurrently with conversion in an in vivo liver model of liver ischemia, an ischemia-reperfusion regimen (1 h of ischemia plus 0.5 h of reperfusion) that resulted in no conversion caused significant elevations in serum glutamic pyruvic transaminase and serum glutamic-oxaloacetic transaminase. Rats depleted of XO by tungsten dieting release 65% less enzyme after the same insult, suggesting that endogenous XO may also participate in the damage process independent of any conversion. SN - 0002-9513 UR - https://www.unboundmedicine.com/medline/citation/3163235/Mechanisms_of_conversion_of_xanthine_dehydrogenase_to_xanthine_oxidase_in_ischemic_rat_liver_and_kidney_ L2 - https://journals.physiology.org/doi/10.1152/ajpgi.1988.254.5.G753?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -