Serum xanthine oxidase in jaundice

Giler, S; Sperling, Oded; Brosh, S; Urca, I; Vries, A. De

doi:10.1016/0009-8981(75)90375-7

Cited by 37 publications

(15 citation statements)

References 9 publications

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“…Other viral illnesses in mice and humans are associated with increased XDH/XO activity. For example, XDH/XO activity is elevated up to 50X normal in the serum of patients with infectious hepatitis (37). The recent studies of Akaike et al (8) provide evidence supporting a central pathologic role for XDH/XO in viral disorders.…”

Section: Discussionmentioning

confidence: 97%

Regulation of xanthine dehydrogenase and xanthine oxidase activity and gene expression in cultured rat pulmonary endothelial cells.

Dupont¹,

Huecksteadt²,

Marshall³

et al. 1992

J. Clin. Invest.

128

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The central importance of xanthine dehydrogenase (XDH) and xanthine oxidase (XO) in the pathobiochemistry of a number of clinical disorders underscores the need for a comprehensive understanding of the regulation of their expression. This study was undertaken to examine the effects of cytokines on XDH/ XO activity and gene expression in pulmonary endothelial cells. The results indicate that IFN-'y is a potent inducer of XDH/XO activity in rat lung endothelial cells derived from both the microvasculature (LMVC) and the pulmonary artery.In contrast, interferon-affi, tumor necrosis factor-a, interleukin-i or -6, lipopolysaccharide and phorbol myristate acetate have no demonstrable effect. The increase in XDH/XO activity requires new protein synthesis. By Northern analysis, IFN-"y markedly increases the level of the 5.0-kb XDH/XO mRNA in LMVC. The increase is due, in part, to increased transcription rate of the XDH/XO gene. Transcriptional activation does not require new protein synthesis. The physiologic relevance of these observations was evaluated by administering IFN-'y to rats. Intraperitoneal administration leads to an increased XDH/XO activity and XDH/XO mRNA level in rat lungs. In sum, IFN-'y is a potent and biologically relevant inducer of XDH/XO expression; the major site of upregulation occurs at the transcriptional level. (J. Clin. Invest. 1992. 89:197-202.)

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Section: Discussionmentioning

confidence: 97%

Regulation of xanthine dehydrogenase and xanthine oxidase activity and gene expression in cultured rat pulmonary endothelial cells.

Dupont¹,

Huecksteadt²,

Marshall³

et al. 1992

J. Clin. Invest.

128

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“…These cascades of events may start after the advent of tissue damage-here due to impediment to the vascular tree-even if followed by volume or pressure resuscitation, as demonstrated herein. Support for this contention can be obtained from cases of limb ischemia [38] and its reperfusion [29], aortic cross-clamping and aneurysmectomy [19,24,29,30,34,38], and other traumatic or ischemic events in humans [39,40], as well as during organ transplant [41] and renal decompensation [42]. Importantly, the linear magnitude of changes of XO and GSH also attest to the role of the pressure in generating stress injury in the various kidneys.…”

Section: Discussionmentioning

confidence: 99%

Renal oxidative stress following CO2 pneumoperitoneum-like conditions

et al. 2008

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Background Physiologic renal changes associated with pneumoperitoneum (PNP) have been described and various underlying mechanisms have been suggested. We investigated the possibility that PNP-associated renal damage is pressure dependent, and that oxidative stress is thereby involved. Materials and methods Seventy Wistar rat kidneys (n = 10 per group) were isolated. They were perfused with oxygenated, warm, Krebs-Henseleit solution containing 5% albumin within an isolated environment and subjected to various CO 2 pressures (0 [control], 3,5,8,12,15, and 18 mmHg) for 60 min. Half of each group was additionally perfused for 30 min at 0 mmHg pressure.Results Renal flow decreased proportionately to the applied pressure as did urine output: both decreased (P \ 0.05) after 60 and 90 min when pressure C8 mmHg was applied. Oxygen extraction decreased (P \ 0.05) during PNP in all pressurized groups. Xanthine oxidase (XO) activity and reduced glutathione in the tissues increased (P \ 0.05) proportionately to pressures C8 mmHg. All parameters slightly reversed toward baseline values, upon the release of the intra-chamber pressure, except for the 18 mmHg group's values. Conclusions CO 2 -PNP pressure induces kidney injury, possibly reversible immediately after pressure is annulled. Pressure is associated with oxidative stress, which interferes with cellular metabolism and function, possibly via an ischemic-reperfusion-like mechanism.

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“…There is only trace XO activity in the plasma and vascular endothelium of healthy humans (36,37). During pathological conditions such as hepatocellular damage (38,39), ischemia-reperfusion (40), atherosclerosis (41), adult respiratory distress syndrome (36), alcoholic liver disease (42), and now SCD, in which organs replete in XOR can release this proinflammatory enzyme into the circulation, plasma XO levels increase. This can lead to an enhancement of vascular oxidant production, often in tissue compartments having minimal defense against oxidative injury.…”

Section: Discussionmentioning

confidence: 99%