Serum thioredoxin levels as an indicator of oxidative stress in patients with hepatitis C virus infection

Sumida, Yoshio; Nakashima, Tomoki; Yoh, Takaharu; Nakajima, Yoshiki; Ishikawa, Hiroki; Mitsuyoshi, Hironori; Sakamoto, Yoshikuni; Okanoue, Takeshi; Kashima, Kei; Nakamura, Hajime; Yodoi, Junji

doi:10.1016/s0168-8278(00)80013-6

Cited by 136 publications

(73 citation statements)

References 43 publications

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“…19 These findings suggest that TRX1 per se and the redox system modulated by TRX1 have a important role in the cellular defense against oxidative stress in cardiomyocytes as well as in other cell types, such as neurons 11 and hepatocytes. 20 Most studies support the view that both an increase in oxidative stress and a decrease in antioxidants play an important role in the pathogenesis of ADR cardiomyopathy. 2,5,6 ADR has been shown to be a potential source of free radicals.…”

Section: Discussionmentioning

confidence: 87%

Overexpression of Thioredoxin-1 in Transgenic Mice Attenuates Adriamycin-Induced Cardiotoxicity

et al. 2002

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Background-Adriamycin (ADR) is an anticancer drug known to cause severe cardiac toxicity by generating free radicals.We investigated the role of a redox-regulating molecule, thioredoxin-1 (TRX1), in ADR-induced cardiotoxicity. Methods and Results-The in vitro study showed that TRX1 was dose-dependently increased concomitant with the formation of hydroxyl radicals in ADR-treated neonatal rat cardiomyocytes. Lactate dehydrogenase-releasing assay showed that treatment with recombinant human TRX1 suppressed cardiomyocyte injury in ADR-treated cardiomyocytes. To examine the biological significance of TRX1 in vivo, we used transgenic mice expressing increased levels of human TRX1 (TRX1-TG mice). Electron microscopy revealed that mitochondria, myofibrils, and other cellular details were much better maintained in ADR-treated TRX1-TG mice than in ADR-treated nontransgenic (WT) mice. The increase in the protein carbonyl content, a marker of cellular protein oxidation, was suppressed in ADR-treated TRX1-TG mice compared with ADR-treated WT mice. The formation of hydroxyl radicals in ADR-treated heart homogenates of TRX1-TG mice was decreased compared with WT mice. For the survival study, all WT mice treated with ADR died within 6 weeks, but 5 of 6 TRX1-TG mice treated with ADR survived Ͼ8 weeks. Conclusions-TRX1 is upregulated by intracellular oxidative stress generated by ADR. TRX1 has a protective role against ADR-induced cardiotoxicity by reducing oxidative stress.

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Section: Discussionmentioning

confidence: 87%

Overexpression of Thioredoxin-1 in Transgenic Mice Attenuates Adriamycin-Induced Cardiotoxicity

et al. 2002

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“…Although the mecha-nism is unclear, HCV infection is known to induce oxidative stress and DNA damage. [46][47][48] Finally, three genes involved in glucose metabolism, glycogen synthase, phosphoenolpyruvate carboxykinase, and GLUT2, were differentially underexpressed in the ACR group. Glycogen synthase catalyzes the rate-limiting step in glycogen synthesis, whereas phosphoenolpyruvate carboxykinase is a key enzyme in gluconeogenesis.…”

Section: Discussionmentioning

confidence: 95%

Differential allograft gene expression in acute cellular rejection and recurrence of hepatitis C after liver transplantation

Raghavakaimal¹

2002

Liver Transplantation

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Treatment of acute cellular rejection (ACR ) is associated with increased viral load, more severe histologic recurrence, and diminished patient and graft survival after liver transplantation for hepatitis C virus (HCV). Recurrence of HCV may be difficult to distinguish histologically from ACR . Because the immunologic mechanisms of ACR and HCV recurrence are likely to differ, we hypothesized that ACR is associated with the expression of a specific subset of immune activation genes that may serve as a diagnostic indicator of ACR and provide mechanistic insight into the pathophysiology of ACR and recurrence of HCV. The goal of the study was to study intragraft gene expression patterns in ACR and during recurrence of HCV in HCVinfected recipients. High-density microarrays were used to determine relative intragraft gene expression in two groups of HCV-infected liver transplant recipients: four with steroid responsive ACR by Banff criteria and four age-and gender-matched HCV-infected recipients with similar necroinflammatory activity but without histological criteria for rejection (no cholangitis or endotheliitis). Immunosuppression was similar in both groups. Other etiologies of graft dysfunction were excluded by ultrasound, cholangiography, and cultures. High-quality total RNA was extracted from snap frozen liver biopsies, reverse transcribed, labeled with biotin, and fragmented according to established protocol. Twenty-five genes were relatively overexpressed, and 15 were relatively underexpressed by >twofold in the ACR when compared with the HCV group. ACR was most notably associated with the relative overexpression of genes associated with major histocompatibility complex I and II, insulin-like growth factor-1 expression, apoptosis induction, and T-cell activation. In HCV-infected liver transplant recipients, ACR is associated with an intragraft gene expression profile that is distinct from that seen during recurrence of HCV. These experiments provide evidence that alloimmunity,

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“…17,18 In hepatitis C virus infection, serum level of Trx is elevated, serving as a possible indicator for the effectiveness of interferon therapy. 19 Circulating Trx prevents neutrophil extravasation and suppresses inflammation. 20 Based on these considerations, we hypothesized that Trx could attenuate oxidative stress-mediated acute hepatitis.…”

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confidence: 99%

Overexpression of Thioredoxin Prevents Acute Hepatitis Caused by Thioacetamide or Lipopolysaccharide in Mice

et al. 2003

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Serum thioredoxin levels as an indicator of oxidative stress in patients with hepatitis C virus infection

Cited by 136 publications

References 43 publications

Overexpression of Thioredoxin-1 in Transgenic Mice Attenuates Adriamycin-Induced Cardiotoxicity

Overexpression of Thioredoxin-1 in Transgenic Mice Attenuates Adriamycin-Induced Cardiotoxicity

Differential allograft gene expression in acute cellular rejection and recurrence of hepatitis C after liver transplantation

Overexpression of Thioredoxin Prevents Acute Hepatitis Caused by Thioacetamide or Lipopolysaccharide in Mice

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