Antioxidant status and glutathione metabolism in peripheral blood mononuclear cells from patients with chronic hepatitis C

Boya, Patricia; Peña, Andrés de la; Beloqui, Óscar; Larrea, Esther; Conchillo, Marian; Castelruiz, Y.; Civeira, M.P.; Prieto, Jesús

doi:10.1016/s0168-8278(99)80281-5

Cited by 104 publications

(82 citation statements)

References 42 publications

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“…Chronic infection was also associated with ROS production in the liver and peripheral blood mononuclear cells (12)(13)(14). ROS, especially superoxide anion (O 2 .…”

Section: Hepatitis C Virus (Hcv)mentioning

confidence: 99%

Nonstructural 3 Protein of Hepatitis C Virus Triggers an Oxidative Burst in Human Monocytes via Activation of NADPH Oxidase

Bureau

Bernad

Chaouche

et al. 2001

Journal of Biological Chemistry

147

121

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It has been shown that oxidative stress occurs in chronic hepatitis C. Release of reactive oxygen species (ROS) from sequestered phagocytes and activated resident macrophages represents the predominant component of oxidative stress in the liver. However, little is known about the ability of the monocyte to produce ROS in response to protein of hepatitis C virus. In this study, we investigated the ROS production in human monocytes stimulated by several viral proteins of hepatitis C virus. Human monocytes from healthy blood donors were incubated with recombinant viral protein: Core, NS3, NS4, and NS5. ROS production was measured by chemiluminescence. Only NS3 triggered ROS production in human monocytes. Generated ROS were mainly the anion superoxide. NS3 also induced a rapid and transient increase in intracellular calcium concentration measured by a video digital microscopy technique. By using different metabolic inhibitors, we showed that ROS production requires calcium influx, tyrosine kinases, and the stress-activated protein kinase, p38. The study of p47 PHOX phosphorylation and translocation showed that NADPH oxidase was activated and involved in ROS production induced by NS3. In a second experiment, NS3 inhibited the oxidative burst induced by phorbol 12-myristate 13-acetate. These results indicate that NS3 activates NADPH oxidase and modulates ROS production, which may be involved in the natural history of hepatitis C infection.

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“…Chronic infection was also associated with ROS production in the liver and peripheral blood mononuclear cells (12)(13)(14). ROS, especially superoxide anion (O 2 .…”

Section: Hepatitis C Virus (Hcv)mentioning

confidence: 99%

Nonstructural 3 Protein of Hepatitis C Virus Triggers an Oxidative Burst in Human Monocytes via Activation of NADPH Oxidase

Bureau

Bernad

Chaouche

et al. 2001

Journal of Biological Chemistry

147

121

View full text Add to dashboard Cite

show abstract

“…Paradis et al (11) also demonstrated MDA-protein adducts immunohistochemically in infected liver tissue. Boya et al (9) showed that the peripheral blood mononuclear cells from patients with chronic hepatitis C had increased MDA concentrations, and enhanced SOD activity. Romero et al (12) showed higher serum MDA values in chronic hepatitis C patients than healthy subjects before the interferon treatment.…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress In Patients With Chronic Hepatitis B And C

Çıragil¹,

Kurutaş²,

Kökoğlu³

et al. 2010

TUTFD

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“…First, oxidative stress is involved in the pathogenesis of chronic liver disease and fibrosis, and increased oxidative stress with impaired antioxidant status at the systemic level has been described in different chronic liver diseases. [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] Second, two previous studies have shown the persistence of increased systemic lipid peroxidation products above normal values in patients with cirrhosis 3 to 12 weeks after OLT that is a likely expression of extrahepatic ROS production. In fact, this time frame from operation is too wide to be compatible with continuous intra-graft production of ROS secondary to ischemia-reperfusion injury and release into the circulation, and it is too small to be expression of chronic liver damage of the transplanted liver.…”

mentioning

confidence: 99%

High preoperative recipient plasma 7β-hydroxycholesterol is associated with initial poor graft function after liver transplantation

et al. 2005

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Oxidative stress is implicated in the pathogenesis of hepatic ischemia-reperfusion injury, a major determinant of initial poor graft function (IPGF) after orthotopic liver transplantation (OLT). We prospectively investigated the association between the recipient plasma preoperative oxidative stress and the occurrence of IPGF after deceased-donor OLT and indirectly studied the sourcehepatic or extra-hepatic-of systemic oxidative stress in vivo in cirrhosis. We used a recently developed specific and sensitive mass spectrometry assay to measure 7␤-hydroxycholesterol and 7-ketocholesterol (oxysterols), markers of oxidative stress, in biological matrices. At univariate analysis, preoperative recipient 7␤-hydroxycholesterol plasma concentration was significantly higher in transplants with subsequent IPGF (n ‫؍‬ 9) compared with those with initial good graft function (IGGF; n ‫؍‬ 23) [mean ؎ SD: 30.63 ؎ 26.42 and 11.57 ؎ 15.76 ng/mL, respectively] (P ‫؍‬ 0.017). In a logistic regression model, which included also the Model for End-Stage Liver Disease (MELD) score, 7␤-hydroxycholesterol plasma concentration was an independent predictor of IPGF with an odds ratio of 1.17 (95% CI, 1.02-1.33, P ‫؍‬ 0.028). Patients with cirrhosis (n ‫؍‬ 32) had increased oxysterol plasma levels compared with healthy controls (n ‫؍‬ 49); livers with cirrhosis (n ‫؍‬ 21), however, had oxysterol content comparable with normal livers obtained from organ donors (n ‫؍‬ 19). Oxysterols persisted elevated in plasma 1 month after OLT (n ‫؍‬ 23). In conclusion, cirrhosis presents upregulated systemic oxidative stress likely of extrahepatic source that is associated with graft failure after OLT. (Liver Transpl 2005;11:1494-1504.)

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Antioxidant status and glutathione metabolism in peripheral blood mononuclear cells from patients with chronic hepatitis C

Cited by 104 publications

References 42 publications

Nonstructural 3 Protein of Hepatitis C Virus Triggers an Oxidative Burst in Human Monocytes via Activation of NADPH Oxidase

Nonstructural 3 Protein of Hepatitis C Virus Triggers an Oxidative Burst in Human Monocytes via Activation of NADPH Oxidase

Oxidative Stress In Patients With Chronic Hepatitis B And C

High preoperative recipient plasma 7β-hydroxycholesterol is associated with initial poor graft function after liver transplantation

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