Nitric oxide production in experimental alcoholic liver disease in the rat: Role in protection from injury

Nanji, Amin A.; Greenberg, Samantha; Tahan, Steven R.; Fogt, Franz; Loscalzo, Joseph; Sadrzadeh, S.M. Hossein; Xie, Jianming; Stamler, Jonathan S.

doi:10.1016/0016-5085(95)90400-x

Cited by 102 publications

(60 citation statements)

References 49 publications

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“…Based on this, they propose that decreased NO from non-parenchymal cells, i.e. endothelial cells and eNOS, and increased NO from hepatocyte iNOS work in concert to exacerbate chronic alcohol mediated liver injury [117,118]. While these data support the hypothesis that the source, site, and concentration of NO produced are critical for determining the functional consequence of NO, i.e.…”

Section: Interplay Between Nitric Oxide and Mitochondria In Fatty LIVmentioning

confidence: 94%

“…In models of chronic alcohol consumption eNOS activity is decreased in liver through increased expression of the inhibitory protein caveolin-1 and/or decreased eNOS phosphorylation [115,116]. Similarly, Nanji and colleagues have demonstrated L-arginine supplementation prevents and reverses chronic alcohol mediated liver injury [117,118]. Based on this, they propose that decreased NO from non-parenchymal cells, i.e.…”

Section: Interplay Between Nitric Oxide and Mitochondria In Fatty LIVmentioning

confidence: 98%

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Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Mantena

King

Andringa

et al. 2008

Free Radical Biology and Medicine

382

302

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Fatty liver disease associated with chronic alcohol consumption or obesity/type 2 diabetes has emerged as a serious public health problem. Steatosis, accumulation of triglyceride in hepatocytes, is now recognized as a critical "first-hit" in the pathogenesis of liver disease. It is proposed that steatosis "primes" the liver to progress to more severe liver pathologies when individuals are exposed to subsequent metabolic and/or environmental stressors or "second-hits". Genetic risk factors can also influence the susceptibility and severity of fatty liver disease. Furthermore, oxidative stress, disrupted nitric oxide (NO) signaling, and mitochondrial dysfunctional are proposed to be key molecular events that accelerate or worsen steatosis and initiate progression to steatohepatitis and fibrosis. This review article will discuss the following topics regarding the pathobiology and molecular mechanisms responsible for fatty liver disease: 1) the "two-hit" or "multi-hit" hypothesis; 2) the role of mitochondrial bioenergetic defects and oxidant stress; 3) interplay between NO and mitochondria in fatty liver disease; 4) genetic risk factors and oxidative stress responsive genes; and 5) the feasibility of antioxidants for treatment.

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Section: Interplay Between Nitric Oxide and Mitochondria In Fatty LIVmentioning

confidence: 94%

Section: Interplay Between Nitric Oxide and Mitochondria In Fatty LIVmentioning

confidence: 98%

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Mantena

King

Andringa

et al. 2008

Free Radical Biology and Medicine

382

302

View full text Add to dashboard Cite

show abstract

“…20 As a result, both cytoprotective and cytotoxic effects of NO have been shown in the liver. Protection was observed following partial hepatectomy, 19 in alcoholic hepatitis, 21 and after GalN/TNF 22 or CCl 4 treatment. 23 However, it was also reported that iNOS induction has hepatotoxic effects, for example, in hemorrhagic shock, 24 in endotoxemia, 25 after GalN/lipopolysaccharide treatment, 15 and in con A-induced hepatitis.…”

mentioning

confidence: 97%

In vivoregulation of inducible NO synthase in immune-mediated liver injury in mice

Koerber

Sass

Kiemer³

et al. 2002

Hepatology

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Inducible nitric oxide synthase (iNOS) has been shown to play an important role in the development of liver injury. iNOS deficiency protects mice from hemorrhage/resuscitation as well as from cytokine-mediated liver injury, for example, after administration of concanavalin A (con A). Here we investigated the in vivo effects of tumor necrosis factor (TNF)-␣ and/or interferon (IFN)-␥, two mediators of con A-induced liver injury, the TNF receptor (TNFR) usage leading to iNOS expression, and its connection with nuclear factor B (NF-B) activation. In conclusion, iNOS expression in vivo is dependent on both TNF-␣ and IFN-␥. Although con A-induced liver injury depends on both TNFR1 and TNFR2, TNF-dependent iNOS expression is mediated exclusively by TNFR1 and requires NF-B activation. (HEPATOLOGY

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“…13,14 In liver, iNOS is now known to be induced in all liver cells including hepatocytes, Kupffer cells, endothelial cells, and stellate cells (lipocytes, Ito cells), 13,15,16 and has been implicated in the pathogenesis of a number of processes including acute hepatocellular injury during endotoxemia, 17 ischemia-reperfusion injury, 18 and toxin-mediated liver injury. 19 NO has also been hypothesized to be important in the pathogenesis of portal hypertension after chronic liver injury. 20 Persistent hepatic injury leads to cirrhosis, a scarring process in the liver that appears to be analogous to wound healing, with components of both increased fibrogenesis and wound contraction.…”

mentioning

confidence: 99%

Stimulation of inducible nitric oxide synthase in rat liver by hyaluronan fragments

et al. 1998

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Nitric oxide production in experimental alcoholic liver disease in the rat: Role in protection from injury

Cited by 102 publications

References 49 publications

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

In vivoregulation of inducible NO synthase in immune-mediated liver injury in mice

Stimulation of inducible nitric oxide synthase in rat liver by hyaluronan fragments

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