Nitric oxide release and enhancement of lipid peroxidation in regenerating rat liver

Carnovale, Cristina E.; Scapini, Celina; Álvarez, María Clara; Favre, Cristián; Monti, Juan A.; Carrillo, María C.

doi:10.1016/s0168-8278(00)80249-4

Cited by 73 publications

(63 citation statements)

References 34 publications

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“…Increased oxidative stress could diminish the regeneration process. Our results showed that MDA, a biomarker of free radical mediated lipid peroxidation, was increased in regenerating liver after PH, which was consistent with previous studies [5,30]. In addition, PH also impairs the antioxidative system, such as SOD and GSH, which can offer protection from cell damage by scavenging superoxide anion radical in the upper stream of reactive oxygen metabolism cascade [37].…”

Section: A B Csupporting

confidence: 92%

“…The role of the antioxidant defence system, which includes SOD and GSH, is well characterised in the liver [28]. Increased oxidative stress during the early phase of liver regeneration had been observed as a cause of surgery and a reactive response of the reduced organ to compensate for the extra functional load [2,5,13]. Hepatic lipid peroxidation peaks at 24 h after PH when GSH content is minimum [1,14,16].…”

Section: A B Cmentioning

confidence: 99%

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The effects of quercetin on liver regeneration after liver resection in rats

Kanter

Tuncer²,

Erboğa³

et al. 2016

Folia Morphol

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Section: A B Csupporting

confidence: 92%

Section: A B Cmentioning

confidence: 99%

The effects of quercetin on liver regeneration after liver resection in rats

Kanter

Tuncer²,

Erboğa³

et al. 2016

Folia Morphol

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“…Given that NO and p38 are involved in the hepatic regenerative response (Hortelano et al, 1995;Spector et al, 1997;Carnovale et al, 2000;Hsu et al, 2006), we evaluated whether the beneficial effects of Ang II receptor antagonists on liver regeneration (AT1R antagonist for nonsteatotic livers and both Ang II receptor antagonists for steatotic ones) could be explained by changes in NO and p38. Our results indicated that NO was not responsible for the beneficial effects of Ang II receptor antagonists on regeneration in either type of liver.…”

Section: Resultsmentioning

confidence: 99%

“…In an attempt to explain the effects of Ang II receptor antagonists on regeneration and damage in both liver types under conditions of partial hepatectomy under I/R, we focused on p38 mitogen-activated protein kinase (p38) and nitric oxide (NO). This approach was based on: 1) numerous studies indicating that changes in p38 activity and NO generation are one of the earliest events in the hepatic regenerative response (Hortelano et al, 1995;Spector et al, 1997;Carnovale et al, 2000;Hsu et al, 2006), 2) the involvement of NO in hepatic damage in conditions of partial hepatectomy under I/R (Kukita et al, 2005), and 3) studies in the heart indicating that Ang II blockers could modulate p38 and NO (Wei et al, 2000;Kajihara et al, 2005).…”

mentioning

confidence: 99%

Are Angiotensin II Receptor Antagonists Useful Strategies in Steatotic and Nonsteatotic Livers in Conditions of Partial Hepatectomy under Ischemia-Reperfusion?

Ramalho

Alfany-Fernandez²,

Casillas-Ramírez³

et al. 2008

J Pharmacol Exp Ther

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We examined whether angiotensin (Ang) II receptor antagonists could be considered a therapeutic strategy in steatotic and nonsteatotic livers in conditions of partial hepatectomy under ischemia-reperfusion (I/R), which is commonly applied in clinical practice to reduce blood loss. We report that Ang II type I receptor (AT1R) antagonist, but not Ang II type II receptor (AT2R) antagonist, increased regeneration in nonsteatotic livers. In the presence of steatosis, both AT1R and AT2R antagonists increased liver regeneration. This effect was stronger when the two were combined. Neither of the Ang II receptor antagonists protected nonsteatotic livers against damage. Only the AT1R antagonist, through nitric oxide inhibition, reduced damage in steatotic livers. The combination of the AT1R and AT2R antagonists in steatotic livers conferred a similar degree of protection to AT1R antagonist alone. Herein, we show that p38 mitogen-activated protein kinase (p38) was a key mechanism in the regeneration induced by the Ang II receptor antagonists in both liver types because when this signaling pathway was inhibited, the beneficial effects of the Ang II receptor antagonists on liver regeneration disappeared, regardless of hepatocyte growth factor or transforming growth factor ␤-hepatic levels. In conclusion, in conditions of partial hepatectomy under I/R, the AT1R antagonist for nonsteatotic livers and the AT1R and AT2R antagonists for steatotic livers improved regeneration in the remnant liver through p38 activation. In addition, the combination of the AT1R and AT2R antagonists in steatotic livers led to stronger liver regeneration than either antagonists used separately and also provided the same protection against damage as that afforded by AT1R antagonist alone.

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“…These situations interfere with the normal regenerative pathways or initiate apoptotic pathways, resulting in a net loss of functional hepatocytes (16). Increased oxidative stress during the early phase of liver regeneration had been observed as a cause of surgery and a reactive response of the reduced organ to compensate for the extra functional load (17)(18)(19). We observed significantly increased oxidative stress and liver function tests levels and significantly decreased liver tissue GSH levels after partial hepatectomy.…”

Section: Discussionmentioning

confidence: 62%