Oxidative stress and hippocampus in a low‐grade hepatic encephalopathy model: protective effects of curcumin

Roselló, Diego Martín; Balestrasse, Karina B.; Coll, Carlos; Coll, Sebastian; Tallis, Silvina; Gurni, Alberto A.; Tomaro, Marı́a L.; Lemberg, A; Perazzo, Juan Carlos

doi:10.1111/j.1872-034x.2008.00377.x

Cited by 13 publications

(9 citation statements)

References 45 publications

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“…Data derived from HE animal models suggest a relationship between impaired functions of brain regions involved in cognition, learning, memory formation, and motor control, as well as elevated markers for oxidative stress in the hippocampus (12,13), cerebral cortex (14), and cerebellum (15,16). Consistently, increased markers for oxidative stress, such as PTN and RNA oxidation, have also been shown in postmortem human brain tissue of patients with liver cirrhosis and HE (17).…”

mentioning

confidence: 48%

Hyperammonemia in gene-targeted mice lacking functional hepatic glutamine synthetase

Qvartskhava

Lang

Görg

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Urea cycle defects and acute or chronic liver failure are linked to systemic hyperammonemia and often result in cerebral dysfunction and encephalopathy. Although an important role of the liver in ammonia metabolism is widely accepted, the role of ammonia metabolizing pathways in the liver for maintenance of whole-body ammonia homeostasis in vivo remains ill-defined. Here, we show by generation of liver-specific Gln synthetase (GS)-deficient mice that GS in the liver is critically involved in systemic ammonia homeostasis in vivo. Hepatic deletion of GS triggered systemic hyperammonemia, which was associated with cerebral oxidative stress as indicated by increased levels of oxidized RNA and enhanced protein Tyr nitration. Liver-specific GS-deficient mice showed increased locomotion, impaired fear memory, and a slightly reduced life span. In conclusion, the present observations highlight the importance of hepatic GS for maintenance of ammonia homeostasis and establish the liver-specific GS KO mouse as a model with which to study effects of chronic hyperammonemia.hepatic encephalopathy | metabolic zonation | oxidative stress | RNA oxidation | glutamine

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mentioning

confidence: 48%

Hyperammonemia in gene-targeted mice lacking functional hepatic glutamine synthetase

Qvartskhava

Lang

Görg

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…Current evidence strongly implicates a close relationship between a low-grade cerebral edema and oxidative stress in the pathogenesis of hepatic encephalopathy, which could offer new therapeutic options [72][73][74][75][76][77]. However, one has to keep in mind that ROS/RNS are also physiological signaling molecules and their complete abrogation may bear the risk of not yet known harmful side-effects.…”

Section: Resultsmentioning

confidence: 99%

Interaction of oxidative stress, astrocyte swelling and cerebral ammonia toxicity

Häussinger

Görg

2010

Current Opinion in Clinical Nutrition and Metabolic Care

115

146

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Oxidative/nitrosative stress and a low-grade cerebral edema as key events in the pathogenesis of ammonia toxicity and hepatic encephalopathy may offer potential new strategies for treatment. Ammonia-induced oxidation of RNA and proteins may impair postsynaptic protein synthesis, which is critically involved in learning and memory consolidation. RNA oxidation offers a novel explanation for multiple disturbances of neurotransmitter systems and gene expression and the cognitive deficits observed in hepatic encephalopathy.

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“…The experimental model of portal vein ligated rats was suggested to reflect clinical features of minimal hepatic encephalopathy (MHE). This model has been evaluated repeatedly and was characterized with respect to functional, behavioural, and cell biological changes [2,28,29]. As shown in the present study, PVL is sufficient to induce oxidative/nitrosative stress in rat brain, as evidenced by a significant increase of cerebral protein tyrosine nitration and RNA oxidation.…”

Section: Discussionmentioning

confidence: 97%

Locomotor impairment and cerebrocortical oxidative stress in portal vein ligated rats in vivo

Bruck

Görg

Bidmon

et al. 2011

Journal of Hepatology

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Oxidative stress and hippocampus in a low‐grade hepatic encephalopathy model: protective effects of curcumin

Abstract: Oxidative stress was found to be implicated in the hippocampal damage and curcumin protected against this oxidative stress in low-grade hepatic encephalopathic rats. These protective effects may be attributed to its anti-oxidant properties.

Cited by 13 publications

References 45 publications

Hyperammonemia in gene-targeted mice lacking functional hepatic glutamine synthetase

Hyperammonemia in gene-targeted mice lacking functional hepatic glutamine synthetase

Interaction of oxidative stress, astrocyte swelling and cerebral ammonia toxicity

Locomotor impairment and cerebrocortical oxidative stress in portal vein ligated rats in vivo

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