Is intestinal cytosolic glutathione S-transferase an alternative detoxification pathway in two-thirds hepatectomized rats?

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

doi:10.1016/0024-3205(95)02024-d

Cited by 9 publications

(4 citation statements)

References 29 publications

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“…The reduction of lipid peroxidation and glutathione oxidation may be attributed to liver regeneration and release of several growth factors and hormones that may influence intestinal oxidative stress [27]. In addition, previous studies demonstrate evidence for activation of the intestinal cytosolic antioxidant enzyme glutathione S-transferase after hepatectomy [28]. Another explanation might be that removal of a large portion of the liver could result in a decrease of oxidants originating from liver, therefore lowering lipid peroxidation in the intestine.…”

Section: Discussionmentioning

confidence: 98%

Oxidative state in intestine and liver after partial hepatectomy in rats. Effect of bombesin and neurotensin

Alexandris

Assimakopoulos

Vagianos

et al. 2004

Clinical Biochemistry

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Section: Discussionmentioning

confidence: 98%

Oxidative state in intestine and liver after partial hepatectomy in rats. Effect of bombesin and neurotensin

Alexandris

Assimakopoulos

Vagianos

et al. 2004

Clinical Biochemistry

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“…33 Thymidine incorporation into DNA, an indicator of liver regeneration, clearly shows that the livers are regenerating along the experimental period to its original size. 34 ROS such as superoxide anion, hydrogen peroxide or hydroxyl radicals are generally produced during the metabolism of drugs and other occasions such as hepatic injury caused after of PH. 8 When these ROS are not efficiently removed, OS can induce cellular damage.…”

Section: Discussionmentioning

confidence: 99%

Role of melatonin in the oxidative damage prevention at different times of hepatic regeneration

González

Contini

Millen

et al. 2012

Cell Biochemistry & Function

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The process of regenerating liver is the result of a balance between stimulating factors and inhibitors of hepatocyte proliferation. Melatonin and its metabolites have been found to protect tissues against oxidative damage generated by a variety of toxic agents and metabolic processes. Furthermore, studies in liver of rats showed a decrease in the liver mitochondrial hydroxylation of drugs returning to the normal state after the administration of antioxidants. This study was designed to determine, in experimental animals, whether the administration of an antioxidant agent such as melatonin could prevent cells events leading to tissue injury and hepatic dysfunction after partial hepatectomy (PH). Biliary flow (BF), oxidative stress in hepatic tissue and Na⁺/K⁺ ATPase activities in whole plasma membrane were determined. PH decreased the Na⁺/K⁺ ATPase activity. PH significantly reduced the BF (36%) and promoted oxidative stress with an increase of lipoperoxidation and decrease of glutathione peroxidase and catalase activities. Treatment with melatonin prevented the decrease of BF in rats with hepatectomy and normalized the Na⁺/K⁺ ATPase activity. Moreover, melatonin markedly attenuated oxidative stress produced by PH. This may be the results of the higher efficacy of melatonin in scavenging various free radicals and also because of its ability in stimulating the antioxidant enzymes. We suggest that oxidative stress before and during liver regeneration has a crucial role in cholestasis, apoptotic/necrotic hepatocellular damage and the impairment in liver transport function induced by PH and that melatonin could modulate the degree of oxidative stress and through it prevent the alterations in liver function carrier.

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“…GST is known to be an early and sensitive marker of liver injury and has been shown to increase after liver ischaemia/reperfusion [ 46 ]. This increased activity of GST could be explained as a compensatory mechanism to protect the organism against injury [ 47 ]. These findings are not only in accord with the diverse signalling pathways related to postoperative liver injury associated with DM ( Figure 1 ) but also indicate the importance of the determination of increased ROS production and its characteristic consequences in postischaemic tissues, permitting the identification of interventions that stimulates ROS detoxification, and consequently protect against reperfusion injury [ 16 ], mainly in a diabetic context ( Figure 1 ).…”

Section: Oxidative Stressmentioning

confidence: 99%

Diabetes Mellitus and Liver Surgery: The Effect of Diabetes on Oxidative Stress and Inflammation

Mendes‐Braz

Martins

2018

Mediators of Inflammation

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Diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycaemia and high morbidity worldwide. The detrimental effects of hyperglycaemia include an increase in the oxidative stress (OS) response and an enhanced inflammatory response. DM compromises the ability of the liver to regenerate and is particularly associated with poor prognosis after ischaemia-reperfusion (I/R) injury. Considering the growing need for knowledge of the impact of DM on the liver following a surgical procedure, this review aims to present recent publications addressing the effects of DM (hyperglycaemia) on OS and the inflammatory process, which play an essential role in I/R injury and impaired hepatic regeneration after liver surgery.

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Is intestinal cytosolic glutathione S-transferase an alternative detoxification pathway in two-thirds hepatectomized rats?

Cited by 9 publications

References 29 publications

Oxidative state in intestine and liver after partial hepatectomy in rats. Effect of bombesin and neurotensin

Oxidative state in intestine and liver after partial hepatectomy in rats. Effect of bombesin and neurotensin

Role of melatonin in the oxidative damage prevention at different times of hepatic regeneration

Diabetes Mellitus and Liver Surgery: The Effect of Diabetes on Oxidative Stress and Inflammation

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