Antioxidant enzyme level in the testes of cirrhotic rats

Abul, H.; Mathew, T.C.; Abul, Fawzi; Al‐Sayer, H.; Dashti, H.

doi:10.1016/s0899-9007(01)00743-2

Cited by 13 publications

(11 citation statements)

References 34 publications

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“…Impairment of the oxidant–antioxidant balance in favour of pro‐oxidants results in cellular damage. The major enzymes with antioxidant activities are SOD, GPx and catalase19, 20. There are several naturally occurring putative antioxidants, such as green tea, carotenoids and α‐tocopherol19, 20.…”

Section: Discussionmentioning

confidence: 99%

Fasting-induced intestinal damage is mediated by oxidative and inflammatory responses

Abdeen

Mathew

Khan

et al. 2009

British Journal of Surgery

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Section: Discussionmentioning

confidence: 99%

Fasting-induced intestinal damage is mediated by oxidative and inflammatory responses

Abdeen

Mathew

Khan

et al. 2009

British Journal of Surgery

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“…Zn administration in rats before CCl 4 exposure inhibited hepatic cell nuclear DNA fragmentation which is linked to apoptosis [66]. The hepatoprotective action of Zn administration against oxidative stress was imposed through the regulation of the metabolism of SOD, MTs, GSH, and other antioxidants such as vitamins E and C [141,158,168].…”

Section: Zn Deficiency and The Pathogenesis Of Liver Fibrosismentioning

confidence: 99%

“…Nevertheless, alcoholic cirrhotic patients had unaffected SOD levels in red blood cells [170], while in the liver only the Cu/Zn-SOD isoenzyme levels were reduced when Mn-SOD levels remained unaffected [171]. In TAA-treated rats, SOD activity was reduced in the liver [168,172]. It has been reported that Zn administration in experimental studies of liver cirrhosis either normalized the SOD levels [173] or did not [141].…”

Section: Zn Deficiency and The Pathogenesis Of Liver Fibrosismentioning

confidence: 99%

Zinc and the Liver: An Active Interaction

2007

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Zinc is an essential trace element, exerting important antioxidant, anti-inflammatory, and antiapoptotic effects. It affects growth and development and participates in processes such as aging and cancer induction. The liver is important for the regulation of zinc homeostasis, while zinc is necessary for proper liver function. Decreased zinc levels have been implicated in both acute and chronic liver disease states, and zinc deficiency has been implicated in the pathogenesis of liver diseases. Zinc supplementation offers protection in experimental animal models of acute and chronic liver injury, but these hepatoprotective properties have not been fully elucidated. In the present review, data on zinc homeostasis, its implication in the pathogenesis of liver diseases, and its effect on acute and chronic liver diseases are presented. It is concluded that zinc could protect against liver diseases, although up to now the underlying pathophysiology of zinc and liver interactions have not been defined.

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“…Free radicals damage DNA, proteins, and lipid membranes [42]. To protect the cells from the attack of free radicals, the mammalian system is equipped with several mechanisms, including the expression of endogenous antioxidant enzymes such as SOD, GPx, and catalase [43,44]. Under normal physiological conditions, within each cell there is a critical equilibrium between free radicals generated and antioxidant activity.…”

Section: Discussionmentioning

confidence: 99%

Exercise may offset nicotine-induced injury in lung tissue: A preliminary histological study based on a rat model

Al‐Obaidi

Mathew

Dean

2012

Experimental Lung Research

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Nicotine appears to be the primary pharmacologic agent that causes smoking-related pulmonary diseases. An understanding of the effect of nicotine on lungs is essential to develop interventions that can be used to counter smoking-related diseases. Further, it is shown that physical exercise may partially reverse smoking-induced pathological changes in experimental animals. Hence, this study focuses on the pathological changes in rat lung following nicotine administration and the role of exercise in reversing the nicotine-induced lung injury. This is a randomized controlled trial with 3 groups of rats. Control (CG), nicotine-exposed (NG), and nicotine-exposed and exercise group (NEG). Control group received no intervention. Both NG and NEG were given 1.5 mg/kg nicotine base, daily, subcutaneously, but NEG were also subjected to an intensive daily swimming protocol. The rats were sacrificed and the lung tissue was processed for light and transmission electron microscopic and immunohistochemical studies. Compared with the control group, the nicotine group showed enlargement and destruction of the alveolar septum, cellular hyperplasia and interstitial fibrosis, and interstitial mononuclear cell infiltration with increased intraluminal macrophages. There was only modest morphological change between the nicotine administered and nicotine and exercise groups. Expression of superoxide dismutase (SOD) and catalase showed a mild increase in the NEG, whereas glutathione peroxidase (GPX) showed mild and moderate increase in the expression in the NG and NEG, respectively. This study shows that nicotine induces substantial pathological changes in the lung and prolonged exercise may have some beneficial effects in partially reversing the nicotine-induced lung injury by inducing the expression of antioxidants.

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Antioxidant enzyme level in the testes of cirrhotic rats

Cited by 13 publications

References 34 publications

Fasting-induced intestinal damage is mediated by oxidative and inflammatory responses

Fasting-induced intestinal damage is mediated by oxidative and inflammatory responses

Zinc and the Liver: An Active Interaction

Exercise may offset nicotine-induced injury in lung tissue: A preliminary histological study based on a rat model

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