Antioxidants, Tissue Damage, and Endurance in Trained and Untrained Young Male Rats

Venditti, Paola; Meo, S. Di

doi:10.1006/abbi.1996.0283

Cited by 174 publications

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“…This outcome was found even in group that didn't receive supplementation, in which we observed the lowest values of antioxidant capacity. However, the skeletal muscle has more limited antioxidant defenses than the heart and the blood 45 , corroborating the results observed in this study, where the presence of an inflammatory process was detected in most of the animals in each group at both phases of Chagas disease.…”

Section: Discussionsupporting

confidence: 91%

Evaluation of antioxidant therapy in experimental Chagas disease

Tieghi

Manca

Garcia

et al. 2017

Rev. Soc. Bras. Med. Trop.

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Introduction: Stimulation of inflammatory mediators such as cytokines and chemokines may cause oxidative stress in Chagas disease. In this study, we evaluated the merit of vitamins C and E as antioxidant therapy to minimize the oxidative stress-induced damage in an experimental model of Chagas disease. Methods: Ninety-six Swiss mice were infected with Trypanosoma cruzi QM2 and treated with vitamins C, E, or both (C/E) for 60 and 120 days, and their effects compared to placebo administration were evaluated in the acute and chronic disease phases. Results: There was no difference in parasitemia among treatment groups. However, histological analysis showed more severe inflammation in the skeletal muscle in the vitamin supplementation groups at both the acute and chronic phases. Biochemical analyses during the acute phase showed increased ferric-reducing ability of plasma (FRAP) and glutathione (GSH) levels in the vitamin C and C/E groups. In the chronic phase, a decrease in GSH levels was observed in the vitamin E group and a decrease in thiobarbituric acid reactive substances (TBARS) was observed in the vitamin C/E group. Moreover, there was a decrease in TBARS in the cardiac tissues of the vitamin C and C/E groups compared to that of the placebo group, although this level was greater in the vitamin E group than in the vitamin C group. Conclusions: The antioxidant action of vitamins C and E reduced oxidative stress in both the acute and chronic phases of Chagas disease, with a marked effect from joint administration, indicating their inherent synergism.

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Section: Discussionsupporting

confidence: 91%

Evaluation of antioxidant therapy in experimental Chagas disease

Tieghi

Manca

Garcia

et al. 2017

Rev. Soc. Bras. Med. Trop.

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“…In Etr subjects, as compared to obese subjects, the ratio of 4-HNE/IMTG was significantly lower suggesting a reduced peroxidation of their IMTG stores. 9 ETr increases skeletal muscle antioxidant capacity, [57][58][59] which may have a positive effect by reducing the amount of lipid peroxidation byproducts and therefore inhibiting the expression of insulindesensitising molecules such as TNFa. Furthermore, both resistance 60 and endurance training (Russell et al, unpublished observations) reduce skeletal muscle TNFa mRNA expression in addition to increasing insulin sensitivity.…”

Section: The Potential Pathways Linking Imtgs With Insulin Resistancementioning

confidence: 99%

Lipotoxicity: the obese and endurance-trained paradox

Russell

2004

Int J Obes

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The potential lipotoxic effect of intramyocellular triglyceride (IMTG) accumulation has been suggested to be a major component in the development of insulin resistance. Increased levels of IMTGs correlate with insulin resistance in both obese and diabetic patients, but this relationship does not exist in endurance trained (ETr) subjects. This may be, in part, related to differences in the gene expression and activities of key enzymes involved in fatty acid transport and oxidation as well as in the perodixation status of the IMTGs in obese/diabetic patients as compared with ETr subjects. Disruptions in fat and lipid homeostasis in skeletal muscle have been shown to activate protein kinase C (PKC), which acts on several downstream signalling pathways, including the insulin and the IkB kinase (IKK)/NFkB signalling pathways. Additionally, an increased peroxidation of IMTGs may reduce insulin sensitivity by increasing TNFa, which is known to increase the expression of suppressor of cytokine signalling proteins (SOCS). A common characteristic observed when activating both PKC and TNFa/SOCS3 is the inhibition of tyrosine phosphorylation of IRS-1 and subsequently an inhibition of its activation of downstream signalling molecules. These may be important players in the development of insulin resistance and understanding their activation and expression in both obese and ETr humans should assist in understanding how and why IMTGs become lipotoxic.

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“…Ischemia results in a decrease in oxygen and substrate availability. The lack of adenosine triphosphate (ATP) due to the inability of anaerobic means to maintain pace with energy demands results in damaging effects [15]. The breakdown of ATP and the activation of xanthine oxidase from xanthine dehydrogenase during ischemia have been related to production of free radicals and tissue damage during reperfusion.…”

Section: Discussionmentioning

confidence: 99%

“…This apparently paradoxical outcome of different exercise protocols has been proposed to be related to upregulation of the antioxidative and repair capacities of cells that are induced by mild oxidative stress [13]. It has been, furthermore, found that training prevents the appearance of some signs of exercise-induced free radical generation [15]. Exercise at moderate intensity, when repeated, induces several changes at the cellular level that may counteract the increased ROS generation more efficiently [19].…”

Section: Discussionmentioning

confidence: 99%

“…2015;17(10):e2195 2 leading to increased oxidative cellular damage, likely due to enhanced production of ROS [14]. It has been found that training prevents the appearance of some signs of exerciseinduced free radical generation [15]. While the effects of physical training on the antioxidant defenses of tissues such as liver, heart, brain, muscle and kidney have been investigated, the potential role of exercise in the gastrointestinal mucosal defense system is less well elucidated [16][17][18][19].…”

Section: Rostami-motamed H Et Almentioning

confidence: 99%

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The Effects of Moderate Exercise on Ethanol-Induced Gastric Injuries in Rats

Rostami-Motamed

Taati

Dezfoulian

et al. 2015

Zahedan J Res Med Sci

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Background:The role of oxygen-derived free radicals in the development of pathogenesis in acute gastric lesions induced by ethanol is well known. The beneficial effects of physical training on the antioxidant defenses of numerous tissues have been proved. Objectives: The present study was designed to evaluate the effects of exercise training on ethanol-induced gastric mucosal injuries in rats. Materials and Methods:In this experimental study, 28 Sprague-Dawley male rats were divided into 4 equal groups: sedentary control, exercise control, sedentary plus ethanol and exercise plus ethanol groups. The rats were subjected to moderate treadmill exercise protocol for 30 consecutive days (one hour per day). Thereafter, ethanol-treated groups received absolute ethanol (1 mL/rat) by gavage to induce gastric ulcer. Antioxidant status and lipid peroxidation of stomach wall were measured by evaluation of glutathione peroxidase (GPx), catalase activities (CAT) and thiobarbituric acid reactive substances (TBARS) concentration, respectively. Results: The histopathological findings of this study showed that moderate exercise training significantly inhibited the ethanol-induced gastric lesions in rats. Biochemical results also showed that administration of ethanol significantly decreased GPx activity and increased TBARS when compared to the sedentary control group (P < 0.05). In contrast, the exercise plus ethanol group showed higher GPx activity and lower TBARS concentration when compared to the ethanol-treated rats (P < 0.05). The catalase activity in ethanol-treated rats tended to be decreased when compared to control group. Conclusions: It seems that the preventive effects of exercise training may be mediated through increasing GPx activity subsequently inhibition of lipid peroxidation in stomach wall of rats. BackgroundThere is extensive evidence documenting the health-promoting effects of exercise [1]. Several reports have studied the useful effects of exercise on the gastrointestinal tract such as protective role against colon cancer, diverticular disease, cholelithiasis and constipation [2,3]. Although the mechanisms underlying these effects are not understood fully, altered gastrointestinal blood flow and motor function, neuroendocrine changes and mechanical effects are probably involved [4].Ulcerative lesions of gastrointestinal tract are one of the major side effects associated with alcohol consumption [5]. Studies have shown alterations in the antioxidant status following ulceration, suggesting that reactive oxygen species (ROS) such as superoxide anion, hydrogen peroxide, and hydroxyl radical play a crucial role in the development of ethanol-induced ulceration in rats [6,7]. ROS induce oxidative damage in membrane lipids and proteins and deplete glutathione level in gastric ulcers [6]. Indeed, "on one hand, ethanol administration reduces mucus production, gastric mucosal blood flow, bicarbonate secretion, endogenous glutathione and prostaglandin levels, and on the other hand it increases the release of histamine, ...

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Antioxidants, Tissue Damage, and Endurance in Trained and Untrained Young Male Rats

Cited by 174 publications

References 0 publications

Evaluation of antioxidant therapy in experimental Chagas disease

Evaluation of antioxidant therapy in experimental Chagas disease

Lipotoxicity: the obese and endurance-trained paradox

The Effects of Moderate Exercise on Ethanol-Induced Gastric Injuries in Rats

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