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      Combination vitamin C and vitamin E prevents enteric diabetic neuropathy in the small intestine in rats

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          Abstract

          The present study evaluated the effects of supplementation with a combination of vitamin C and vitamin E on NADH-diaphorase-positive (NADH-d+) and neuronal nitric oxide synthase (nNOS)-immunoreactive myenteric neurons in the duodenum and ileum in diabetic rats. Forty rats were distributed into the following groups: normoglycemic (N), normoglycemic supplemented with vitamin C and vitamin E (NS), diabetic (D), and diabetic supplemented with vitamin C and vitamin E (DS). Vitamin C was added to the drinking water, and vitamin E was incorporated in the diet (1%). After 120 days, the animals were euthanized, and the duodenum and ileum were subjected to NADH-d and nNOS staining. Quantitative and morphometric analyses of myenteric neurons were performed. Diabetes reduced NADH-d+ neurons in the D group. The density of nitrergic neurons was not changed by diabetes or vitamin treatment. Hypertrophy of the cell body area of NADH-d+ and nNOS-immunoreactive neurons was observed in both intestinal segments. Combined supplementation with vitamin C and vitamin E prevented the reduction of the density of NADH-d+ neurons and hypertrophy, demonstratred by both techniques. Supplementation with a combination of vitamin C and vitamin E promoted myenteric neuroprotection in the small intestine in diabetic rats.

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          Oxidative stress in the pathogenesis of diabetic neuropathy.

          Oxidative stress results from a cell or tissue failing to detoxify the free radicals that are produced during metabolic activity. Diabetes is characterized by chronic hyperglycemia that produces dysregulation of cellular metabolism. This review explores the concept that diabetes overloads glucose metabolic pathways, resulting in excess free radical production and oxidative stress. Evidence is presented to support the idea that both chronic and acute hyperglycemia cause oxidative stress in the peripheral nervous system that can promote the development of diabetic neuropathy. Proteins that are damaged by oxidative stress have decreased biological activity leading to loss of energy metabolism, cell signaling, transport, and, ultimately, to cell death. Examination of the data from animal and cell culture models of diabetes, as well as clinical trials of antioxidants, strongly implicates hyperglycemia-induced oxidative stress in diabetic neuropathy. We conclude that striving for superior antioxidative therapies remains essential for the prevention of neuropathy in diabetic patients.
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            Fixation of ejaculated spermatozoa for electron microscopy.

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              Diabetes and endothelial dysfunction: a clinical perspective.

              The main etiology for mortality and a great percent of morbidity in patients with diabetes mellitus is atherosclerosis. A hypothesis for the initial lesion of atherosclerosis is endothelial dysfunction, defined pragmatically as changes in the concentration of the chemical messengers produced by the endothelial cell and/or by blunting of the nitric oxide-dependent vasodilatory response to acetylcholine or hyperemia. Endothelial dysfunction has been documented in patients with diabetes and in individuals with insulin resistance or at high risk for developing type 2 diabetes. Factors associated with endothelial dysfunction in diabetes include activation of protein kinase C, overexpression of growth factors and/or cytokines, and oxidative stress. Several therapeutic interventions have been tested in clinical trials aimed at improving endothelial function in patients with diabetes. Insulin sensitizers may have a beneficial effect in the short term, but the virtual absence of trials with cardiovascular end-points preclude any definitive conclusion. Two trials offer optimism that treatment with ACE inhibitors may have a positive impact on the progression of atherosclerosis. Although widely used, the effect of hypolipidemic agents on endothelial function in diabetes is not clear. The role of antioxidant therapy is controversial. No data have been published regarding the effects of hormonal replacement therapy on endothelial dysfunction in postmenopausal women with type 2 diabetes.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Journal
                babt
                Brazilian Archives of Biology and Technology
                Braz. arch. biol. technol.
                Instituto de Tecnologia do Paraná - Tecpar (Curitiba )
                1678-4324
                August 2015
                : 58
                : 4
                : 504-511
                Affiliations
                [1 ] Universidade Estadual de Maringá Brazil
                [2 ] Universidade Federal de Mato Grosso do Sul Brazil
                Article
                S1516-89132015000400504
                10.1590/S1516-8913201500414
                cbedb415-f859-46d7-b6c3-ee38e0b8a919

                http://creativecommons.org/licenses/by/4.0/

                History
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                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=1516-8913&lng=en
                Categories
                BIOLOGY

                General life sciences
                ascorbic acid,α-tocopherol,diabetes mellitus,myenteric plexus,enteric nervous system

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