Changes in Rat Alveolar Macrophageal Antioxidant Defense and Reactive Oxygen Species Release by High Dietary Vitamin E.

Pathania, V.; Syal, Nidhi; Pathak, Chander Mohan; Khanduja, Krishan Lal

doi:10.3177/jnsv.44.491

Cited by 5 publications

(3 citation statements)

References 38 publications

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“…40 Indeed, diabetic tissues have an increased rate of H 2 O 2 production as indicated previously, 41 and vitamin E inhibits H 2 O 2 production effectively. 42 In our study, although kidney MDA levels were not significantly changed by diabetes, they were markedly inhibited by vitamin E treatment in both diabetic and non-diabetic control animals. This was concomitant with the parallel decrease in both kidney calcium levels and Ca 2þ -ATPase activity in vitamin E-treated rats, tending to confirm the hypothesis that the occurrence of oxidant reactions is an important reason for impaired calcium metabolism in diabetic membranes.…”

Section: Discussioncontrasting

confidence: 51%

Effects of vitamin E on microsomal Ca²⁺‐ATPase activity and calcium levels in streptozotocin‐induced diabetic rat kidney

Pekiner

Evcimen

Ulusu

et al. 2003

Cell Biochemistry & Function

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Vitamin E treatment has been found to be beneficial in preventing or reducing diabetic nephropathy. Increased tissue calcium and abnormal microsomal Ca(2+)-ATPase activity have been suggested as contributing factors in the development of diabetic nephropathy. This study was undertaken to test the hypothesis that vitamin E reduces lipid peroxidation and can prevent the abnormalities in microsomal Ca(2+)-ATPase activity and calcium levels in kidney of streptozotocin (STZ)-induced diabetic rats. Male rats were rendered diabetic by a single STZ injection (55 mg x kg(-1) i.p.). After diabetes was verified, diabetic and age-matched control rats were untreated or treated with vitamin E (400-500 IU kg(-1) x day(-1), orally) for 10 weeks. Ca(2+)-ATPase activity and lipid peroxidation (MDA) were determined spectrophotometrically. Blood glucose levels increased approximately five-fold (> 500 mg x dl(-1)) in untreated-diabetic rats but decreased to 340+/-27 mg x dl(-1) in the vitamin E treated-diabetic group. Kidney MDA levels did not significantly change in the diabetic state. However, vitamin E treatment markedly inhibited MDA levels in both control and diabetic animals. Ca(2+)-ATPase activity was 0.483+/-0.008 U l(-1) in the control group and significantly increased to 0.754+/-0.010 U l(-1) in the STZ-diabetic group (p < 0.001). Vitamin E treatment completely prevented the diabetes-induced increase in Ca(2+)-ATPase activity (0.307+/-0.025 U l(-1), p < 0.001) and also reduced the enzyme activity in normal control rats. STZ-diabetes resulted in approximately two-fold increase in total calcium content of kidney. Vitamin E treatment led to a significant reduction in kidney calcium levels of both control and diabetic animals (p < 0.001). Thus, vitamin E treatment can lower blood glucose and lipid peroxidation, which in turn prevents the abnormalities in kidney calcium metabolism of diabetic rats. This study describes a potential biochemical mechanism by which vitamin E supplementation may delay or inhibit the development of cellular damage and nephropathy in diabetes.

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Section: Discussioncontrasting

confidence: 51%

Effects of vitamin E on microsomal Ca²⁺‐ATPase activity and calcium levels in streptozotocin‐induced diabetic rat kidney

Pekiner

Evcimen

Ulusu

et al. 2003

Cell Biochemistry & Function

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“…We chose this early time point and faulty level of diabetic control to evaluate penile function without extensive end organ damage, believing these animals would be the most likely to show a reversible effect of therapy (Soriano et al, 2001). There is supporting evidence from the literature concerning the beneficial role of vitamin E in the aorta, lung, and other organs (Pathania et al, 1998; Lang et al, 2000). Vitamin E appears to be the first line of defense against the peroxidation of polyunsaturated fatty acids that are contained in cellular and subcellular membrane phospholipids, because it binds to peroxyl free radicals and forms stable molecules (Mayes, 2000; van Haaften et al, 2003).…”

Section: Discussionmentioning

confidence: 66%

Oxidative Stress and Antioxidant Therapy: Their Impact in Diabetes‐Associated Erectile Dysfunction

Young

Bateman

et al. 2004

Journal of Andrology

129

105

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Oxidative stress is believed to affect the development of diabetic-associated vasculopathy, endothelial dysfunction, and neuropathy within erectile tissue. Our hypothesis is that, given adequate concentrations of the oxygen free radical scavenger vitamin E, enhanced levels of circulating nitric oxide (NO) should improve erectile function with the potential for a synergistic effect with a phosphodiesterase type 5 (PDE5) inhibitor. Twenty adult male Sprague-Dawley streptozotocin-induced (60 mg/kg intraperitoneally) diabetic rats were placed in 4 therapeutic groups (n ϭ 5 per group) as follows: 1) peanut oil only (diabetic control), 2) 20 IU of vitamin E per day, 3) 5 mg/kg of sildenafil per day, and 4) vitamin E plus sildenafil using oral gavage for 3 weeks. In addition, 5 age-matched rats served as normal nondiabetic controls (normal). Erectile function was assessed by measuring the rise in intracavernous pressure (ICP) following cavernous nerve electrostimulation. Penile tissue was evaluated for neuronal NO synthase (nNOS), smooth muscle ␣-actin, nitrotyrosine, and endothelial cell integrity. Urine nitrite and nitrate (NO x ) concentration was quantified, and electrolytes were tested by a serum biochemistry panel. A significant decrease in ICP was recorded in the diabetic animals, with improvement measured in the animals receiving PDE5 inhibitors either with or without vitamin E; the controls had a pressure of 54.8 Ϯ 5.3 cm H 2 O, the vitamin E group had a pressure of 73.5 Ϯ 6.6 cm H 2 O, the sildenafil group had a pressure of 78.4 Ϯ 10.77 cm H 2 O, and the vitamin E plus sildenafil group had a pressure of 87.9 Ϯ 5.5 cm H 2 O (P Ͻ .05), compared with the normal cohorts at 103.0 Ϯ 4.8 cm H 2 O. Histoexaminations showed improved nNOS, endothelial cell, and smooth muscle cell staining in the vitamin E plus sildenafil group compared to the control animals. Urine NO x increased significantly in all the diabetic groups but was blunted in the vitamin E and vitamin E plus sildenafil groups. A significant increase in positive staining for nitrotyrosine was observed in the vitamin E plus sildenafil group. Vitamin E enhanced the therapeutic effect of the PDE5 inhibitor in this study, supporting the potential use of oxygen free radical scavengers in salvaging erectile function in diabetic patients.

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“…There is supporting evidence from the literature concerning the role of vitamin E in the aorta, lung and other organs. 38,39 Vitamin E is an active nonenzymatic antioxidant, highly lipid soluble, associated with structures such as cell membranes, and chemically deactivates relatively hydrophobic reactive species. Vitamin E appears to be the first line of defense against peroxidation of polyunsaturated fatty acids contained in cellular and subcellular membrane phospholipids.…”

Section: Vitamin E Vit E + Sildenafilmentioning

confidence: 99%

Effect of PDE5 inhibition combined with free oxygen radical scavenger therapy on erectile function in a diabetic animal model

Young

Freeman

et al. 2003

Int J Impot Res

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Phosphodiesterase (PDE) inhibitors represent an important advance in the treatment of erectile dysfunction (ED). In spite of widespread use and generally good efficacy, as a class they remain ineffective in 15-57% of men. Specific cohorts of patients with severe vascular or neurogenic basis to their ED, such as diabetic men or those who have undergone radical pelvic surgery, demonstrate lower response rates with PDE inhibition treatment. We believe that circulating levels of nitric oxide (NO) may be enhanced through delivery of adequate concentrations of free oxygen radical scavenger molecules such as vitamin E. Higher levels of NO, theoretically, should produce increased penile blood flow with the potential for a synergistic effect when combined with a PDE5 inhibitor. With this hypothesis in mind, 20 adult male Sprague-Dawley streptozotocin-induced (60 mg/kg i.p.) diabetic rats were divided into four therapeutic groups (n ¼ 5). Group IFcontrol animals received peanut oil, group IIFvitamin E 20 IU/day, group IIIFsildenafil 5 mg/kg/day and group IVFvitamin E 20 IU/day plus sildenafil 5 mg/kg/day, by oral gavage daily for 3 weeks. Erectile function was assessed as a rise in intracavernous pressure following cavernous nerve electrostimulation. Penile tissue was harvested to determine the changes in tissue morphology including neuronal nitric oxide synthase, smooth muscle a-actin and endothelial cell integrity. PDE5 protein content and activity were measured. Significant increases in intracavernous pressure were measured in the animals receiving combined vitamin E plus sildenafil treatment. Immunohistochemical staining showed increases of neuronal nitric oxide synthase, endothelial cell and smooth muscle cell staining. Western blot analysis did not show significant differences of PDE5 protein between the groups. However, higher PDE5 activity was measured in the sildenafil group and lower activity of PDE5 was recorded in the cohort receiving vitamin E with sildenafil. Vitamin E enhanced the therapeutic effect of the PDE5 inhibitor in a meaningful way in this animal model of diabetes. This study indicates a potential means of salvaging erectile function among patients who are refractory to sildenafil.

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Changes in Rat Alveolar Macrophageal Antioxidant Defense and Reactive Oxygen Species Release by High Dietary Vitamin E.

Cited by 5 publications

References 38 publications

Effects of vitamin E on microsomal Ca²⁺‐ATPase activity and calcium levels in streptozotocin‐induced diabetic rat kidney

Effects of vitamin E on microsomal Ca²⁺‐ATPase activity and calcium levels in streptozotocin‐induced diabetic rat kidney

Oxidative Stress and Antioxidant Therapy: Their Impact in Diabetes‐Associated Erectile Dysfunction

Effect of PDE5 inhibition combined with free oxygen radical scavenger therapy on erectile function in a diabetic animal model

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Changes in Rat Alveolar Macrophageal Antioxidant Defense and Reactive Oxygen Species Release by High Dietary Vitamin E.

Cited by 5 publications

References 38 publications

Effects of vitamin E on microsomal Ca2+‐ATPase activity and calcium levels in streptozotocin‐induced diabetic rat kidney

Effects of vitamin E on microsomal Ca2+‐ATPase activity and calcium levels in streptozotocin‐induced diabetic rat kidney

Oxidative Stress and Antioxidant Therapy: Their Impact in Diabetes‐Associated Erectile Dysfunction

Effect of PDE5 inhibition combined with free oxygen radical scavenger therapy on erectile function in a diabetic animal model

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Product

Resources

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Effects of vitamin E on microsomal Ca²⁺‐ATPase activity and calcium levels in streptozotocin‐induced diabetic rat kidney

Effects of vitamin E on microsomal Ca²⁺‐ATPase activity and calcium levels in streptozotocin‐induced diabetic rat kidney