Evaluation of the effect of oxidative stress and vitamin E supplementation on renal function in rats with streptozotocin-induced Type 1 diabetes

Haidara, Mohamed A; Mikhailidis, Dimitri P.; Rateb, Moshira; Ahmed, Zeinab; Yassin, Hanaa Z.; Ibrahim, Ibrahim M.; Rashed, Laila Ahmed

doi:10.1016/j.jdiacomp.2008.02.011

Cited by 88 publications

(69 citation statements)

References 42 publications

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“…Clinical studies using antioxidant interventions in diabetic nephropathy have, to date, shown disappointing results [39,40], possibly due to starting treatment when established damage already exists. However, in animal studies, where antioxidant intervention is started prior to or at the onset of diabetes, kidney damage can be prevented [9,41]. Therefore, kidney function was evaluated after 7 weeks of chronic CoQ10 treatment starting prior to the onset of hyperglycaemia.…”

Section: Discussionmentioning

confidence: 99%

Coenzyme Q10 prevents GDP-sensitive mitochondrial uncoupling, glomerular hyperfiltration and proteinuria in kidneys from db/db mice as a model of type 2 diabetes

Persson¹,

Franzén²,

Catrina

et al. 2012

Diabetologia

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Aims/hypothesis Increased oxygen consumption results in kidney tissue hypoxia, which is proposed to contribute to the development of diabetic nephropathy. Oxidative stress causes increased oxygen consumption in type 1 diabetic kidneys, partly mediated by uncoupling protein-2 (UCP-2)-induced mitochondrial uncoupling. The present study investigates the role of UCP-2 and oxidative stress in mitochondrial oxygen consumption and kidney function in db/db mice as a model of type 2 diabetes. Methods Mitochondrial oxygen consumption, glomerular filtration rate and proteinuria were investigated in db/db mice and corresponding controls with and without coenzyme Q10 (CoQ10) treatment. −1 ). UCP-2 protein levels were similar in untreated control and db/db mice (67± 9 vs 67± 4 optical density; OD) but were reduced in CoQ10 treated groups (43±2 and 38±7 OD). Conclusions/interpretation db/db mice displayed oxidative stress-mediated activation of UCP-2, which resulted in mitochondrial uncoupling and increased oxygen consumption. CoQ10 prevented altered mitochondrial function and morphology, glomerular hyperfiltration and proteinuria in db/db mice, highlighting the role of mitochondria in the pathogenesis of diabetic nephropathy and the benefits of preventing increased oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Coenzyme Q10 prevents GDP-sensitive mitochondrial uncoupling, glomerular hyperfiltration and proteinuria in kidneys from db/db mice as a model of type 2 diabetes

Persson¹,

Franzén²,

Catrina

et al. 2012

Diabetologia

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show abstract

“…However, the debate about the protective properties of vitamins C and E and erdosteine against the development of renal I/R injury in aging males is not settled. Dietary vitamins C and E have been shown to improve the metabolic abnormalities caused by diabetic nephropathy (13)(14)(15)(16). Hence, the experimental data support that vitamins C and E could be useful agents in diabetic nephropathy in younger animals (13,14).…”

Section: Introductionmentioning

confidence: 94%

Protective effects of erdosteine, vitamin E, and vitamin C on renal injury induced by the ischemia-reperfusion of the hind limbs in rats

Sirmali¹,

Armağan²,

Öktem³

et al. 2015

Turk J Med Sci

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Background/aim: To compare the protective efficacy of erdosteine and vitamins C and E against renal injury caused by hind limb ischemia-reperfusion (I/R).Materials and methods: Rats were split into 4 groups: group I as the control, group II as I/R, group III as I/R + erdosteine, and group IV as I/R + vitamins C and E. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA) tissue levels were determined.Results: MDA levels were found comparable with the control group in groups II and III. However, they were considerably decreased in group IV when compared to group II (P < 0.01). Additionally, SOD, CAT, and GSH-Px activities were considerably (P < 0.05) decreased in group II. While CAT and GSH-Px activities were restored (P < 0.01) by vitamin E and C treatment, SOD activity was not significantly affected. While GSH-Px activities were higher (P < 0.05) with erdosteine administration, SOD and CAT activities were unchanged. Conclusion:The protective effect of vitamins C and E is higher than that of erdosteine treatment in reducing the oxidative stress after renal ischemia in this animal model.

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“…Experimental researches established the role of oxidative stress as a central factor in onset and progression of diabetic nephropathy (11)(12)(13)(14). Human studies also showed that oxidative stress markers such as 8-oxodG (oxo-2′-deoxyguanosine) (15)(16)(17)(18)(19), and MDA (21) increased in diabetic patients.…”

Section: Resultsmentioning

confidence: 99%

“…Interestingly, oxidative stress has been suggested as a common product of much of mechanisms that are involved in pathogenesis of diabetic nephropathy (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). In fact, in the tangle web of diabetic nephropathy pathogenesis, oxidative stress activates other pathogenic pathways, other pathways make injury via oxidative stress, and oxidative stress directly leads to injury.…”

Section: Resultsmentioning

confidence: 99%

Diabetic nephropathy and antioxidants

Tavafi¹

2013

J Nephropathol

132

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Evaluation of the effect of oxidative stress and vitamin E supplementation on renal function in rats with streptozotocin-induced Type 1 diabetes

Cited by 88 publications

References 42 publications

Coenzyme Q10 prevents GDP-sensitive mitochondrial uncoupling, glomerular hyperfiltration and proteinuria in kidneys from db/db mice as a model of type 2 diabetes

Coenzyme Q10 prevents GDP-sensitive mitochondrial uncoupling, glomerular hyperfiltration and proteinuria in kidneys from db/db mice as a model of type 2 diabetes

Protective effects of erdosteine, vitamin E, and vitamin C on renal injury induced by the ischemia-reperfusion of the hind limbs in rats

Diabetic nephropathy and antioxidants

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