The glutathione levels are reduced in Goto-Kakizaki rat retina, but are not influenced by aminoguanidine treatment

Agardh, Carl‐David; Agardh, Elisabet; Hultberg, Björn; Qian, Yuning; Östenson, Claes‐Göran

doi:10.1076/ceyr.17.3.251.5217

Cited by 23 publications

(11 citation statements)

References 23 publications

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“…13 The contribution of glycation/glycoxidation to oxidative stress in the diabetic retina has been examined using aminoguanidine, which was found to have a protective effect against oxidative damage in models of type I 14 but not type II diabetes. 15 However, these results can not be seen as conclusive as, in addition to its capacity to react with carbonyls thereby inhibiting AGE formation, aminoguanidine can directly act as an antioxidant 16 and inhibits nitric oxide production. 17 Glycated proteins may contribute to oxidative stress in other ways as it has been observed that glycated forms of some proteins, including elastin, can chelate transition metals in a redox-active form and thus catalyse free radical generation via Fenton-type reactions.…”

Section: Oxidative Reactions Involving Glucosementioning

confidence: 95%

The retina: oxidative stress and diabetes

2003

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A prominent and early feature of the retinopathy of diabetes mellitus is a diffuse increase in vascular permeability. As the disease develops, the development of frank macular oedema may result in vision loss. That reactive oxygen species production is likely to be elevated in the retina, and that certain regions of the retina are enriched in substrates for lipid peroxidation, may create an environment susceptible to oxidative damage. This may be more so in the diabetic retina, where hyperglycaemia may lead to elevated oxidant production by a number of mechanisms, including the production of oxidants by vascular endothelium and leukocytes. There is substantial evidence from animal and clinical studies for both impaired antioxidant defences and increased oxidative damage in the retinae of diabetic subjects that have been, in the case of animal studies, reversible with antioxidant supplementation. Whether oxidative damage has a causative role in the pathology of diabetic retinopathy, and thus whether antioxidants can prevent or correct any retinal damage, has not been established, nor has the specific nature of any damaging species been characterised.

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Section: Oxidative Reactions Involving Glucosementioning

confidence: 95%

The retina: oxidative stress and diabetes

2003

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“…NIDDM has been studied in several animal models including the GK rat, which was selected for this study because it represents a good model of hereditary non-obese NIDDM that develops into a moderate and stable diabetic state with age [20,31]. Several reports showed that increased levels of glucose found in NIDDM patients are responsible not only Fig.…”

Section: Discussionmentioning

confidence: 99%

Diabetes and mitochondrial oxidative stress: A study using heart mitochondria from the diabetic Goto-Kakizaki rat

Santos¹,

Palmeira²,

Seiça³

et al. 2003

Vascular Biochemistry

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Increasing evidence shows that the overproduction of reactive oxygen species, induced by diabetic hyperglycemia, contributes to the development of several cardiopathologies. The susceptibility of diabetic hearts to oxidative stress, induced in vitro by ADP-Fe 2+ in mitochondria, was studied in 12-month-old Goto-Kakizaki rats, a model of non-insulin dependent diabetes mellitus, and normal (non-diabetic) Wistar rats. In terms of lipid peroxidation the oxidative damage was evaluated on heart mitochondria by measuring both the O 2 consumption and the concentrations of thiobarbituric acid reactive substances. Diabetic rats display a more intense formation of thiobarbituric acid reactive substances and a higher O 2 consumption than nondiabetic rats. The oxidative damage, assessed by electron microscopy, was followed by an extensive effect on the volume of diabetic heart mitochondria, as compared with control heart mitochondria. An increase in the susceptibility of diabetic heart mitochondria to oxidative stress can be explained by reduced levels of endogenous antioxidants, so we proceeded in determining α-tocopherol, GSH and coenzyme Q content. Although no difference of α-tocopherol levels was found in diabetic rats as compared with control rat mitochondria, a significant reduction in GSH (21.5% reduction in diabetic rats) and coenzyme Q levels of diabetic rats was observed. The data suggest that a significant decrease of coenzyme Q 9 , a potent antioxidant involved in the elimination of mitochondria-generated reactive oxygen species, may be responsible for an increased susceptibility of diabetic heart mitochondria to oxidative damage. (Mol Cell Biochem 246: 163-170, 2003)

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“…One important antioxidant is glutathione (GSH), which protects proteins against oxidative damage in the retina. 11 In various animal models of diabetes, retinal GSH levels [12][13][14][15] and the GSH/cysteine ratio 16 decrease by time, implicating that the abnormalities of retinal metabolism in diabetes result in deterioration of this antioxidant defence system. Retinal GSH levels are likely to be regulated by Müller cells, 17 and Pow and Crook 18 found immunocytochemical evidence for high levels of reduced GSH in retinal glial and as well as in horizontal cells.…”

Section: Introductionmentioning

confidence: 99%