Abnormal incorporation and utilization of α-tocopherol in erythrocyte membranes of streptozotocin-induced diabetic rats

Shinozaki, Kazushi; Takeda, Hiroshi; Inazu, Masato; Matsumiya, Teruhiko; Takasaki, Masaya

doi:10.1016/s0014-2999(02)02618-3

Cited by 8 publications

(5 citation statements)

References 41 publications

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“…Vitamin E has been more broadly examined in diabetes models. Interestingly, the incorporation of vitamin E into erythrocyte membranes is impaired in the hyperglycemic state; therefore, decreased antioxidant defense may be further exacerbated in poorly controlled diabetes (188). Rat models of diabetes show some therapeutic benefit in the presence of vitamin E therapy.…”

Section: B Vitamins E and Cmentioning

confidence: 99%

Oxidative Stress in the Pathogenesis of Diabetic Neuropathy

et al. 2004

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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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Section: B Vitamins E and Cmentioning

confidence: 99%

Oxidative Stress in the Pathogenesis of Diabetic Neuropathy

et al. 2004

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“…30 In accordance with this expectation, it has been found that αTQ levels are significantly elevated in new-borns compared with their mothers both in plasma and red blood cells (RBCs) when expressed per total lipids, but not when expressed as mole/ml. 31 An increase in the αTQ/αT ratio has been reported for aged rats, 32 streptodotocin-induced diabetic rats, 33 and rats under stress of hyperoxia. 34 The exposure of C3H mice to UV light and free radicals was found to induce epidermal accumulation of αTQ and αTQH 2 .…”

Section: Formation and Distributionmentioning

confidence: 94%

Tocopherylquinone and tocopherylhydroquinone

Niki

2007

Redox Report

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Tocopherylquinone (TQ) is formed in the antioxidant action of tocopherol (T). TQ was found in human subjects and it was observed that the ratio alphaTQ/ alphaT increased in general with increasing oxidative stress. TQ is reduced to tocopheryl hydroquinone (TQH2) but the ratio TQH2/TQ in vivo has not been reported. TQH2 acts as a potent radical-scavenging antioxidant. alphaTQH2 is more reactive toward radicals than ubiquinol, a reduced form of coenzyme Q, and alphaT. The overall efficacy of TQH2 as an antioxidant is determined by the fate of semiquinone radical formed from TQH2 as well as the reactivity toward oxygen radicals. Partly substituted gammaTQ, but not alphaTQ, exerts cytotoxicity by both redox cycling and reaction with protein thiols and glutathione.

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“…Moreover, ethanol feeding reduced liver α -Toc content and caused a marked increase in liver TQ, especially in the microsomal fraction (Kawase et al 1989 ). In diabetic rats, the ratio of TQ/ α -Toc in the erythrocyte membrane was increased (Shinozaki et al 2002 ). The ratio of TQ/ α -Toc and/or TQ level may be a good marker of oxidative stress, but only limited studies are available.…”

Section: α -Tocopheryl Quinonementioning

confidence: 99%