α‐Tocopherol and Endothelial Nitric Oxide Synthesis

Heller, Regine; Werner-Felmayer, Gabriele; Werner, Ernst R.

doi:10.1196/annals.1331.007

Cited by 41 publications

(24 citation statements)

References 67 publications

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“…Several antioxidants such as α-lipoic acid, taurine, acetyl-Lcarnitine, M40403 and β-carotene have demonstrated to ameliorate nerve function deficit in experimental diabetic neuropathy (Cameron and Cotter, 1999;Coppey et al, 2001a, b;Heller et al, 2004;Karasu et al, 1995;Love et al, 1996;Nickander et al, 1996;Rosen et al, 1995). These reports suggest that reducing oxidative stress may inhibit the development of diabetic neuropathy.…”

Section: Introductionmentioning

confidence: 92%

Effects of U83836E on nerve functions, hyperalgesia and oxidative stress in experimental diabetic neuropathy

2006

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Oxidative stress has been implicated to play an important role in the pathogenesis of diabetic neuropathy, which is the most common complication of diabetes mellitus affecting more than 50% of diabetic patients. In the present study, we have investigated the effect of U83836E], a potent free radical scavenger in streptozotocin (STZ)-induced diabetic neuropathy in rats. STZ-induced diabetic rats showed significant deficit in motor nerve conduction velocity (MNCV), nerve blood flow (NBF) and thermal hyperalgesia after 8 weeks of diabetes induction, indicating development of diabetic neuropathy. Antioxidant enzyme (superoxide dismutase and catalase) levels were reduced and malondialdehyde (MDA) levels were significantly increased in diabetic rats as compared to the age-matched control rats, this indicates the involvement of oxidative stress in diabetic neuropathy. The 2-week treatment with U83836E (3 and 9 mg/kg, i.p.) started 6 weeks after diabetes induction significantly ameliorated the alterations in MNCV, NBF, hyperalgesia, MDA levels and antioxidant enzymes in diabetic rats. Results of the present study suggest the potential of U83836E in treatment of diabetic neuropathy.

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Section: Introductionmentioning

confidence: 92%

Effects of U83836E on nerve functions, hyperalgesia and oxidative stress in experimental diabetic neuropathy

2006

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“…The most studied mechanism whereby they act is partly based on their ability to directly reduce ROS. In addition to its ROS scavenging functions, these two antioxidants exert their action in a synergistic way: when α-tocopherol losses an electron and is left as α-tocopheroxyl radical, vitamin C reduces it at the level of the lipidwater interphase, so that it can thus recover its antioxidant properties [72,73]. In contrast, in the absence of efficient reducers, vitamin E cannot be recycled into its antioxidant form, leading to the formation of tocopheryl quinone, molecule that could compete in mitochondrial respiratory chain reactions.…”

Section: Biological Properties and Synergism Of Vitamins C And Ementioning

confidence: 99%

“…Furthermore it has been hypothesized that one of the mechanisms by which classic anti-AF drugs act is related with the ability to ROS scavenging and protection against membrane lipid peroxidation [71]. However, Vitamin C (ascorbate) and Vitamin E (α-tocopherol) deserve special mention among other antioxidants, gathering several biochemical and empiric evidence that makes them excellent candidates to be used in the treatment and/or prevention of POAF [72,73].…”

Section: Prevention Of Poaf By Antioxidant Vitamin Supplementationmentioning

confidence: 99%

Use of vitamins C and E as a prophylactic therapy to prevent postoperative atrial fibrillation

Rodrigo

Vinay

Castillo

et al. 2010

International Journal of Cardiology

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“…120 In fact, the effect of a-tocopherol seems to be dependent on tissue saturation with vitamin C, and both vitamins may function synergistically to provide optimal conditions for endothelial NO formation. 121 Thus, the association of vitamins C and E is expected to have an antihypertensive effect, probably because this combined therapy provides a reinforcement of their individual properties through a complementary effect. 122 Despite the biological effects of both vitamin C and E, long-term clinical trials have failed to consistently support their antihypertensive effects in high-risk cardiovascular patients.…”

Section: Endogenous Antioxidantsmentioning

confidence: 99%

The role of oxidative stress in the pathophysiology of hypertension

2011

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Hypertension is considered to be the most important risk factor in the development of cardiovascular disease. An increasing body of evidence suggests that oxidative stress, which results in an excessive generation of reactive oxygen species (ROS), has a key role in the pathogenesis of hypertension. The modulation of the vasomotor system involves ROS as mediators of vasoconstriction induced by angiotensin II, endothelin-1 and urotensin-II, among others. The bioavailability of nitric oxide (NO), which is a major vasodilator, is highly dependent on the redox status. Under physiological conditions, low concentrations of intracellular ROS have an important role in the normal redox signaling maintaining vascular function and integrity. However, under pathophysiological conditions, increased levels of ROS contribute to vascular dysfunction and remodeling through oxidative damage. In human hypertension, an increase in the production of superoxide anions and hydrogen peroxide, a decrease in NO synthesis and a reduction in antioxidant bioavailability have been observed. In turn, antioxidants are reducing agents that can neutralize these oxidative and otherwise damaging biomolecules. The use of antioxidant vitamins, such as vitamins C and E, has gained considerable interest as protecting agents against vascular endothelial damage. Available data support the role of these vitamins as effective antioxidants that can counteract ROS effects. This review discusses the mechanisms involved in ROS generation, the role of oxidative stress in the pathogenesis of vascular damage in hypertension, and the possible therapeutic strategies that could prevent or treat this disorder. Hypertension Research (2011) 34, 431-440; doi:10.1038/hr.2010.264; published online 13 January 2011Keywords: antioxidants; endothelial dysfunction; oxidative stress INTRODUCTION Hypertension is considered the most important risk factor for the occurrence of cardiovascular disease. 1 Oxidative stress has gained attention as one of the fundamental mechanisms responsible for the development of hypertension. Reactive oxygen species (ROS) have an important role in the homeostasis of the vascular wall; hence, they could be part of the mechanism that leads to hypertension. 2-4 Thus, increased ROS production, reduced nitric oxide (NO) levels and reduced antioxidant bioavailability were demonstrated in experimental and human hypertension. Vascular superoxide is primarily derived from nicotinamide adenine dineucleotide phosphate (NADPH) oxidase when stimulated by hormones, such as angiotensin II (AT-II), endothelin-1 (ET-1) and urotensin II. In addition, increased ROS production may be generated by mechanical stimuli on the vascular wall, which increase with hypertension. ROS-induced vasoconstriction results from increased intracellular calcium concentration, thereby contributing to the pathogenesis of hypertension. 2 Vasomotor tone is dependent on a delicate balance between vasoconstrictor and vasodilator forces that result from the interaction between the components of...

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α‐Tocopherol and Endothelial Nitric Oxide Synthesis

Cited by 41 publications

References 67 publications

Effects of U83836E on nerve functions, hyperalgesia and oxidative stress in experimental diabetic neuropathy

Effects of U83836E on nerve functions, hyperalgesia and oxidative stress in experimental diabetic neuropathy

Use of vitamins C and E as a prophylactic therapy to prevent postoperative atrial fibrillation

The role of oxidative stress in the pathophysiology of hypertension

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