Correlations between Endothelial Functions and ROS Detection in Diabetic Microvascular Wall:<i>Early and Late Ascorbic Acid Supplementation</i>

Sridulyakul, Pattarin; Wongeakin, Natchaya; Patumraj, Suthiluk

doi:10.1155/2012/709695

Cited by 7 publications

(8 citation statements)

References 27 publications

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“…Diabetes is associated with various micro vascular and macro vascular complications. Hyperglycaemia in diabetes is responsible for micro vascular ROS generation which causes endothelial dysfunction [167] and vitamin C blocks acute hyperglycaemic impairment of endothelial function in diabetic subjects [168]. One of the most important micro vascular complications is diabetic nephropathy.…”

Section: Vitamin C and Diabetesmentioning

confidence: 99%

Vitamin C in Disease Prevention and Cure: An Overview

et al. 2013

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The recognition of vitamin C is associated with a history of an unrelenting search for the cause of the ancient haemorrhagic disease scurvy. Isolated in 1928, vitamin C is essential for the development and maintenance of connective tissues. It plays an important role in bone formation, wound healing and the maintenance of healthy gums. Vitamin C plays an important role in a number of metabolic functions including the activation of the B vitamin, folic acid, the conversion of cholesterol to bile acids and the conversion of the amino acid, tryptophan, to the neurotransmitter, serotonin. It is an antioxidant that protects body from free radical damage. It is used as therapeutic agent in many diseases and disorders. Vitamin C protects the immune system, reduces the severity of allergic reactions and helps to fight off infections. However the significance and beneficial effect of vitamin C in respect to human disease such as cancer, atherosclerosis, diabetes, neurodegenerative disease and metal toxicity however remains equivocal. Thus further continuous uninterrupted efforts may open new vistas to understand its significance in disease management.

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Section: Vitamin C and Diabetesmentioning

confidence: 99%

Vitamin C in Disease Prevention and Cure: An Overview

et al. 2013

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“…Accumulating evidence indicates that hyperglycemia in diabetes is associated with a decrease in the antioxidant potential and an increase in ROS generation [ 13 , 14 , 15 ]. In addition, diabetes has been shown to be a proinflammatory state that increases the risk of vascular complications [ 16 , 17 ]. Thus, the enhanced oxidative stress and inflammatory responses in the diabetic state may substantially contribute to the aggravation of cerebral injury caused by transient ischemia and subsequent reperfusion.…”

Section: Introductionmentioning

confidence: 99%

Orally Administrated Ascorbic Acid Suppresses Neuronal Damage and Modifies Expression of SVCT2 and GLUT1 in the Brain of Diabetic Rats with Cerebral Ischemia-Reperfusion

et al. 2014

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Diabetes mellitus is known to exacerbate cerebral ischemic injury. In the present study, we investigated antiapoptotic and anti-inflammatory effects of oral supplementation of ascorbic acid (AA) on cerebral injury caused by middle cerebral artery occlusion and reperfusion (MCAO/Re) in rats with streptozotocin-induced diabetes. We also evaluated the effects of AA on expression of sodium-dependent vitamin C transporter 2 (SVCT2) and glucose transporter 1 (GLUT1) after MCAO/Re in the brain. The diabetic state markedly aggravated MCAO/Re-induced cerebral damage, as assessed by infarct volume and edema. Pretreatment with AA (100 mg/kg, p.o.) for two weeks significantly suppressed the exacerbation of damage in the brain of diabetic rats. AA also suppressed the production of superoxide radical, activation of caspase-3, and expression of proinflammatory cytokines (tumor necrosis factor-α and interleukin-1β) in the ischemic penumbra. Immunohistochemical staining revealed that expression of SVCT2 was upregulated primarily in neurons and capillary endothelial cells after MCAO/Re in the nondiabetic cortex, accompanied by an increase in total AA (AA + dehydroascorbic acid) in the tissue, and that these responses were suppressed in the diabetic rats. AA supplementation to the diabetic rats restored these responses to the levels of the nondiabetic rats. Furthermore, AA markedly upregulated the basal expression of GLUT1 in endothelial cells of nondiabetic and diabetic cortex, which did not affect total AA levels in the cortex. These results suggest that daily intake of AA attenuates the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to anti-apoptotic and anti-inflammatory effects via the improvement of augmented oxidative stress in the brain. AA supplementation may protect endothelial function against the exacerbated ischemic oxidative injury in the diabetic state and improve AA transport through SVCT2 in the cortex.

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“…This in turn could cause an increase in DNA damage. In order to test this hypothesis, ascorbic acid was used, as it has been shown in the literature to reduce the production of reactive oxygen species (ROS) [29] . The results show that, in fact, when cells were irradiated, addition of DEXA and ascorbic acid led to the return of gamma-H2AX foci to basal levels, suggesting that at least one of the mechanisms of DEXA in the DNA damage pathway is increasing ROS, which would in turn lead to an increase in the levels of gamma-H2AX foci ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone acts as a radiosensitizer in three astrocytoma cell lines via oxidative stress

Ortega-Martínez

2015

Redox Biology

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Glucocorticoids (GCs), which act on stress pathways, are well-established in the co-treatment of different kinds of tumors; however, the underlying mechanisms by which GCs act are not yet well elucidated. As such, this work investigates the role of glucocorticoids, specifically dexamethasone (DEXA), in the processes referred to as DNA damage and DNA damage response (DDR), establishing a new approach in three astrocytomas cell lines (CT2A, APP.PS1 L.1 and APP.PS1 L.3). The results show that DEXA administration increased the basal levels of gamma-H2AX foci, keeping them higher 4 h after irradiation (IR) of the cells, compared to untreated cells. This means that DEXA might cause increased radiosensitivity in these cell lines. On the other hand, DEXA did not have an apparent effect on the formation and disappearance of the 53BP1 foci. Furthermore, it was found that DEXA administered 2 h before IR led to a radical change in DNA repair kinetics, even DEXA does not affect cell cycle. It is important to highlight that DEXA produced cell death in these cell lines compared to untreated cells. Finally and most important, the high levels of gamma-H2AX could be reversed by administration of ascorbic acid, a potent blocker of reactive oxygen species, suggesting that DEXA acts by causing DNA damage via oxidative stress. These exiting findings suggest that DEXA might promote radiosensitivity in brain tumors, specifically in astrocytoma-like tumors.

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Correlations between Endothelial Functions and ROS Detection in Diabetic Microvascular Wall:Early and Late Ascorbic Acid Supplementation

Cited by 7 publications

References 27 publications

Vitamin C in Disease Prevention and Cure: An Overview

Vitamin C in Disease Prevention and Cure: An Overview

Orally Administrated Ascorbic Acid Suppresses Neuronal Damage and Modifies Expression of SVCT2 and GLUT1 in the Brain of Diabetic Rats with Cerebral Ischemia-Reperfusion

Dexamethasone acts as a radiosensitizer in three astrocytoma cell lines via oxidative stress

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