Effect of Ascorbic Acid Supplementation on Certain Oxidative Stress Parameters in the Post Reperfusion Patients of Myocardial Infarction

Bhakuni, Pushpa; Chandra, M.; Misra, M. K.

doi:10.1007/s11010-006-9182-y

Cited by 22 publications

(21 citation statements)

References 32 publications

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“…Incorporation of allopurinol, a specific inhibitor of XO, is capable of protecting the myocardium from ischemia/reperfusion induced injury and thus it is clear that the generation of OFR by XO during ischemia/reperfusion play a major role in tissue damage [25]. Free radical production during ischemia is further increased upon reperfusion [26,27]. Oxy free radicals are removed by SOD, but during ischemia, SOD is inhibited by excess H 2 O 2 and hence fails to cope up with the increased production of free radicals and H 2 O 2 resulting in excessive injury.…”

Section: Discussionmentioning

confidence: 99%

Protective Role of l-Arginine Against Free-Radical Mediated Oxidative Damage in Patients with Unstable Angina

Tripathi

Chandra²,

Misra

2010

Indian J Clin Biochem

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Unstable angina is a critical condition of heart resulting from narrowing of vessels supplying blood to heart. Ischemia of the myocardium leads to oxidative stress and severe tissue damage. The objective of the present study was to determine the effect of l-arginine administration on the oxidant-antioxidant homeostasis which otherwise gets imbalanced in patients with cardiovascular diseases. The results obtained, show improvement in the oxidant-antioxidant levels of the subjects upon incorporation of l-arginine. Our findings suggest that supplementation of l-arginine along with regular anti-anginal therapy may be beneficial to the patients of unstable angina.

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Section: Discussionmentioning

confidence: 99%

Protective Role of l-Arginine Against Free-Radical Mediated Oxidative Damage in Patients with Unstable Angina

Tripathi

Chandra²,

Misra

2010

Indian J Clin Biochem

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“…It is not possible to exclude that all these aspects may be related to the high prevalence of inflammatory gene polymorphism demonstrated in these young subjects with AMI. [35][36][37][38][39] The persistence of an impaired oxidative stress 12 months after AMI requires 2 different considerations: first, the use of antioxidant therapy after AMI may be advisable [40][41][42][43] ; moreover, the altered oxidative status observed much later after AMI may be present also before AMI. Regarding this latter aspect, our project of reevaluating the same AMI subjects 2 years or even later after AMI may give further information.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress in Young Subjects With Acute Myocardial Infarction: Evaluation at the Initial Stage and After 12 Months

LoPresti

Catania

D'Amico

et al. 2007

Clin Appl Thromb Hemost

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In 105 subjects (97 men and 8 women) aged <46 years (mean age 39.6 +/- 5.5 years), with recent acute myocardial infarction (T1), thiobarbituric acid reactive substances and total antioxidant status were determined; NO production was evaluated by measuring the nitrite and nitrate (NOx) concentration. The patients with acute myocardial infarction were subdivided according to the main risk factors, number of risk factors, and extent of coronary lesions. The evaluation was repeated after 12 months (T2). In these subjects, thiobarbituric acid reactive substances and NOx were significantly increased and total antioxidant status was significantly decreased at T1. In single risk factor, only NO metabolites were significantly lower in acute myocardial infarction subjects who smoke than in subjects who do not. Subdividing the subjects according to the number of risk factors and number of stenosed coronary vessels, there were no significant differences between the subgroups. At T2, thiobarbituric acid reactive substances and NOx were decreased and total antioxidant status was increased, but all parameters were still altered.

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“…Furthermore, in patients subjected to thrombolysis, SOD in the blood was found significantly reduced; whereas the activity of the oxidant enzyme XO, and malondialdehyde levels were found significantly increased. However, oral supplementation of vitamin C to the post reperfusion patients restored these parameters back to normal or near normal levels (Bhakuni et al, 2006). These effects could be related to the modulation of ROS production by vitamin C. A major enzymatic source of ROS is given by their production via NADPH oxidase, an enzyme subjected to downregulation by vitamin C. In addition, vitamin C prevents the oxidation of tetrahydrobiopterin, a cofactor of eNOS that is highly sensitive to oxidation.…”

Section: Prevention Of Postoperative Atrial Fibrillationmentioning

confidence: 99%

Prevention of Postoperative Atrial Fibrillation: Novel and Safe Strategy Based on the Modulation of the Antioxidant System

Rodrigo¹

2012

Front. Physio.

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Postoperative atrial fibrillation (AF) is the most common arrhythmia following cardiac surgery with extracorporeal circulation. The pathogenesis of postoperative AF is multifactorial. Oxidative stress, caused by the unavoidable ischemia–reperfusion event occurring in this setting, is a major contributory factor. Reactive oxygen species (ROS)-derived effects could result in lipid peroxidation, protein carbonylation, or DNA oxidation of cardiac tissue, thus leading to functional and structural myocardial remodeling. The vulnerability of myocardial tissue to the oxidative challenge is also dependent on the activity of the antioxidant system. High ROS levels, overwhelming this system, should result in deleterious cellular effects, such as the induction of necrosis, apoptosis, or autophagy. Nevertheless, tissue exposure to low to moderate ROS levels could trigger a survival response with a trend to reinforce the antioxidant defense system. Administration of n−3 polyunsaturated fatty acids (PUFA), known to involve a moderate ROS production, is consistent with a diminished vulnerability to the development of postoperative AF. Accordingly, supplementation of n−3 PUFA successfully reduced the incidence of postoperative AF after coronary bypass grafting. This response is due to an up-regulation of antioxidant enzymes, as shown in experimental models. In turn, non-enzymatic antioxidant reinforcement through vitamin C administration prior to cardiac surgery has also reduced the postoperative AF incidence. Therefore, it should be expected that a mixed therapy result in an improvement of the cardioprotective effect by modulating both components of the antioxidant system. We present novel available evidence supporting the hypothesis of an effective prevention of postoperative AF including a two-step therapeutic strategy: n−3 PUFA followed by vitamin C supplementation to patients scheduled for cardiac surgery with extracorporeal circulation. The present study should encourage the design of clinical trials aimed to test the efficacy of this strategy to offer new therapeutic opportunities to patients challenged by ischemia–reperfusion events not solely in heart, but also in other organs such as kidney or liver in transplantation surgeries.

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Effect of Ascorbic Acid Supplementation on Certain Oxidative Stress Parameters in the Post Reperfusion Patients of Myocardial Infarction

Cited by 22 publications

References 32 publications

Protective Role of l-Arginine Against Free-Radical Mediated Oxidative Damage in Patients with Unstable Angina

Protective Role of l-Arginine Against Free-Radical Mediated Oxidative Damage in Patients with Unstable Angina

Oxidative Stress in Young Subjects With Acute Myocardial Infarction: Evaluation at the Initial Stage and After 12 Months

Prevention of Postoperative Atrial Fibrillation: Novel and Safe Strategy Based on the Modulation of the Antioxidant System

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