Enzymatic oxidant and antioxidants of human blood platelets in unstable angina and myocardial infarction

Pandey, Nalini; Kaur, Gurjeet; Chandra, M.; Sanwal, G.G.; Misra, M. K.

doi:10.1016/s0167-5273(00)00344-2

Cited by 35 publications

(29 citation statements)

References 23 publications

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“…Buczinsky et al 1993 117 Kaur et al 2000, 118 Pandey et al 2000 119 Nitrate tolerance Enhanced platelet NAD(P)H-oxidase-dependent ROS production McVeigh et al 2002 42 Nitrate tolerance in stable angina pectoris (SAP) Enhanced platelet O 2 Ϫ production in patients with SAP Chirkov et al 1999 120 Nitrate tolerance in chronic heart failure Ascorbic acid renders platelets sensible to the inhibitory effects of NO.…”

Section: Cardiovascular Risk Factors and Diseases Associated With Enhmentioning

confidence: 99%

Reactive Oxygen Species

Krötz

Sohn

Pohl

2004

ATVB

404

122

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Abstract-Platelets participate not only in thrombus formation but also in the regulation of vessel tone, the development of atherosclerosis, angiogenesis, and in neointima formation after vessel wall injury. It is not surprising, therefore, that the platelet activation cascade (including receptor-mediated tethering to the endothelium, rolling, firm adhesion, aggregation, and thrombus formation) is tightly regulated. In addition to already well-defined platelet regulatory factors, such as nitric oxide (NO), prostacyclin (PGI 2 ), and adenosine, reactive oxygen species (ROS) participate in the regulation of platelet activation. Although exogenously derived ROS are known to affect the regulation of platelet activation, recent data suggest that the platelets themselves generate ROS. Intracellular ROS signaling in activated platelets could be of significant relevance after transient platelet contact with the vessel wall, during the recruitment of additional platelets, and in thrombus formation. This review discusses the potential cellular and enzymatic sources of ROS in platelets, their molecular mechanisms of action in platelet activation, and summarizes in vitro and in vivo evidence for their physiological and potential therapeutic relevance. Key Words: platelets Ⅲ reactive oxygen species Ⅲ NAD(P)H-oxidase Ⅲ aggregation Ⅲ adhesion Ⅲ thrombus formation P latelet interaction with the vessel wall serves numerous physiological and pathophysiological functions. This is reflected by the fact that platelets release growth factors, 1 lipid mediators, 2,3 and cytokines. 4 Consequently, the regulation of platelet activity plays a role not only for thrombus formation and the regulation of vascular tone 5 but also for the vascular pathophysiology of angiogenesis and inflammation. Moreover, platelets participate in the development of atherothrombotic disease by promoting atherosclerotic lesion 6 and neointima formation. 7 Not surprisingly, the activation of platelets is regulated and modulated by numerous factors, blood-borne and cell-derived. Most of these factors are relatively well-characterized. 8 However, in recent time, several publications have suggested that reactive oxygen species (ROS) represent a new modulator of platelet activity. It has been known for some time that ROS exert critical regulatory functions within the vascular wall and it is therefore plausible that platelets represent a relevant target for their action.Within the vessel wall (where endothelial cells, vascular smooth muscle cells, and fibroblasts express a variety of ROS-generating enzymes), there is a constant, low-quantity flux of ROS. It is already established that enhanced ROS release from the vascular wall can indirectly affect platelet activity by scavenging nitric oxide (NO), thereby decreasing the antiplatelet properties of the endothelium. 9 In addition to their exposure to ROS derived from the vascular wall, platelets themselves also can generate ROS, and there is some evidence for a more direct role of ROS in the control of platelet activi...

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Section: Cardiovascular Risk Factors and Diseases Associated With Enhmentioning

confidence: 99%

Reactive Oxygen Species

Krötz

Sohn

Pohl

2004

ATVB

404

122

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“…The increased level of free radical generating system and malondialdehyde (MDA) and lowered levels of free radical scavenging systems seem to have critical role in ischemic heart condition (Pandry et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effect of amlodipine in oxidative stress induced by experimental myocardial infarction in rats

Begum

Akhter

2008

Bangladesh J Pharmacol

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The present study investigated whether the administration of amlodipine ameliorates oxidative stress induced by experimental myocardial infarction in rats. Adrenaline was administered and myocardial damage was evaluated biochemically [significantly increased serum aspertate aminotransferase (AST), lactate dehydrogenase (LDH) and malondialdehyde (MDA) levels of myocardial tissue] and histologically (morphological changes of myocardium). Amlodipine was administered as pretreatment for 14 days in adrenaline treated rats. Statistically significant amelioration in all the biochemical parameters supported by significantly improved myocardial morphology was observed in amlodipine pretreatment. It was concluded that amlodipine afforded cardioprotection by reducing oxidative stress induced in experimental myocardial infarction of catecholamine assault.

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“…Xanthine oxidoreductase, under normal conditions, exists in dehyrogenase form and uses NAD + and there is no or very little production of superoxide anion (3). Under ischemic conditions, there is depletion of ATP and subsequent loss of membrane Ca 2+ gradient.…”

mentioning

confidence: 99%