Oxidative Stress and Platelets

Abstract

Abstract-Platelet-dependent thrombus formation may be influenced by alteration of platelet or vascular redox state, the presence of endogenous or exogenous antioxidants, as well as the formation of reactive oxygen and nitrogen species. Specifically, settings and pathways that influence the formation of superoxide and nitric oxide, as well as their metabolism, may influence platelet function and thrombus formation. Although some antioxidant regimens have been associated with bleeding and hemorrhagic stroke, the therapeutic value of antioxidants in clinical syndromes that lead to platelet-dependent thrombosis is not clear, as supplemental antioxidants have not been generally associated with better cardiovascular outcome. R edox changes occur as a function of normal platelet activation; however, the introduction of additional oxidative stress in certain settings may be prothrombotic. Modulation of platelet or vascular redox status, the presence of reactive oxygen species, and the addition of exogenous antioxidants can alter platelet activation in vitro and in vivo and may have (patho)physiological ramifications.The clinical role of oxidative stress in platelet function and thrombosis is not straightforward. Although earlier epidemiological studies found that dietary antioxidant consumption was inversely associated with the development of coronary artery disease, more recent studies of vitamin supplementation have presented conflicting or negative results. 1 Interestingly, some of the negative side effects of antioxidant therapies, such as enhanced hemorrhagic stroke, may be attributed to changes in the thrombotic response. Although the effects of antioxidants were attributed to the prevention of oxidative modification of low-density lipoprotein (LDL) and the inhibition of atherogenesis, other effects may be relevant, including regulation of platelet activation, which is dependent on the balance between oxidative stress and redox state. As platelet function has also been implicated in the development of atherosclerosis and in the acute occlusion of coronary vessels, 2,3 oxidative processes and platelet redox status may have far reaching effects on the homeostasis of vasculature. Platelet Activation, Cardiovascular Events, and the Role of AntioxidantsThrombus formation within a coronary vessel is the precipitating event in myocardial infarction and unstable angina. 4 Normally, the intact endothelium prevents adhesion and activation of platelets. Adhesion of platelets to the endothelium is prevented by several mechanisms, including endothelial cell production of prostacyclin and nitric oxide (NO). 5,6 The occurrence of superficial intimal injury caused by endothelial denudation and deep intimal injury caused by plaque rupture expose collagen and von Willebrand factor (vWF) to platelets. Platelets then adhere directly to collagen or indirectly via the binding of vWF to the glycoprotein (GP) Ib/IX matrix. Local platelet activation stimulates further thrombus formation and additional platelet recruitment by supporting ce...

Creation of a blood-compatible surface: A novel strategy for suppressing blood activation and coagulation using a nitroxide radical-containing polymer with reactive oxygen species scavenging activity

“…ROS scavenging character worked effectively on the suppression of blood cell activations. Freedman reported that NO rapidly reacts with ROS to result in suppression of blood activation [38]. The ROS scavenging character of NRP might influence the role of NO, which will be investigated further and will be published elsewhere.…”

In Vitro Susceptibility of Wistar Rat Platelets to Hydrogen Peroxide and AAPH-Induced Oxidative Stress

“…Catalase was insignificant in H 2 O 2 platelets which can be due to (i) hydroperoxides produced by the platelets are also metabolized by GSH-Px present in the platelets, at lower concentrations of H 2 O 2 [3,44] and (ii) H 2 O 2 at concentrations other than 0.025, 0.05 and 0.075 mM decrease CAT activity [45]. AAPH triggers the formation of H 2 O 2 in addition to the endogenous H 2 O 2 [3], also observed in our results of 1.0 mM AAPH (30 min).…”

“…Superoxide is known to enhance platelet aggregation. Low concentrations (lM/L) of hydrogen peroxide (H 2 O 2 ) inhibit platelet function, although high concentrations (mM/L) of H 2 O 2 have been shown to stimulate platelet aggregation [1][2][3].…”

GC-MS analysis, evaluation of phytochemicals, anti-oxidant, thrombolytic and anti-inflammatory activities of <i>Exacum bicolor</i>

“…The free radical scavenging molecules such as flavonoids, phenols, tannins, alkaloids, amines, vitamins and other metabolites possess anti-inflammatory, thrombolytic, anti-carcinogenic, antibacterial and antiviral activities (Filomena et al, 2008). Inflammation is a key factor in all aspects of coronary disease including the initiation and progression of atherosclerotic plaque, plaque rupture, and thrombosis (atherothrombosis) where the oxidative stress is known to play a significant role (Freedman, 2008). Oxidative stress and inflammation are intimately linked with both the evolution of cardiovascular disease and acute coronary syndromes (Pashkow, 2011).…”