Abstract
The potential of antioxidants as tools for lowering the incidence of diseases, including cardiovascular events, is of growing interest. Some antioxidants (e.g. vitamin E and acetyl-salicylic acid) have been described as effective on cardiovascular diseases with mechanisms that differ from other scavenging agents. Currently, vitamin C is used to open occluded long-term central venous catheters, which avoids the process of reinserting a new one and injuring the patient. In this work, we investigated the vitamin C antihemostatic profile by evaluating its effects on the coagulation process. We used different assays, including prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time (TT) and ancrod time tests. We also examined the overall pH disturbance caused by vitamin C at different concentrations and its effect on the thrombin-initiated fibrin polymerization assay. Our results revealed a significant anticoagulant activity of vitamin C at high plasma concentrations (surpassing the normal 100 ?mol/L ratio) in a cell-independent mechanism. Our results suggest that vitamin C may affect blood coagulation by a direct impairment of fibrin assembly and further formation of a cohesive clot microstructure. This study supports the literature that points to the antihemostatic ability of antioxidant agents, and clarifies the mechanism of vitamin C in opening occluded long-term central venous catheters.
Highlights
Vitamin C is a water-soluble antioxidant and an enzyme cofactor that can be found in many biological systems of different origin [1,2,3]
Macedo and Kang reported the clinical usage for vitamin C in flow-recovery from occluded long-term central venous catheters, instead of streptokinase or tissue plasminogen activator, establishing its application as an ongoing practice in hospitals for over 13 years [18]. These results revealed the influence of high doses of vitamin C on the fibrinolytic process, no studies have clarified its role in blood coagulation and/or its direct influence in the plasma phase of clot formation
We propose an anticoagulant mechanism based on the antioxidant potential of the active agent, where the substrate cleavage of the E-portion of fibrinogen by thrombin removes the N-terminal 16 and 14 peptides known as fibrinopeptides A (FPA) and B (FPB), respectively (Fig. 5)
Summary
Vitamin C is a water-soluble antioxidant and an enzyme cofactor that can be found in many biological systems of different origin [1,2,3]. The human population obtains this molecule mainly through fruits, vegetables and pharmaceutical supplements [4]. International guidelines, such as the United States Department of Agriculture and National Cancer Institute publications, recommend the ingestion of an average of five fruits daily (200-300 mg of ingested vitamin C, depending on the fruit consumed) [5]. The literature points to the positive effects of polyphenols and other antioxidants on lipid profile, rates of myocardial infarction and cardiomyocyte apoptosis, decreasing the overall risk of cardiovascular disease [8,9,10], prompting to their cardioprotective ability [11,12]. Recent studies show that vitamin C may develop a protective role in ischemic heart disease due to its ability to increase the overall time of thrombus formation, decrease platelet aggregation rates and superoxide anion generation [13,14]
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