Vitamin C: historical perspectives and heart failure
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Vitamin C: historical perspectives and heart failure Akshi Malik 1 & Ashim K. Bagchi 1 & Kartik Vinayak 1 & Gauri Akolkar 2 & Jan Slezak 3 & Adriane Belló-Klein 4 & Davinder S. Jassal 1,5 & Pawan K. Singal 1 Accepted: 30 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Vitamin C (Vit C) is an ideal antioxidant as it is easily available, water soluble, very potent, least toxic, regenerates other antioxidants particularly Vit E, and acts as a cofactor for different enzymes. It has received much attention due to its ability in limiting reactive oxygen species, oxidative stress, and nitrosative stress, as well as it helps to maintain some of the normal metabolic functions of the cell. However, over 140 clinical trials using Vit C in different pathological conditions such as myocardial infarction, gastritis, diabetes, hypertension, stroke, and cancer have yielded inconsistent results. Such a divergence calls for new strategies to establish practical significance of Vit C in heart failure or even in its prevention. For a better understanding of Vit C functioning, it is important to revisit its transport across the cell membrane and subcellular interactions. In this review, we have highlighted some historical details of Vit C and its transporters in the heart with a particular focus on heart failure in cancer chemotherapy. Keywords Vit C transporters . Nitric oxide . Nitric oxide synthases (NOS) . Doxorubicin . Tetrahydrobiopterin (BH4)
Introduction Vitamin C (Vit C) is a wide spectrum antioxidant effective against a wide variety of reactive oxygen (ROS) and nitrosative (RNS) species such as superoxide radicals, peroxides, hydroxyl radical, and peroxynitrites [1]. Although Vit C intake has been suggested to contribute in the prevention of chronic diseases [1, 2], disappointing results have been obtained from phase III randomized controlled trials (RCTs) in the prevention of cardiovascular (CV) diseases and cancer [3–5]. These studies have raised the skepticism for the use of Vit C in
* Pawan K. Singal [email protected] 1
Department of Physiology and Pathophysiology, Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, University of Manitoba, 351 Tache Avenue, Winnipeg, MB R2H 2A6, Canada
2
University of Ottawa Heart Institute, Ottawa, Canada
3
Centre of Experimental Medicine, Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic
4
Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil
5
Section of Cardiology, Department of Internal Medicine; Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada
cardiovascular diseases. Some reports claim design flaws as an explanation of failure of phase III RCTs [6–8]. Another explanation for failure of observable beneficial effects of Vit C could be due to poor Vit C uptake through its transporters in the target tissues, particularly, during
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