Abstract

Objectives: Smoking causes endothelial dysfunction, but it still remains unclear whether oral administration of anthocyanin brings benefits to endothelial function and redox states in young healthy smokers. We tested the hypothesis that supplement anthocyanin may rescue endothelial dysfunction and redox states in young healthy smokers. Methods: Young healthy male non-smoker (n = 8) and smokers (n = 14) were enrolled to measure the derivatives of reactive oxygen metabolites (d-ROMs) and biological antioxidant potential (BAP) levels and brachial artery flow-mediated dilation (FMD) before and 2 hours after one cigarette smoking or resting under administration of blackcurrant supplements (anthocyanins 210 mg) or not. Results: FMD, d-ROMs, and BAP at baseline were similar between non-smokers and smokers. One cigarette smoking induced a decrease in FMD at 2 hours (9.0% ± 2.6% vs 7.5% ± 2.3%, p < 0.05) without affecting plasma levels of d-ROMs and BAP in young healthy smokers. Single oral administration of anthocyanin at 210 mg abolished smoking-induced decrease in FMD (8.3% ± 3.4% vs 9.5% ± 3.6%, p = ns) without changes in plasma levels of d-ROMs and BAP in young smokers. In non-smokers, however, administration of anthocyanin at 210 mg slightly but significantly elevated plasma level of d-ROMs at 2 hours (249.6 ± 30.3 vs 265.5 ± 36.3 U CARR, p < 0.05) without affecting plasma level of BAP and FMD. Conclusions: Single oral administration of anthocyanin rescued smoking-induced endothelial dysfunction in young healthy smokers, but facilitated oxidative stress in non-smokers. When anthocyanin is taken as supplements, it seems important to pay attention to the dose and timing of administration.

Highlights

  • Lifestyle-related disease has become an object of public concern, and arteriosclerosis is attributable to the pathogenesis of lifestyle-related diseases such as cardiovascular disease

  • Oxidative stress derivatives of reactive oxygen metabolites (d-ROMs), antioxidant capacity biological antioxidant potential (BAP), and endothelial function at baseline were similar between young healthy smokers and non-smokers

  • Oxidative stress d-ROMs, antioxidant capacity BAP, and endothelial function assessed by flow-mediated dilation (FMD) measurement were all similar between young healthy smokers and non-smokers

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Summary

Introduction

Lifestyle-related disease has become an object of public concern, and arteriosclerosis is attributable to the pathogenesis of lifestyle-related diseases such as cardiovascular disease. Smoking is predisposed to arteriosclerosis and regarded as one of the major risk factors for the development of cardiovascular diseases [1]. Smoking comprises free radicals such as superoxide and reactive oxygen and several other materials of carbon monoxide, nitrogen, and nicotine [2]. Reactive oxygen species and reactive nitrogen species constituents in both the tar and gas phases of smoke are associated with various diseases like arteriosclerosis, diabetes or cancer [3]. Recent evidence showed that young smokers have a higher risk to develop vascular functional and histological abnormalities which are early hallmarks of atherosclerosis [5]. It is important to develop new therapeutic strategies to prevent negative effects on the cardiovascular system by smoking

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