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Review
. 2024 Mar 7;25(6):3114.
doi: 10.3390/ijms25063114.

Vitamin C as Scavenger of Reactive Oxygen Species during Healing after Myocardial Infarction

Huabo Zheng  1   2 , Yichen Xu  2   3 , Elisa A Liehn  2   4 , Mihaela Rusu  5
Affiliations
Review

Vitamin C as Scavenger of Reactive Oxygen Species during Healing after Myocardial Infarction

Huabo Zheng et al. Int J Mol Sci. .

Abstract

Currently, coronary artery bypass and reperfusion therapies are considered the gold standard in long-term treatments to restore heart function after acute myocardial infarction. As a drawback of these restoring strategies, reperfusion after an ischemic insult and sudden oxygen exposure lead to the exacerbated synthesis of additional reactive oxidative species and the persistence of increased oxidation levels. Attempts based on antioxidant treatment have failed to achieve an effective therapy for cardiovascular disease patients. The controversial use of vitamin C as an antioxidant in clinical practice is comprehensively systematized and discussed in this review. The dose-dependent adsorption and release kinetics mechanism of vitamin C is complex; however, this review may provide a holistic perspective on its potential as a preventive supplement and/or for combined precise and targeted therapeutics in cardiovascular management therapy.

Keywords: antioxidant capacity; cardiovascular diseases; myocardial infarction; oxidative stress; preventive strategy; reactive oxidative species (ROS); vitamin C supplementation.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Metabolism of vitamin C in vivo vs. in vitro. In vivo, vitamin C is oxidized to dehydroascorbic acid (DHA) when reacts with ROS. In vitro, ascorbate autoxidizes easily to O2•− and ASC•−.
Figure 2
Figure 2
Schematic diagram of various sources of ROS generation and its effect on mitochondrial activity in CVD (brown arrows point to the enzymatic sources of ROS formation). Oxidized ubiquinol receives two electrons from Fe-S clusters of complexes I (A) [154] and II (B) [122] to form ubiquinol; ubiquinol transports electrons to Fe-S clusters in complex III. Cyt c mediates the transport of electrons from complex III (C) to complex IV (D) [126]. Complex IV delivers the electrons to O2 and forms H2O. Hydrogen ions are pumped by complexes I [154], III [126], and IV [137] from the mitochondrial matrix to the mitochondrial intermembrane space to generate the H+ electrochemical gradient for ATP generation. MnSOD [75], Cu/Zn-SOD [74], CAT [76], GPx [76], TRx [77], and GSH are vital for the scavenging of ROS in the mitochondria. Cu/Zn-SOD, CAT, GPx, thioredoxins, and GSH also play important roles in scavenging ROS in the cytosol [74,76,78,155]. Complex V (ATP synthase) synthesizes ATP molecules [148] (E). Complex V dimers participate in the formation of MPTP, which also includes VDAC, ANT, and CypD. The overproduction of ROS in the mitochondria causes the opening of MPTP, producing a large amount of mtROS [156]. The opening of MPTP can even activate Bax and then lead to the release of cyt c, the activation of caspase 3 [50,120], and apoptotic cell death [152,157] (E).
Figure 3
Figure 3
Overview of the effect of vitamin C on scavenging mitochondria-produced ROS in CVD. Vitamin C in the mitochondria reduces O2•− [159], OH•− [78], and H2O2 [78] produced by mitochondrial complexes I (A), II (B), III (C), IV (D), and V (E), and is oxidized to DHA or ASC•−. Vitamin C is also reported to increase the activity or levels of GSH [78], Mn-SOD [165,185], GPx [165], CAT [166,186], Cu/Zn-SOD [185,186] (A–D), and therefore enhance the ability to scavenge ROS in the mitochondria in the CVD condition.
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