Next Article in Journal
Salicylic Acid and Melatonin Alleviate the Effects of Heat Stress on Essential Oil Composition and Antioxidant Enzyme Activity in Mentha × piperita and Mentha arvensis L.
Next Article in Special Issue
Sulforaphane Protects Cells against Lipopolysaccharide-Stimulated Inflammation in Murine Macrophages
Previous Article in Journal
Evidence for an Allosteric S-Nitrosoglutathione Binding Site in S-Nitrosoglutathione Reductase (GSNOR)
Previous Article in Special Issue
Salivary Antioxidants Status Following Progressive Aerobic Exercise: What Are the Differences between Waterpipe Smokers and Non-Smokers?
Open AccessArticle

Assessing the Efficacy of Dietary Selenomethionine Supplementation in the Setting of Cardiac Ischemia/Reperfusion Injury

1
Heart Research Institute, Sydney 2042, Australia
2
Sydney Medical School, University of Sydney, Sydney 2006, Australia
3
School of Mathematical and Physical Sciences, Faculty of Science, University of Technology Sydney, Sydney 2007, Australia
4
Department of Biomedical Sciences, Panum Institute, University of Copenhagen, DK-2100 Copenhagen, Denmark
*
Author to whom correspondence should be addressed.
Antioxidants 2019, 8(11), 546; https://doi.org/10.3390/antiox8110546
Received: 29 October 2019 / Revised: 7 November 2019 / Accepted: 11 November 2019 / Published: 13 November 2019
Oxidative stress is a major hallmark of cardiac ischemia/reperfusion (I/R) injury. This partly arises from the presence of activated phagocytes releasing myeloperoxidase (MPO) and its production of hypochlorous acid (HOCl). The dietary supplement selenomethionine (SeMet) has been shown to bolster endogenous antioxidant processes as well as readily react with MPO-derived oxidants. The aim of this study was to assess whether supplementation with SeMet could modulate the extent of cellular damage observed in an in vitro cardiac myocyte model exposed to (patho)-physiological levels of HOCl and an in vivo rat model of cardiac I/R injury. Exposure of the H9c2 cardiac myoblast cell line to HOCl resulted in a dose-dependent increase in necrotic cell death, which could be prevented by SeMet supplementation and was attributed to SeMet preventing the HOCl-induced loss of mitochondrial inner trans-membrane potential, and the associated cytosolic calcium accumulation. This protection was credited primarily to the direct oxidant scavenging ability of SeMet, with a minor contribution arising from the ability of SeMet to bolster cardiac myoblast glutathione peroxidase (GPx) activity. In vivo, a significant increase in selenium levels in the plasma and heart tissue were seen in male Wistar rats fed a diet supplemented with 2 mg kg−1 SeMet compared to controls. However, SeMet-supplementation demonstrated only limited improvement in heart function and did not result in better heart remodelling following I/R injury. These data indicate that SeMet supplementation is of potential benefit within pathological settings where excessive HOCl is known to be generated but has limited efficacy as a therapeutic agent for the treatment of heart attack. View Full-Text
Keywords: ischemia/reperfusion (I/R); hypochlorous acid (HOCl); myeloperoxidase (MPO); selenomethionine (SeMet) ischemia/reperfusion (I/R); hypochlorous acid (HOCl); myeloperoxidase (MPO); selenomethionine (SeMet)
Show Figures

Figure 1

MDPI and ACS Style

Reyes, L.; Bishop, D.P.; Hawkins, C.L.; Rayner, B.S. Assessing the Efficacy of Dietary Selenomethionine Supplementation in the Setting of Cardiac Ischemia/Reperfusion Injury. Antioxidants 2019, 8, 546.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop