Addition of oh8dG to Cardioplegia Attenuated Myocardial Oxidative Injury through the Inhibition of Sodium Bicarbonate Cotransporter Activity.

Antioxidants (Basel)

Department of Health Sciences and Technology, Lee Gil Ya Cancer and Diabetes Institute, GAIHST, Gachon University, 155 Getbeolro, Yeonsu-gu, Incheon 21999, Korea.

Published: August 2022

AI Article Synopsis

  • - The biomarker 8-hydroxy-2'-deoxyguanosine (oh8dG) is linked to DNA damage caused by oxidative stress and is thought to impact sodium bicarbonate cotransporter (NBC) activity in heart cells due to reactive oxygen species (ROS) production.
  • - In experiments with isolated heart tissues and cells, oh8dG treatment was found to reduce NBC activity and ROS levels while also mitigating markers of cardiac damage associated with oxidative stress.
  • - Overall, oh8dG appears to protect heart cells from oxidative damage and could be a promising approach for improving heart function in conditions involving oxidative stress.

Article Abstract

The biomarker 8-hydroxy-2'-deoxyguanosine (oh8dG) is derived from oxidized nucleic acids or products of oxidant-mediated DNA damage. Enhanced sodium bicarbonate cotransporter (NBC) activity is caused by reactive oxygen species (ROS) production in ventricular myocytes. Thus, we hypothesized that cardioplegia-solution-mediated ROS generation may be involved in the regulation of NBC activity in cardiomyocytes and that oh8dG treatment may modulate ROS and associated NBC activity. Langendorff-free cardioplegia-arrested cardiac strips and cardiomyocytes were isolated to determine the NBC activity and effects of oh8dG on oxidative-stress-mediated cardiac damage markers. We first determined the histidine-tryptophan-ketoglutarate (HTK) solution mediated NBC activity in cardiac strips and cells. The oh8dG treatment attenuated NBC activity in the electroneutral or electrogenic form of NBC. Additionally, exposure to HTK solution induced ROS, whereas co-administration of oh8dG attenuated ROS-mediated NBC activity, reduced ROS levels, and decreased the expression of apoptotic markers and fibrosis-associated proteins in cardiac cells. The oh8dG-administrated cardiac tissues were also protected from enhanced HTK-induced damage markers, heat shock protein 60 and polyADP-ribose. Our results show that oh8dG has a protective role against myocardial oxidative damage and provides a useful treatment strategy for restoring cardiac function.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9495749PMC
http://dx.doi.org/10.3390/antiox11091641DOI Listing

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