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. 2020 Jul 28;10:12653. doi: 10.1038/s41598-020-69501-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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α-Hemolysin induces oxidative stress in mitochondria of THP-1m and inhibition of potassium efflux brought glutathione-redox status to normal. GSH:GSSG estimation was performed to evaluate the effect of α-hemolysin (HlyA) on THP-1m mitochondrial redox state. Additionally, the effect of glibenclamide and potassium chloride were also assessed on hemolysin induced oxidative stress in THP-1m. THP-1m pre-treated with glibenclamide (100 μM, 30 min prior to stimulation) and KCl (140 mM, 30 min prior to stimulation) were stimulated with HlyA for 2 h. Data shown is the average of three independent experiments. Comparisons between multiple groups were made using one-way ANOVA with Bonferroni’s post test. P value is shown as *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001.