Pyroptotic cell death by exposure to 1-butanol in H9c2 cardiomyoblastoma cells

Abstract

The aim of this study is to examine the molecular mechanism of cytotoxicity caused by direct exposure to short chain alcohol. We showed previously that exposing H9c2 cardiomyoblastoma cells to 150 mM 1-butanol results in cell death within 1 h through an intrinsic apoptotic pathway. The cell death is accompanied by plasma membrane blebbing and caspase-3 activation. Here we show that a higher concentration (200 mM) of 1-butanol, as well as prolonged exposure (3-6 h) to 150 mM 1-butanol, induces plasma membrane ballooning, a characteristic feature of pyroptosis. Although gasderminD (GSDMD) cleavage by caspase-1 was not observed, GSDME cleavage by caspase-3 was observed during exposure to 150 mM 1-butanol for 6 h. We conclude that pyroptotic cell death by 1-butanol in H9c2 cardiomyoblastoma cells should occur via the caspase-3-GSDME pathway, revealing that 1butanol could induce not only apoptosis but also pyroptosis in the cells.

Biological effects of sub-lethal doses of glyphosate and AMPA on cardiac myoblasts

“…Signs of cell damage are still present after 24 h ( Figure 2 , bottom panels). Coupled to the reduction in cell viability, these morphologic alterations suggest an involvement of apoptotic pathways ( Sardão et al, 2009 ; Gui et al, 2012 ; Zhang et al, 2018 ; Noritake et al, 2020 ). Benachour and Séralini (2009) showed that in vitro pure Gly treatment caused apoptosis via caspase (cas)-3 and -7 activation, already after 6 h, in three different human cell lines.…”