Effects of chloromethylisothiazolinone/methylisothiazolinone on cytotoxicity and mitochondrial dysfunction in bronchial epithelial cells.

A mixture of 5-chloro-2-methyl-4-isothiazolin-3-one (CMIT) and 2-methyl-4-isothiazolin-3-one (MIT) is frequently utilized as a biocide in various personal care products (PCP). However, toxicity attributed to this mixture remains poorly understood. Therefore, this study aimed to investigate effects of CMIT/MIT on the respiratory system using human bronchial epithelial BEAS-2B cells as a model. In this study, the mechanisms underlying CMIT/MIT-induced toxicity were examined with particular focus on mitochondria-mediated apoptotic and autophagy cell death using BEAS-2B cells. Notably, CMIT-MIT initiated cytotoxic effects on BEAS-2B cell viability at concentrations of 10 μg/mL following 1 h treatment. In addition, CMIT-MIT treatment inhibited complex II in a concentration-dependent manner, diminished mitochondrial membrane potential and altered dynamic balance between mitochondrial fission and fusion indicative of mitochondrial damage. Further, exposure to 10 μg/mL CMIT-MIT for 1 h induced cellular damage, elevated mitochondrial reactive oxygen species (ROS) levels and concomitantly increased levels of apoptosis and autophagy. Taken together our findings indicate the potential of CMIT/MIT exposure to disrupt mitochondrial functions, thereby initiating apoptotic and autophagic processes in human bronchial epithelial BEAS-2B cells.