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Toxicological assessment of 3‐monochloropropane‐1,2‐diol (3‐MCPD) as a main contaminant of foodstuff in three different in vitro models: Involvement of oxidative stress and cell death signaling pathway
Author(s) -
Nazari Firouzeh,
Naserzadeh Parvaneh,
Dizaji Rana,
Manjili Hamidreza Kheiri,
Bahrami Hadis,
Soleimani Mina,
Sharafi Ali,
Hosseini MirJamal
Publication year - 2020
Publication title -
journal of food science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 150
eISSN - 1750-3841
pISSN - 0022-1147
DOI - 10.1111/1750-3841.15471
Subject(s) - oxidative stress , toxicity , programmed cell death , mitochondrion , reactive oxygen species , oxidative phosphorylation , kidney , glutathione , cell culture , carcinogen , cytotoxicity , chemistry , biology , apoptosis , biochemistry , in vitro , endocrinology , enzyme , genetics , organic chemistry
Abstract 3‐Monochloropropane‐1,2‐diol (3‐MCPD) as a main source of food contamination has always been known as a carcinogenic agent. Kidney, liver, testis, and heart seem to be the main target organs for 3‐MCPD. Because oxidative stress and mitochondrial dysfunction have been realized to be involved in 3‐MCPD‐induced cytotoxicity, the present study aimed to investigate the probable toxicity mechanisms of 3‐MCPD in isolated mitochondria, HEK‐293 cell line, and cell isolated from the rats’ liver and kidney through measuring multiparametric oxidative stress assay. Based on the data indicating no significant difference between 3‐MCPD‐treated groups and control group, metabolites of 3‐MCPD have a key role in organ toxicity caused by them. To further investigating the suggested hypothesis, the effect of 3‐MCPD toxicity on HEK‐293 cell line was examined. Although the proliferation declined after exposure to a low dose of 3‐MCPD (10 to 200 µM), controversial responses in higher concentration (2 to 10 mM) have led to studies on the effect of oxidative stress and cell death signaling on isolated kidney and liver cells. Treatment of the isolated kidney and liver cells with 3‐MCPD resulted in an increase in the level of reactive oxygen species (ROS), the collapse of mitochondrial membrane potential (MMP), and activation of cell death signaling without creating any significant difference in the amount of reduced glutathione. In fact, 3‐MCPD can disrupt the mitochondrial electron transfer in isolated cells, which is correlated with the impairment of mitochondrial oxidative phosphorylation system, the rise of ROS level, and the failure of MMP, leading to the release of cytochrome c from mitochondria to cytosol and finally the activation of cell death signaling.