Insight into the health risk implicated in mitochondrial toxicity of dibutyl phthalate exposure on zebrafish (Danio rerio) cells

Mitochondrial DNA Stress-Mediated Health Risk to Dibutyl Phthalate Contamination on Zebrafish (Danio rerio) at Early Life Stage

“…Detection of Mitochondrial Function. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were used to observe the mitochondrial morphology and ultrastructure; 19 the samples are from the dorsal muscle of zebrafish larvae at 96 hpf. The mitochondrial membrane potential was labeled by a JC-1 fluorescent probe and evaluated by a flow cytometer (BD FACSAria III).…”

“…When mtDNA is damaged or stressed, it can be released from mitochondria into the cytosol and acts as damage-associated molecular patterns (DAMPs) to stimulate the innate immune response. , Herein, the cytosolic DNA sensor of cyclic GMP-AMP synthase (cGAS) is activated and promotes the stimulator of interferon genes (STING), TANK binding kinase 1 (TBK1), and interferon regulatory factor 3 (IRF3) signaling to elevate type I interferon (IFN) and other pro-inflammatory cytokines responses . Increasing evidence suggests that mitochondria and mtDNA are critically vulnerable to environmental pollutants, and previous studies have provided novel insight into the health risk implicated in mitochondrial toxicity of DBP. ,, Therefore, mitochondria and mtDNA stress-dependent physiological or pathological responses to pollutant exposure would be noteworthy topics, shedding light on public health and ecotoxicity research under realistic environmental contamination.…”

“…16−18 Previous works suggest that the potential mechanisms underlying toxicity of DBP may result from oxidative stress, inflammation, and epigenetic modifications, as well as further raising concerns at the subcellular level. 19 Due to the hydrophobic nature of DBP with a high K ow (octanol−water partition coefficients: 3.74) and low vapor pressure, it is not unexpected that DBP tends to be attracted to lipid-rich organelles inside the cell such as mitochondria, the well-known predictive targets of chemical agents. Mitochondria are crucial organelles that produce ATP through oxidative phosphorylation and regulate homeostasis of reactive oxygen species (ROS), programmed cell death, and immune response, etc.…”

“…25 Increasing evidence suggests that mitochondria and mtDNA are critically vulnerable to environmental pollutants, and previous studies have provided novel insight into the health risk implicated in mitochondrial toxicity of DBP. 19,26,27 Therefore, mitochondria and mtDNA stress-dependent physiological or pathological responses to pollutant exposure would be noteworthy topics, shedding light on public health and ecotoxicity research under realistic environmental contamination.…”

“…DBP is classified as an endocrine-disrupting chemical and potentially causes teratogenicity, mutagenicity, and carcinogenicity. Several studies have reviewed the association between DBP exposure and reproductive diseases, cardiovascular diseases, thyroid diseases, and other adverse effects that were confirmed by some cohort studies and animal model experiments. − Previous works suggest that the potential mechanisms underlying toxicity of DBP may result from oxidative stress, inflammation, and epigenetic modifications, as well as further raising concerns at the subcellular level . Due to the hydrophobic nature of DBP with a high K ow (octanol–water partition coefficients: 3.74) and low vapor pressure, it is not unexpected that DBP tends to be attracted to lipid-rich organelles inside the cell such as mitochondria, the well-known predictive targets of chemical agents.…”