Dysregulation of fatty acid metabolism associated with esophageal inflammation of ICR mice induced by nitrosamines exposure

Hu, Zhang; Zhao, Chunjiang; Liu, Qiwei; Zhang, Ying; Luo, Kai; Pu, Yuepu; Yin, Lu

doi:10.1016/j.envpol.2021.118680

Cited by 11 publications

(8 citation statements)

References 60 publications

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“…The health damage caused by nitrosamines in humans has received attention globally (Luo et al, 2020). Nitrosamines caused the potential toxicological effects of cytotoxicity, genotoxicity, developmental toxicity, and neurobehavioral toxicity (Zhang, Zhao, et al, 2021). Therefore, nitrosamines, especially NDMA, were regulated in drinking water by several countries and regions, including Ontario (9 ng/L), Massachusetts (10 ng/L), California (10 ng/L), Canada (40 ng/L), the Netherlands (12 ng/L), WHO (100 ng/L), and Australia (100 ng/L) (Drinkwaterbesluit, n.d.).…”

Section: Discussionmentioning

confidence: 99%

“…LPS has been demonstrated to cause NLRP3‐caspase‐1 pathway pyroptosis in bronchial epithelial cells through the activation of NLRP3 inflammasome‐mediated pyroptosis in cardiomyocytes along with increased positive PI staining and LDH release (Qiu et al, 2019). Cigarette smoke caused NLRP3‐caspase‐1 pathway pyroptosis, cell membrane pore formation, and increased LDH release in bronchial epithelial cells (Zhang, Zhao, et al, 2021). High glucose could mediate pyroptosis via NLRP3‐Caspase‐1‐GSDMD pathway, which ultimately led to pericyte damage in the retina (Gan et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

“…NLRP3 inflammasome activation could promote mtROS production, reduce mitochondrial membrane potential, and increase mitochondrial permeability through the activation of caspase‐1 protease, causing mitochondrial damage and accelerating pyroptosis (He et al, 2016; Yu et al, 2014). The BPA disturbed bone health and caused pyroptotic death of osteocytes via ROS/NLRP3/Caspase‐1 pathway (Zhang, Zhao, et al, 2021). This study inhibited NLRP3 inflammasome activation by constructing the NLRP3 low expressed Het‐1A cell line, which was accompanied by the decrease of the percentage of PI staining, LDH release, caspase‐1, and GSDMD protein levels, indicating that the inhibiting NLRP3 inflammasome activation could reduce caspase‐1 protease activation and cell pyroptosis caused by nitrosamines exposure in Het‐1A cells.…”

Section: Discussionmentioning

confidence: 99%

Section: The Pyroptosis In Het-1a Cells Exposed To Nitrosaminesmentioning

confidence: 99%

“…The Het‐1A cell line was derived from normal human esophageal epithelial cells and commonly used to study the mechanisms of damage and toxicity in normal esophageal cells exposed to environmental contaminants (Zhang, Zhao, et al, 2021). In this study, the Het‐1A cells were used as the model to investigate the activation and potential mechanisms of the NLRP3 inflammasome by nitrosamines co‐exposure, and the relationship between NLRP3 inflammasome activation and cell pyroptosis, to provide more information for an insight into the toxic effects of nitrosamines.…”

Section: Introductionmentioning

confidence: 99%

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Reactive oxygen species‐mediated activation of NLRP3 inflammasome associated with pyroptosis in Het‐1A cells induced by the co‐exposure of nitrosamines

Liu

Zhao

Zhou

et al. 2022

J of Applied Toxicology

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Nitrosamines were a class of important environmental carcinogens associated with digestive tract neoplasms. As the early toxic effect of nitrosamines, inflammatory response participated in the malignant transformation of cells and promoted the occurrence and development of tumors. However, the role of NLRP3 inflammasome in the nitrosamines-induced inflammatory response was unclear. In this study, the human esophageal epithelial cells (Het-1A) were used to explore potential mechanisms of the activation of NLRP3 inflammasome under co-exposure to nine nitrosamines commonly found in drinking water at the doses of 0, 4, 20, 100, 500, and 2500 ng/mL. The results showed that nitrosamines stimulated activation of the NLRP3 inflammasome and induced cellular oxidative damage in a dose-dependent manner. Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species (mtROS) scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mtROS. Furthermore, we found that nitrosamines co-exposure also promoted cell pyroptosis through the NLRP3/caspase-1/GSDMD pathway, which was demonstrated by adding the caspase-1 inhibitor Z-YVAD-FMK and constructing NLRP3 downregulated Het-1A cell line. This study revealed the underlying mechanism of the activation of NLRP3 inflammasome initiated by nitrosamines co-exposure and provided new perspectives on the toxic effects of nitrosamines.

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Section: Discussionmentioning

confidence: 99%