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Mechanisms and pathogenesis underlying environmental chemical-induced necroptosis

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Abstract

Necroptosis is a regulated cell death that is governed by mixed lineage kinase domain-like, receptor-interacting serine-threonine kinase 3 and commonly displays with necrosis morphological characteristics. This study examined the molecular mechanisms involved in the chemical-induced necroptosis where a systematic evaluation of experimental studies addressing this issue is missing. We strictly reviewed all scientific reports related to our search terms including “necroptosis” or “programmed necrosis”, “environmental chemicals” or “air pollutants” or “pesticides” or “nanoparticles” and “Medicines” from 2009 to 2019. Manuscripts that met the objective of this study were included for further evaluations. Studies showed that several pathological contexts like cancer, neurodegenerative disorders, and inflammatory diseases were related to necroptosis. Furthermore, multiple chemical-induced cytotoxic effects, such as DNA damage, mitochondrial dysregulation, oxidative damage, lipid peroxidation, endoplasmic reticulum disruption, and inflammation are also associated with necroptosis. The main environmental exposures that are related to necroptosis are air pollutants (airborne particulate matter, cadmium, and hydrogen sulfide), nanoparticles (gold, silver, and silica), pesticides (endosulfan, cypermethrin, chlorpyrifos, and paraquat), and tobacco smoke. To sum up, air pollutants, pesticides, and nanoparticles could potentially affect human health via disruption of cell growth and induction of necroptosis. Understanding the exact molecular pathogenesis of these environmental chemicals needs further comprehensive research to provide innovative concepts for the prevention approaches and introduce novel targets for the amelioration of a range of human health problems.

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Abbreviations

cIAP:

cellular inhibitor of apoptosis protein

COPD:

chronic obstructive pulmonary disease

DAMPs:

aamage-associated molecular patterns

FADD:

Fas-associated protein with a death domain

IKK:

IκB kinase

IL-1β:

interleukin 1 beta

LUBAC:

linear ubiquitin chain assembly complex

MAPK:

mitogen-activated protein kinase

MLKL:

mixed lineage kinase domain-like

NOX1:

NADPH oxidase 1

Nec-1:

necroptosis-specific inhibitor-1

NEMO:

nuclear factor-κB essential modulator

NF-kB:

nuclear factor kappa B

RHIM:

RIP homotypic interaction motif

RIP:

receptor-interacting protein

RIPK:

receptor-interacting protein kinase

ROS:

reactive oxygen species

PMA:

phorbol 12-myristate 13-acetate

TAK:

transforming growth factor β-activated kinase 1

TRAF:

TNFR-associated factor

TLR:

Toll-like receptor

TRADD:

TNFα receptor-associated death domain

TNF:

tumor necrosis factor

TNFR:

Tumor necrosis factor receptor

TRAIL:

TNF-related apoptosis-inducing ligand

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Funding

This study was supported by the University of Zabol, Zabol, Iran, (UOZ-GR-9618-5) received by the corresponding author Dr. N. Sanadgol.

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M-R Sepand and N. Sanadgol conceived the study and designed the study; M-R Sepand, M. Aliomrani, and Y. Hasani-Nourian conducted the searches; N. Sanadgol, M-H Farzaei, and M-R Kalhori interpreted the finding; all authors contributed in writing and commented on the manuscript.

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Correspondence to Nima Sanadgol.

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Responsible Editor: Lotfi Aleya

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Highlights

• Necroptosis can be triggered in response to the activation of multiple cell-surface receptors.

• Abnormal and extreme activation of necroptosis may be concerned with cellular/tissue damage and ultimately lead to pathological abnormalities.

• Air pollutants, pesticides, nanoparticles, and tobacco smoke could potentially mediate chemicals-induced necroptosis.

• Cell type, exposure duration, and does play an essential role in chemicals-induced necroptosis.

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Sepand, MR., Aliomrani, M., Hasani-Nourian, Y. et al. Mechanisms and pathogenesis underlying environmental chemical-induced necroptosis. Environ Sci Pollut Res 27, 37488–37501 (2020). https://doi.org/10.1007/s11356-020-09360-5

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  • DOI: https://doi.org/10.1007/s11356-020-09360-5

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