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Environmental Toxicants and Carcinogenicity: Role of Oxidative Stress

Role of oxidative stress

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Handbook of Oxidative Stress in Cancer: Mechanistic Aspects

Abstract

The transformation of a normal cell to a malignant one is a multifactorial process. Over the last decade, it has been established that redox homeostasis is one of the major factors for cancer initiation and progression. Due to indiscriminate use, toxicants (pesticides, heavy metals, and plastics) enter into different environmental compartments (air, water, and soil), where they accumulate and show various health adversities in an exposed organism, including cancer. Oxidative stress is a prime response in organisms against the exposures to environmental pollutants. Oxidative stress not only generates a constant threat to cellular macromolecules (protein, lipid, and DNA) but also is linked with several cell survival and cell death pathways. Accumulation of oxidative DNA damage leads to genomic instability and encourages mutations; however, cellular stress response attempts to mitigate this damage. Moreover, increased oxidative stress can modulate growth, inflammation, apoptosis, and cell cycle regulation, eventually leading to carcinogenicity. Evidences are available on research database showing the relation between cancer and environmental toxicants. This chapter enlightens various portfolios of toxicants and their impact on carcinogenesis with emphasis on the role of cellular redox status.

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Abbreviations

16-HBE:

Human bronchial epithelial

8-OHdG:

8-Oxo-2'-deoxyguanosine

A549:

Adenocarcinomic human alveolar basal epithelial cells

BEAS-2B:

Human bronchial epithelium

COX2:

Cyclooxygenase-2

DDE:

Dichlorodiphenyldichloroethylene

DSB:

Double strand breaks

HaCaT:

Human keratinocytes

HIF-1α:

Hypoxia-inducible factor 1-alpha

HOSE:

Human ovary surface epithelial cells

MAPK:

Mitogen-activated protein kinase

MDA:

Malondialdehyde

miR-21-PDCD4:

Programmed cell death 4

NAC:

N-acetyl-cysteine

NFAT:

Nuclear factor of activated T-cells

NF-κB:

Nuclear factor kappa B

NHEJ:

Nonhomologous end joining

Nkx2.1:

NK2 homeobox 1

Nrf2:

Nuclear factor erythroid 2-related factor 2

OSCC:

Oral squamous cell carcinoma

PBDEs:

Polybrominated diphenyl ethers

PCDD/Fs:

Polychlorinated dibenzo-p-dioxinsanddibenzo furans

PCNA:

Proliferating cell nuclear antigen

RNS:

Reactive nitrogen species

ROS:

Reactive oxygen species

Smad2:

Mothers against decapentaplegic homolog 2

SV-HUC-1:

Human uroepithelial cells

TAC:

Total antioxidant capacity

TCDD:

2,3,7,8-Tetrachlorodibenzo-p-dioxin

VEGF:

Vascular endothelial growth factor

β-HCH:

β-Hexachlorocyclohexane

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Acknowledgment

We sincerely apologize to all those researchers, whose works have not been discussed in the book chapter due to space restriction. The authors are thankful to the Director, CSIR – Indian Institute of Toxicology Research, Lucknow, and Nitte University Centre for Science Education and Research, Mangalore. AS thanks Science and Engineering Research Board (ECR/2016/001863). Financial support to JGP and SS from CSIR, as RA and SRF, respectively (Fellowship nos. 09/1257(0001)/2019-EMR-I and 31/29(0291)/2018-EMR-I), are thankfully acknowledged. IITR communication number of the book chapter is 3622.

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Correspondence to Anurag Sharma or Debapratim Kar Chowdhuri .

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Saini, S., Paithankar, J.G., Sharma, A., Kar Chowdhuri, D. (2021). Environmental Toxicants and Carcinogenicity: Role of Oxidative Stress. In: Chakraborti, S., Ray, B.K., Roychowdhury, S. (eds) Handbook of Oxidative Stress in Cancer: Mechanistic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-15-4501-6_35-1

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  • DOI: https://doi.org/10.1007/978-981-15-4501-6_35-1

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