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Mechanisms of Nickel Carcinogenesis

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Essential and Non-essential Metals

Part of the book series: Molecular and Integrative Toxicology ((MOLECUL))

Abstract

Nickel (Ni) is a naturally occurring metal that is widely used in an array of industries such as nickel plating, refinery, welding, as well as in the manufacturing of stainless steel, jewelry, coins, batteries, and medical devices. Despite tremendous economic values, exposure to this carcinogenic metal either through acute dermal contact or chronic inhalation in occupational settings can elicit a wide range of health problems including contact dermatitis, cardiovascular diseases, and respiratory tract cancer. Nickel-induced carcinogenesis has long been validated and studied by scientists; however despite extended studies in cell culture, animal, and epidemiology, the precise mechanism of Ni carcinogenesis is still uncertain. This chapter will seek to provide a comprehensive overview of the mechanistic roles, genetic and epigenetic alterations, in Ni carcinogenesis, as well as a review of recent advances in the area.

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Abbreviations

AcCoA:

Acetyl coenzyme A

BEAS-2B:

Human bronchial epithelial cells

CpG:

5′-C-phosphate-G-3′

DNMT:

DNA methyltransferase

GPT:

Glutamic-pyruvate transaminase

IARC:

International Agency for Research on Cancer

JMJD1A:

Jumonji domain containing 1A

JMJD3:

Jumonji domain containing 3

Ni(C2H3O2):

Nickel acetate

Ni3S2:

Nickel sulfide

NiSO4:

Nickel (II) sulfate

pri-miRNA:

Primary miRNA

PTEN:

Phosphatase and tensin homolog

RARB2:

Retinoic acid receptor beta

RASSF1A:

Ras association domain family 1 isoform A

RISC:

RNA-induced silencing complex

ROS:

Reactive oxygen species

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Chen, Q.Y., Brocato, J., Laulicht, F., Costa, M. (2017). Mechanisms of Nickel Carcinogenesis. In: Mudipalli, A., Zelikoff, J. (eds) Essential and Non-essential Metals. Molecular and Integrative Toxicology. Humana Press, Cham. https://doi.org/10.1007/978-3-319-55448-8_8

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