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EC number: 231-901-9
CAS number: 7778-39-4
Chronic arsenic poisoning is a world public
health issue. Long-term exposure to inorganic arsenic (As) from drinking
water has been documented to induce cancers in lung, urinary bladder,
kidney, liver and skin in a dose-response relationship.
Oxidative stress, chromosomal abnormality
and altered growth factors are possible modes of action in arsenic
Arsenic tends to accumulate in the skin.
Skin hyperpigmentation and hyperkeratosis have long been known to be the
hallmark signs of chronic As exposure. There are significant
associations between these dermatological lesions and risk of skin
The most common arsenic-induced skin cancers
are Bowen's disease (carcinoma in situ), basal cell carcinoma (BCC) and
squamous cell carcinoma (SCC). Arsenic-induced Bowen's disease (As-BD)
is able to transform into invasive BCC and SCC. Individuals with As-BD
are considered for more aggressive cancer screening in the lung and
urinary bladder. As-BD provides an excellent model for studying the
early stages of chemical carcinogenesis in human beings. Arsenic
exposure is associated with G2/M cell cycle arrest and DNA aneuploidy in
both cultured keratinocytes and As-BD lesions. These cellular
abnormalities relate to the p53 dysfunction induced by arsenic. The
characteristic clinical figures of arsenic-induced skin cancer are: (i)
occurrence on sun-protected areas of the body; (ii) multiple and
Both As and UVB are able to induce skin
cancer. Arsenic treatment enhances the cytotoxicity, mutagenicity and
clastogenicity of UV in mammalian cells. Both As and UVB induce
apoptosis in keratinocytes by caspase-9 and caspase-8 signaling,
respectively. Combined UVB and As treatments resulted in the
antiproliferative and proapoptotic effects by stimulating both caspase
pathways in the keratinocytes. UVB irradiation inhibited mutant p53 and
ki-67 expression, as well as increased in the number of apoptotic cells
in As-BD lesions which resulted in an inhibitory effect on
proliferation. As-UVB interaction provides a reasonable explanation for
the rare occurrences of arsenical cancer in the sun-exposed skin.
The multiple and recurrent skin lesions are
associated with cellular immune dysfunction in chronic arsenism. A
decrease in peripheral CD4+ cells was noticed in the inhabitants of
arsenic exposure areas. There was a decrease in the number of Langerhans
cells in As-BD lesion which results in an impaired immune function on
the lesional sites. Since CD4+ cells are the target cell affected by As,
the interaction between CD4+ cells and epidermal keratinocytes under As
affection might be closely linked to the pathogenesis of multiple
occurrence of arsenic-induced skin cancer.
In the review article, the pathomechanisms
of arsenic skin cancer and the relationship to its characteristic
figures was reported.
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