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Immunological profile of arsenic toxicity: a hint towards arsenic-induced carcinogenesis.

Abstract
Arsenic (a Group I carcinogen in humans) contamination and poisoning of human populations in different parts of Southeast and Eastern Asia, including West Bengal and Bangladesh, has become a major environmental concern. Arsenic intoxication affects diverse human organs including the lungs, liver, skin, bladder and kidney. This metalloid acts as a promoter of carcinogenesis, exerting toxic effects on the immune system. The present study was aimed at investigating arsenic-induced carcinogenesis and effects on the immune system in an animal model. Tumors were induced using ethylnitrosourea (ENU) and arsenic was used as a promoter. To investigate specific effects on the immune system, cytokine (TNF-α, IFNγ, IL4, IL6, IL10, IL12) production of lymphocytes was evaluated by FACS. The damaging consequences of treatment were assessed by evaluating the specific programmed cell death cascade in lymphocytes, assessed by FACS readings. The results revealed that under arsenic influence, and more so with arsenic+ENU, marked neoplastic changes were noted, which were corroborated with histological changes, cytokine modulation and apoptosis hinted at marked neoplastic changes.
AuthorsSagar Acharya, Suhnrita Chaudhuri, Sirshendu Chatterjee, Pankaj Kumar, Zarina Begum, Shyamal Dasgupta, S J S Flora, Swapna Chaudhuri
JournalAsian Pacific journal of cancer prevention : APJCP (Asian Pac J Cancer Prev) Vol. 11 Issue 2 Pg. 479-90 ( 2010) ISSN: 2476-762X [Electronic] Thailand
PMID20843137 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Alkylating Agents
  • Cytokines
  • Caspases
  • Arsenic
  • Ethylnitrosourea
Topics
  • Alkylating Agents (toxicity)
  • Animals
  • Apoptosis (drug effects)
  • Arsenic (pharmacokinetics, toxicity)
  • Caspases (metabolism)
  • Cell Transformation, Neoplastic (drug effects)
  • Cytokines (metabolism)
  • Ethylnitrosourea (toxicity)
  • Female
  • Humans
  • Male
  • Mice
  • Neoplasms, Experimental (chemically induced, immunology, metabolism)
  • Tissue Distribution

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