Review
Version 1
Preserved in Portico This version is not peer-reviewed
Toxicity Tolerance in the Carcinogenesis of Environmental Cadmium
Version 1
: Received: 13 January 2024 / Approved: 15 January 2024 / Online: 15 January 2024 (10:27:42 CET)
A peer-reviewed article of this Preprint also exists.
Cirovic, A.; Satarug, S. Toxicity Tolerance in the Carcinogenesis of Environmental Cadmium. Int. J. Mol. Sci. 2024, 25, 1851. Cirovic, A.; Satarug, S. Toxicity Tolerance in the Carcinogenesis of Environmental Cadmium. Int. J. Mol. Sci. 2024, 25, 1851.
Abstract
Cadmium (Cd) is an environmental toxicant of worldwide public health significance. Diet is the main non-workplace Cd exposure source other than smoking. The intestinal absorption of Cd involves the transporters for iron, zinc, copper, and calcium. These metal transporters essentially determine the body burden of Cd because only 0.001-0.005% of Cd accumulated in the body can be excreted in urine each day. The International Agency for Research on Cancer listed Cd as a human lung carcinogen. Current evidence, however, suggests that environmental Cd may increase the prevalence of many types of cancer, notably lung, liver, breast, pancreas, and kidney. A two-year bioassay that mimics a lifelong exposure demonstrates Cd caused neoplasms in multiple tissues of mice. Also, several non-tumorigenic human cell lines underwent malignant cell transformation, when they were exposed to a sublethal dose of Cd for a prolonged time. Cd does not directly damage DNA, but it can profoundly affect gene expression through its interactions with various proteins, and Cd can thus be viewed as a transcription modulator. The present review highlights epidemiological studies that connected an enhanced risk of various neoplastic diseases to chronic exposure to environmental Cd. Special emphasis is on the impact of body iron stores on the absorption rate of Cd, and its implications for breast cancer prevention in highly susceptible subpopulation groups of women. Resistance to cell death and other cancer phenotypes acquired during Cd-induced cancer-cell transformation, under in vitro conditions, are briefly discussed. The potential role for ZnT1 efflux transporter in cellular acquisition of tolerance to Cd cytotoxicity are highlighted.
Keywords
cadmium; cancer; cell transformation; copper; intestinal absorption; iron store status; zinc transporters
Subject
Public Health and Healthcare, Public, Environmental and Occupational Health
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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