Mechanisms of chromium toxicity, carcinogenicity and allergenicity: Review of the literature from 1985 to 2000

  title={Mechanisms of chromium toxicity, carcinogenicity and allergenicity: Review of the literature from 1985 to 2000},
  author={Anthony D Dayan and Alan J. Paine},
  journal={Human and Experimental Toxicology},
  pages={439 - 451}
  • A. Dayan, A. Paine
  • Published 1 September 2001
  • Medicine, Chemistry, Biology
  • Human and Experimental Toxicology
Laboratory and clinical reports about the pathogenesis of the carcinogenicity and allergenicity of chromium compounds published between 1985 and 2000 have been reviewed as a basis for consideration of the pathogenetic mechanisms involved. There is good evidence from the clinic and the laboratory that Cr[VI] is the ion responsible for most of the toxic actions, although much of the under lying molecular damage may be due to its intracellular reduction to the even more highly reactive and short… 
Ch chromium induced cytotoxicity can be attributed to oxidative stress started from glutathione mediated metal reductive activation and continued by mitochondrial/lysosomal toxic interaction.
To assess the health effects and carcinogenic potential of chromium exposure in tannery workers with special emphasis on the different job categories for better and detailed evaluation of adverse effects and for more targeted efforts of safety and prevention.
Mathematical Modelling of Toxicity Associated with Intracellular Chromium Reduction
A conceptual model examining the intracellular reduction of chromium through reductants such as glutathione and ascorbic acid is devised and a mathematical model describing these events in detail is built to clarify the key steps in the process of Chromium reduction within cells.
Mechanism of Nickel and Chromium-Induced Immunotoxicity and Oxidative Stress: A Comparative Study
The aim of this study is to investigate the oxidative stress and their potential effects on glutathione peroxidase (GPx) among workers exposed to both metals during electroplating process and highlight the possible immunotoxic potential of both Cr and Ni in occupationally exposed workers.
Potassium Dichromate Induced Cytotoxicity, Genotoxicity and Oxidative Stress in Human Liver Carcinoma (HepG2) Cells
It is demonstrated that potassium dichromate was highly cytotoxic to HepG2 cells, and its cytotoxicity seems to be mediated by oxidative stress and DNA damage.
Study the effect of hexavalent chromium on some biochemical, citotoxicological and histopathological aspects of the Orechromis spp. fish.
  • H. Abbas, F. K. Ali
  • Environmental Science
    Pakistan journal of biological sciences : PJBS
  • 2007
Results showed a significant decrease in total glycogen, total lipids and total protein of liver, muscles and gills after 24 and 96 h of exposure to 96 h LC50 of hexavalent chromium (43.7 mg L(-1).
An Overview of Carcinogenic Heavy Metal: Molecular Toxicity Mechanism and Prevention
The analyzed data showed that Arsenic, cadmium, chromium, and nickel induce oxidative stress, DNA damage, and cell death processes, resulting in increase the risk of cancer and cancer-related diseases.
Oxidative stress, DNA damage, and antioxidant enzyme activity induced by hexavalent chromium in Sprague‐Dawley rats
The results obtained showed that Cr (VI) could induce dose‐ and time‐dependent effects on DNA damage, both liver and kidney show defense against chromium‐induced oxidative stress by enhancing their antioxidant enzyme activity, however, liver was found to exhibit more antioxidant defense than the kidney.
Cytogenetic Assays of Genotoxic Effects and Cancer Risk of Chromium on Tannery Workers in Bangladesh
Evidence is provided that the duration of exposure to C r compounds in human peripheral lymphocytes results in induction of DNA damage and chromosomal instability, and it is suggested that occupational exposure to Cr could lead to eased levels of DNADamage and chromosom instability.
Molecular mechanisms of hexavalent chromium-induced apoptosis in human bronchoalveolar cells.
This is the first report indicating strict correlation of Cr(VI) apoptosis to PUMA induction on primary human bronchoalveolar cells in short-term cultures and establishes p53 as the "necessary" player in Cr( VI)-induced apoptosis.


Mechanisms of chromium carcinogenicity and toxicity.
The chemical nature of chromium compounds and how these properties impact upon the interactions ofchromium with cellular and genetic targets, including animal and human hosts, are discussed.
Reduction of chromium(VI) and its relationship to carcinogenesis.
This article summarizes recent studies on the reduction of Cr(VI) by ascorbate, diol- and thiol-containing molecules, certain flavoenzymes, cell organelles, intact cells, and whole animals; free-radical production with emphasis on hydroxy radical generation via Fenton or Haber-Weiss type reactions; and free- radical-induced cellular damage.
Toxicity and carcinogenicity of Cr(VI) in animal models and humans.
  • M. Costa
  • Biology
    Critical reviews in toxicology
  • 1997
There is suggestive evidence that hexavalent Cr causes increased risk of bone, prostate, lymphomas, Hodgkins, leukemia, stomach, genital, renal, and bladder cancer, reflecting the ability of Hexavalent chromate to penetrate all tissues in the body.
Reduction of carcinogenic chromium(vi) on the skin of living rats
The results demonstrate that skin represents one route for chromium to enter into animals and humans and indicate the potential for in vivo EPR spectroscopy for studying the metabolism of paramagnetic reactive species in chemical and biochemical reactions occurring in/on the skin of both small and large animals, and possibly humans.
Occupational exposures to Cd, Ni, and Cr modulate titers of antioxidized DNA base autoantibodies.
This study was undertaken to establish whether occupational exposures to derivatives of carcinogenic metals evoke inflammatory immune responses, as determined by the presence of elevated titers of
Chromium Toxicity: Reductive Activation by Human Enzymes.
Chromium(VI) reduction by human lung is similar to that in liver, with significant rates of reduction using chromium( VI) concentrations anticipated for occupational exposure, and individuals who are simultaneously exposed to chromium and quinones are likely at greater risk for chromium toxicity.
Chromium occurrence and function in biological systems.
  • W. Mertz
  • Chemistry
    Physiological reviews
  • 1969
An extensive review of the biogeochemistry of chromium is presented, dealing with its occurrence in nature, chromium's interactions with proteins, nucleic acids, bacteria, yeasts and red blood cells, and the biochemical aspects of low-chromium states.
Utilization of DNA-protein cross-links as a biomarker of chromium exposure.
Human exposure to carcinogenic Cr(VI) compounds is found among workers in a large number of professional groups, and it can also occur through environmental pollution. A significant number of toxic
Metabolism of the carcinogen chromate by cellular constituents
The redox chemistry of chromium(VI) is discussed with respect to the cellular metabolism of the carcinogen chromate in vivo and some redox proteins are active in reducing chromate.
Immunotoxicologic effects of inhaled chromium: role of particle solubility and co-exposure to ozone.
Results indicate that, while immunomodulatory effects of inhaled Cr6+ upon PAM are related to particle solubility, the co-inhalation of O3 apparently does not cause further modifications of the metal-induced effects.