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Published on: May 10, 2016
Cytogenomics of hexavalent chromium (Cr 6+) exposed cells: a comprehensive review
Akanksha Nigam, Shivam Priya, Preeti Bajpai
1Environmental Carcinogenesis Division, CSIR-Indian Institute of Toxicology Research, Lucknow, India.
Abstract:
The altered cellular gene expression profile is being hypothesized as the possible molecular basis navigating the onset or progress of various morbidities. This hypothesis has been evaluated here in respect of Cr 6+ induced toxicity. Several studies using gene microarray show selective and strategic dysregulations of cellular genes and pathways induced by Cr 6+. Relevant literature has been reviewed to unravel these changes in different test systems after exposure to Cr 6+ and also to elucidate association if any, of the altered cytogenomics with Cr 6+ induced toxicity or carcinogenicity. The aim was to verify the hypothesis for critical role of altered cytogenomics in onset of Cr 6+ induced biological/clinical effects by identifying genes modulated commonly by the toxicant irrespective of test system or test concentrations/doses, and by scrutinizing their importance in regulation of the flow of mechanistically linked events crucial for resultant morbidities. Their probability as biomarkers to monitor the toxicant induced biological changes is speculative. The modulated genes have been found to cluster under the pathways that manage onset of oxidative stress, DNA damage, apoptosis, cell-cycle regulation, cytoskeleton, morphological changes, energy metabolism, biosynthesis, oncogenes, bioenergetics, and immune system critical for toxicity. In these studies, the identity of genes has been found to differ remarkably; albeit the trend of pathways' dysregulation has been found to remain similar. We conclude that the intensity of dysregulation of genes or pathways involved in mechanistic events forms a sub-threshold or threshold level depending upon the dose and type (including speciation) of the toxicant, duration of exposure, type of target cells, and niche microenvironment of cells, and the intensity of sub-threshold or threshold level of the altered cytogenomics paves way in toxicant exposed cells eventually either to opt for reversal to differentiation and growth, or to result in toxicity like dedifferentiation and apoptosis, respectively.
Insights
Altered gene expression (cytogenomics) is linked to Cr 6+ toxicity. Pathway dysregulation, not specific genes, is key to understanding toxic effects and potential biomarkers.
Area of Science:
- Environmental Toxicology
- Molecular Biology
- Genomics
Background:
- Altered cellular gene expression is hypothesized to drive disease onset and progression.
- Hexavalent chromium (Cr 6+) exposure is known to induce cellular toxicity.
- Gene microarray studies reveal specific gene and pathway dysregulations following Cr 6+ exposure.
Purpose of the Study:
- To evaluate the hypothesis linking altered cytogenomics to Cr 6+ induced toxicity.
- To identify commonly modulated genes by Cr 6+ across different test systems and doses.
- To assess the role of altered cytogenomics in Cr 6+ induced biological and clinical effects.
Main Methods:
- Literature review of studies on Cr 6+ induced gene expression changes.
- Analysis of gene microarray data to identify dysregulated genes and pathways.
- Scrutiny of identified genes' roles in critical cellular events.
Main Results:
- Cr 6+ exposure modulates genes involved in oxidative stress, DNA damage, apoptosis, cell cycle, and more.
- While specific gene identities vary, pathway dysregulation trends remain consistent.
- Modulated genes cluster within pathways critical for toxicity, including oncogenes and immune responses.
Conclusions:
- The intensity of gene/pathway dysregulation determines toxic outcomes.
- Cr 6+ toxicity depends on dose, exposure duration, cell type, and microenvironment.
- Altered cytogenomics can lead to either cellular recovery or toxicity (dedifferentiation, apoptosis).
