How does toxicants alter gene expression by affecting mRNAs?
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Toxicants can alter gene expression by affecting mRNAs through various mechanisms. Transcriptomics studies have shown that toxicants like organophosphorus pesticides, thyroid peroxidase inhibitors, and hepatic enzyme inducers can induce characteristic gene expression changes in response to exposure. Gene expression profiles in polymorphonuclear leukocytes (PMNL) have been used as surrogates for toxicant target organs, enabling the monitoring of gene expression alterations due to toxicant exposure. Additionally, environmental stressors like arsenic and cadmium have been found to impact gene expression responses and network coordination in organisms like killifish and water fleas. Furthermore, toxic metals can influence gene expression through epigenetic mechanisms, altering DNA methylation, histone modification, and non-coding RNA expression. These findings highlight the diverse ways in which toxicants can modulate gene expression at the mRNA level.
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59 Citations | Toxicants alter gene expression by influencing epigenetic features like DNA methylation, histone modification, and non-coding RNA expression, rather than directly affecting mRNAs. |
Open access•Dissertation 01 Dec 2017 1 Citations | Toxicants like arsenic reduce gene expression responses and coordination during osmotic shock, while cadmium increases responses and network coordination, impacting mRNA expression patterns in response to environmental stress. |
| Toxicants like thyroid peroxidase inhibitors alter gene expression by affecting mRNAs involved in the thyroid hormone synthesis pathway, providing insights into thyroid toxicity modes of action. | |
05 Jan 2022 | Toxicants like organophosphate pesticides can moderate gene expression by downregulating signaling pathways and transcription factors that control detoxifying enzymes, esterases, polyamine metabolism, and regulatory pathways in Rhinella arenarum larvae. |
Open access 01 Jan 2013 1 Citations | Toxicants alter gene expression by affecting mRNA levels in polymorphonuclear leukocytes (PMNL), serving as surrogates for target organ toxicity, enabling monitoring and characterization of toxicant exposure effects. |
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