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Related Concept Videos

Gene-Environment Interactions01:20

Gene-Environment Interactions

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Gene expression is a dynamic process that is significantly influenced by environmental factors. This interaction underlies the complex nature of biological development and the phenotypic differences observed among individuals, even among those with identical genetic makeups. Factors such as radiation, temperature, behavior, nutrition, and stress play pivotal roles in determining how genes are expressed. The concept of the reaction range is central to understanding this interaction. It posits...
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Humans continually engage with an environment rich in potentially harmful chemicals. These are introduced to our bodies through inhalation, ingestion, or skin contact. These chemicals exist in various forms, such as air and environmental pollutants, agricultural chemicals, organic solvents, and heavy metals.
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Although the genetic makeup of an organism plays a major role in determining the phenotype, there are also several environmental factors, such as temperature, oxygen availability, presence of mutagens, that can alter an organism’s phenotype.
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When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
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Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
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Drugs, encompassing various chemical compounds from natural sources, lab synthesis, or genetic engineering, elicit different biological responses in living organisms. Some of these responses are desirable or therapeutic, while others are undesirable. The primary goal of administering a drug is to achieve a therapeutic effect, that is, to address a specific disease or health condition. Any concurrent effects outside of this therapeutic outcome are considered undesirable. These undesirable...
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G × E interactions as a basis for toxicological uncertainty.

Ilinca Suciu1, David Pamies2, Roberta Peruzzo3

  • 1In Vitro Toxicology and Biomedicine, Department Inaugurated By the Doerenkamp-Zbinden Foundation, University of Konstanz, Universitaetsstr. 10, 78457, Constance, Germany.

Archives of Toxicology
|May 31, 2023
PubMed
Summary
This summary is machine-generated.

This study proposes a quantitative approach to toxicology, moving beyond traditional safety factors. It emphasizes understanding compound-specific uncertainties by considering genetic expression and exposure timing interactions for more accurate human risk assessment.

Keywords:
AOPEpigeneticsModel systemResilienceSafety factorToxicokinetics

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Area of Science:

  • Toxicology and Risk Assessment
  • Genomics and Environmental Health
  • Computational Biology and Predictive Modeling

Background:

  • Current toxicological assessments rely on standardized safety factors to extrapolate animal data to humans, which may not fully capture individual variability.
  • The traditional genotype-by-environment (G×E) interaction concept in toxicology is largely qualitative and requires quantitative refinement.
  • Understanding biological variability is crucial for accurate prediction of chemical toxicity across different populations and exposure scenarios.

Discussion:

  • This work introduces a refined concept, Ge×Et, integrating gene expression dynamics (Ge) with exposure timing (Et) to model compound-specific toxicological uncertainties.
  • It highlights the need for research programs to identify and quantify major biological variabilities influencing toxicity and to explore adverse outcome pathways (AOPs) in diverse biological contexts.
  • The study advocates for a precise definition of 'genetic' influence, encompassing not only gene sequence but also gene expression regulation.

Key Insights:

  • Accurate toxicological predictions require moving beyond generic safety factors to model compound-specific uncertainties.
  • Incorporating dynamic gene expression (Ge) and exposure timing (Et) provides a more nuanced understanding of G×E interactions in toxicity.
  • This quantitative Ge×Et framework can enhance the application of New Approach Methodologies (NAMs) for improved human health risk assessment.

Outlook:

  • Future research should focus on detailed case studies to elucidate the role of genetic backgrounds in chemical-induced adverse effects.
  • Further investigation into modulatory and counter-regulatory steps within adverse outcome pathways is essential for a comprehensive understanding.
  • Developing and validating quantitative models based on the Ge×Et concept will be critical for advancing predictive toxicology.