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Related Concept Videos

Toxic Reactions: Overview01:26

Toxic Reactions: Overview

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.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
Toxicity Testing in Animals01:23

Toxicity Testing in Animals

Toxicity tests in animals are grounded on two main assumptions: first, the effects observed in laboratory animals can be extrapolated to humans, especially when adjusted for body surface area; second, high-dose exposure in animals is essential to identify potential human hazards from lower doses. This is based on the quantal dose-response concept, which faces the challenge of extrapolating results from relatively few test animals to much larger human populations. For example, a 0.01% incidence...
Toxicokinetics: Overview01:21

Toxicokinetics: Overview

Studies that assess how a drug is absorbed, distributed, metabolized, and excreted (ADME) at toxic doses are termed toxicokinetics. Understanding toxicokinetics helps predict adverse drug reactions (ADRs) and manage toxicity in humans.Toxicokinetics differs from pharmacokinetics mainly in the dose levels studied, with toxicokinetics focusing on higher toxic doses. The kinetics at these levels can be non-linear due to altered physiological processes. Toxicodynamics examines the relationship...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
Drug Toxicity: Overview01:00

Drug Toxicity: Overview

Drug toxicity quantifies the harm a compound causes to an organism, varying by dose and potentially impacting whole systems or specific organs like the liver. Toxic reactions may arise from venomous insect or spider bites, with effects ranging from mild symptoms to severe outcomes such as brain damage or death. Common forms of acute poisoning include ethanol intoxication and overdose of pain or fever medications, with substances like GHB and heroin being particularly lethal at doses close to...
Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...

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Mixture toxicity revisited from a toxicogenomic perspective.

Rolf Altenburger1, Stefan Scholz, Mechthild Schmitt-Jansen

  • 1Department Bioanalytical Ecotoxicology, UFZ - Helmholtz Centre for Environmental Research, Permoser Street 15, 04318 Leipzig, Germany. rolf.altenburger@ufz.de

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Summary

New genomic techniques aid mixture toxicology by analyzing combined chemical effects. This review highlights studies using toxicogenomic approaches to understand low-dose interactions and proposes a framework for better quantitative analysis.

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Area of Science:

  • Environmental toxicology
  • Genomics and bioinformatics
  • Molecular biology

Background:

  • Advancements in genomic techniques offer new possibilities for investigating complex toxicological questions, particularly concerning chemical mixtures.
  • Understanding the mechanisms of low-dose interactions within chemical mixtures remains a significant challenge in toxicology.
  • Toxicogenomic approaches, including transcriptomics, metabolomics, and proteomics, have emerged as powerful tools for studying joint exposures.

Purpose of the Study:

  • To review experimental studies from the past decade (2002-2011) that utilized toxicogenomic techniques to address mixture toxicology.
  • To assess the diagnostic and mechanistic insights gained from these studies regarding the combined effects of chemical mixtures.
  • To propose a conceptual framework for improving the assessment of mixture toxicity.

Main Methods:

  • Systematic review of 41 studies published between 2002 and 2011 focusing on mixture toxicity assessment.
  • Analysis of studies employing multiplexed gene transcript quantification, metabolomics, and proteomics.
  • Evaluation of bioinformatic analysis tools and statistical treatments used in toxicogenomic data.

Main Results:

  • While standard practices for data handling have improved, bioinformatic analysis of toxicogenomic data remains diverse and evolving.
  • Many studies primarily compared mixture outcomes to individual components, limiting a comprehensive understanding of joint effects.
  • Receptor-based assays showed promise in establishing quantitative exposure-response relationships, whereas transcriptomic interpretations were often ambiguous.

Conclusions:

  • Current mixture toxicology studies often provide anecdotal evidence due to limitations in study design and analysis.
  • A conceptual framework integrating established mixture effect models with toxicokinetic/dynamic principles is proposed.
  • Recommendations include designing studies for quantitative dose-time-response relationships, adopting mixture toxicity models, utilizing advanced bioinformatics, and incorporating stress response concepts.