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Related Concept Videos

Types of Toxins01:36

Types of Toxins

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.
Air pollutants, primarily gases, pose significant threats to respiratory health, leading to conditions like hypoxia, lung cancer, and in extreme cases, death.
Environmental pollutants like...
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,...
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...
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: 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...

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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

Published on: March 6, 2018

Developmental origin of chronic diseases: toxicological implication.

Stefan Bezek1, Eduard Ujházy, Mojmír Mach

  • 1Institute of Experimental Pharmacology, Slovak Academy of Sciences, 841 04 Bratislava, Slovakia.

Interdisciplinary Toxicology
|January 11, 2011
PubMed
Summary

Early life environments permanently alter health, influencing adult disease risk. Developmental programming and epigenetic changes due to suboptimal conditions like intrauterine growth restriction (IUGR) are key factors.

Keywords:
chronic diseasesdevelopmental programmingdiabetesepigeneticsprenatal and postnatal development

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Area of Science:

  • Developmental biology
  • Epigenetics
  • Public Health

Background:

  • Suboptimal fetal and neonatal environments profoundly impact adult physiological function and disease risk.
  • Early life adaptations to conditions like intrauterine growth restriction (IUGR) can lead to permanent alterations in tissue development, increasing vulnerability to chronic diseases.
  • The concept of Developmental Origins of Adult Diseases (DOHaD) is supported by animal studies demonstrating precise outcomes of specific early-life exposures.

Purpose of the Study:

  • To explore how early life environmental exposures, including nutritional and chemical factors, influence long-term health outcomes.
  • To elucidate the role of developmental programming and epigenetics in the etiology of adult diseases.
  • To understand the mechanisms by which environmental toxicants impact fetal development and permanent organ system alterations.

Main Methods:

  • Review of human epidemiological and experimental animal studies.
  • Analysis of molecular, cellular, metabolic, endocrine, and physiological adaptations during critical developmental periods.
  • Investigation of epigenetic modifications resulting from early-life exposures.

Main Results:

  • Early life suboptimal environments cause permanent alterations in cellular proliferation and differentiation, manifesting as chronic diseases in adulthood.
  • Intrauterine growth restriction (IUGR) is linked to essential hypertension, diabetes mellitus, ischemic heart disease, osteoporosis, and respiratory, neuropsychiatric, and immune system diseases.
  • Environmental pollutants and toxicants can permanently alter fetal organ structure and function, increasing disease susceptibility.

Conclusions:

  • Early life exposures establish epigenetic codes that influence disease development later in life.
  • Developmental epigenetics aims to create adaptive phenotypes, but mismatches with later-life environments elevate disease risk.
  • Conflicts between programmed adaptations and modern environmental factors may explain rising disease rates.