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Positive and negative feedback loops are crucial for regulating biological signaling systems. These feedback loops are processes that connect output signals to their inputs.
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Related Experiment Video

Updated: Jul 3, 2026

Measurements of Physiological Stress Responses in C. Elegans
10:36

Measurements of Physiological Stress Responses in C. Elegans

Published on: May 21, 2020

Hormesis and adaptive cellular control systems.

Qiang Zhang1, Jingbo Pi, Courtney G Woods

  • 1Division of Computational Biology, The Hamner Institutes for Health Sciences, 6 Davis Drive, Research Triangle Park, NC 27709, USA.

Dose-Response : a Publication of International Hormesis Society
|July 24, 2008
PubMed
Summary

Hormetic dose responses, often U-shaped, arise from cellular adaptive mechanisms protecting against environmental stressors. These adaptations, while beneficial, incur energetic costs, influencing cellular functions and risk assessment models.

Keywords:
Hormesisadaptive responsechlorinehomeostasisoxidative stress

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Using Caenorhabditis elegans as a Model System to Study Protein Homeostasis in a Multicellular Organism
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Using Caenorhabditis elegans as a Model System to Study Protein Homeostasis in a Multicellular Organism

Published on: December 18, 2013

Area of Science:

  • Environmental toxicology
  • Cellular biology
  • Biophysics

Background:

  • Hormetic dose-response relationships are observed for numerous endpoints following exposure to environmental stressors.
  • Cellular U- or inverted U-shaped responses may stem from adaptive mechanisms that protect cells in stressful environments.

Purpose of the Study:

  • To investigate the hypothesis that adaptive responses to stressors, like chlorine, lead to U- or inverted U-shaped dose-response curves.
  • To explore the energetic trade-offs associated with cellular adaptation and their impact on basal cellular functions.
  • To refine risk assessment practices by incorporating adaptive response dynamics.

Main Methods:

  • Utilized cellular studies to examine dose-response relationships.
  • Performed gene expression analysis to understand stress response pathways.
  • Employed computational modeling to simulate the activation of control networks.

Main Results:

  • Observed discrete cellular states (normal, adaptive, stressed, toxic) contingent on exposure concentration and duration.
  • Demonstrated that adaptive pathways extend cellular homeostasis but incur energetic costs.
  • Identified potential for U- or inverted U-shaped curves in precursor endpoints due to resource trade-offs.

Conclusions:

  • Cellular adaptive responses to environmental stressors can result in non-linear dose-response curves.
  • The energetic cost of adaptation influences cellular function and may explain observed response patterns.
  • Findings suggest a need to update risk assessment methodologies to account for adaptive responses.