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Related Concept Videos

Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
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Cellular Injury II: Classification

Cellular injury is any process that disrupts a cell’s ability to maintain homeostasis, leading to structural or functional changes. It is broadly classified based on etiology (cause) and mechanism of damage.Classification by EtiologyCellular injury may result from several causes. Hypoxic injury happens due to reduced oxygen delivery, most commonly from inadequate blood supply, such as arterial obstruction; for example, coronary artery thrombosis can cause myocardial infarction. Chemical injury...

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Updated: Jul 15, 2026

Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors
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Oxidative stress detection: what for? Part II.

B Palmieri1, V Sblendorio

  • 1Department of General Surgery and Surgical Specialties, University of Modena and Reggio Emilia Medical School, Surgical Clinic, Modena, Italy. palmieri@unimo.it

European Review for Medical and Pharmacological Sciences
|April 5, 2007
PubMed
Summary

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have dual roles in health and disease. Their overproduction causes oxidative stress, a factor in many illnesses linked to cell signaling disruptions.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathophysiology

Background:

  • Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are biologically active molecules with significant roles in cellular processes.
  • These species can exert both beneficial and detrimental effects depending on their concentration and cellular context.
  • An imbalance in ROS/RNS production and scavenging leads to oxidative stress, a condition implicated in numerous diseases.

Purpose of the Study:

  • To elucidate the dual role of ROS/RNS in biological systems.
  • To define oxidative stress as the cumulative generation of ROS/RNS.
  • To highlight the link between oxidative stress and diseases involving altered cellular redox regulation.

Main Methods:

  • Literature review on ROS/RNS biology and oxidative stress.
  • Analysis of cellular signaling pathways affected by redox regulation.
  • Correlation of oxidative stress markers with disease pathogenesis.

Main Results:

  • ROS/RNS exhibit context-dependent beneficial and deleterious functions.
  • Oxidative stress results from the cumulative generation of ROS/RNS from endogenous and exogenous sources.
  • Altered redox regulation of cellular signaling is a common feature in diseases associated with oxidative stress.

Conclusions:

  • Understanding the dual role of ROS/RNS is crucial for comprehending cellular homeostasis and disease.
  • Oxidative stress is a significant pathological factor in a wide range of diseases.
  • Targeting redox regulation pathways may offer therapeutic strategies for oxidative stress-related conditions.