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Updated: May 24, 2026

Production and Detection of Reactive Oxygen Species (ROS) in Cancers
Published on: November 21, 2011
Mitochondria and reactive oxygen species. Which role in physiology and pathology?
1Dipartimento di Biochimica, Università di Bologna, Bologna, Italy. giorgio.lenaz@unibo.it
Abstract:
Oxidative stress is among the major causes of toxicity due to interaction of Reactive Oxygen Species (ROS) with cellular macromolecules and structures and interference with signal transduction pathways. The mitochondrial respiratory chain, specially from Complexes I and III, is considered the main origin of ROS particularly under conditions of high membrane potential, but several other sources may be important for ROS generation, such as mitochondrial p66(Shc), monoamine oxidase, α-ketoglutarate dehydogenase, besides redox cycling of redox-active molecules. ROS are able to oxidatively modify lipids, proteins, carbohydrates and nucleic acids in mitochondria and to activate/inactivate signalling pathways by oxidative modification of redox-active factors. Cells are endowed with several defence mechanisms including repair or removal of damaged molecules, and antioxidant systems, either enzymatic or non-enzymatic. Oxidative stress is at the basis of ageing and many pathological disorders, such as ischemic diseases, neurodegenerative diseases, diabetes, and cancer, although the underlying mechanisms are not always completely understood.
Insights
Oxidative stress, caused by reactive oxygen species (ROS), damages cells and contributes to aging and diseases. Cells possess defense mechanisms against ROS, but understanding these processes is key to combating associated pathologies.
Area of Science:
- Biochemistry
- Cell Biology
- Pathology
Background:
- Oxidative stress arises from an imbalance between reactive oxygen species (ROS) production and cellular antioxidant defenses.
- Mitochondria, particularly Complexes I and III, are primary ROS sources, but other enzymes and molecules also contribute.
- ROS can damage cellular components like lipids, proteins, and DNA, and alter signaling pathways.
Purpose of the Study:
- To elucidate the multifaceted origins and consequences of oxidative stress.
- To highlight the cellular defense mechanisms against ROS-induced damage.
- To underscore the role of oxidative stress in aging and various diseases.
Main Methods:
- Review of existing literature on ROS generation and cellular responses.
- Analysis of molecular mechanisms underlying oxidative damage.
- Examination of the link between oxidative stress and pathological conditions.
Main Results:
- Identified key intracellular sources of ROS, including mitochondrial complexes and specific enzymes.
- Described the damaging effects of ROS on cellular macromolecules and signaling pathways.
- Highlighted the presence of enzymatic and non-enzymatic antioxidant systems for cellular protection.
Conclusions:
- Oxidative stress is a significant factor in cellular toxicity, aging, and diseases like cancer and neurodegeneration.
- Cellular defense systems play a crucial role in mitigating ROS-induced damage.
- Further research is needed to fully understand the complex mechanisms involved in oxidative stress and its pathological implications.
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