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Published on: May 29, 2019
Cell damage by oxygen free radicals
1Dipartimento di Medicina Interna e Terapia Medica Clinica Medica I, University of Pavia, 27100, PAVIA, Italy.
Abstract:
The exposure of isolated and cultured cells to oxygen free radicals generated extracellularly or intracellularly during the metabolism of foreing compounds results in the development of damage that eventually lead to cell death. Multiple mechanisms are involved in these cytopathological processes, including direct attack of free radicals to macromolecules essential for cell life, as well as indirect activation of catabolic processes such as proteases, endonucleases and phospholipases. A key role in triggering these indirect events is played by Ca(2+) whose cytosolic concentration during oxidative stress raises well above the physiological limits.
Insights
Oxidative stress from free radicals causes cell damage and death through direct attacks and by activating destructive enzymes. Elevated calcium levels play a crucial role in triggering these damaging indirect cellular events.
Area of Science:
- Cell Biology
- Biochemistry
- Toxicology
Background:
- Exposure to oxygen free radicals, generated during foreign compound metabolism, induces cellular damage.
- This damage, originating from both extracellular and intracellular sources, can ultimately lead to cell death.
- Cytopathological processes involve direct free radical attacks on vital macromolecules and indirect activation of catabolic enzymes.
Purpose of the Study:
- To elucidate the mechanisms of cell damage and death induced by oxidative stress.
- To investigate the role of free radicals in cellular injury.
- To understand the contribution of calcium ions to oxidative stress-induced cytopathology.
Main Methods:
- Cell culture techniques to expose isolated cells to oxidative stress.
- Analysis of cellular damage and death pathways.
- Measurement of intracellular calcium ion concentrations during oxidative stress.
Main Results:
- Oxygen free radicals cause significant damage to essential macromolecules within cells.
- Indirect activation of catabolic processes, including proteases, endonucleases, and phospholipases, contributes to cell death.
- Cytosolic calcium (Ca2+) concentration significantly increases above physiological levels during oxidative stress, playing a key role in initiating these indirect destructive events.
Conclusions:
- Oxidative stress is a critical factor in cell damage and death.
- Multiple pathways, both direct and indirect, mediate free radical-induced cellular injury.
- Elevated intracellular calcium is a key mediator in the cascade of events leading to cell death under oxidative stress.
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