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Polimorphonuclear cell-mediated oxidative stress: sink for reactive oxygen species and cell various type damage
M Sisto1, A Acquafredda, V Mitolo
1Department of Human Anatomy and Histology, University of Bari, Policlinico, Italy. m.sisto@anatomia.uniba.it
Abstract:
Reactive oxygen species (ROS) are produced in animals and humans under physiologic and pathologic conditions. Polymorphonuclear cells (PMNs) and other professional phagocytes are able to generate large amounts of ROS that have not only antimicrobial capacity but are also deleterious to mammalian cells and responsible for many chronic diseases. In particular, ROS produced in large amounts by the massively infiltrating leukocytes in inflammed tissues are believed to constitute a major tissue-destructive force and may contribute significantly to the pathogenesis of several inflammatory diseases. Inflammation can accelerate the development of cancer: in fact, it seems that a part of the predisposition to cancer may be attributed to the oxidants released by the phagocytes at inflammatory site and then to the effects of continuous damage over a life span by ROS. The focus of this study was to investigate the differential capacity of ROS capture and the relative cellular damage degree in gastric, intestinal and fibroblastic cell lines. These various cell types were in vitro used as sink for ROS released by co-cultured fMLP-stimulated human polymorphonuclear cells. Our data demonstrated that cell lines showed a differential capacity of ROS capture correlated to cellular damage, probably due to a different cell susceptibilty to the oxidative challenge produced by stimulated PMNs.
Insights
Reactive oxygen species (ROS) cause cellular damage and chronic diseases. Different cell types exhibit varying susceptibility to ROS-induced damage, impacting disease pathogenesis.
Area of Science:
- Biochemistry
- Cell Biology
- Immunology
Background:
- Reactive oxygen species (ROS) are generated during physiological and pathological processes.
- Polymorphonuclear cells (PMNs) produce ROS with antimicrobial functions, but also cause cellular damage and contribute to chronic diseases.
- Inflammation-associated ROS are implicated in tissue destruction and cancer development.
Purpose of the Study:
- To investigate the differential capacity of ROS capture among various cell lines.
- To assess the relative cellular damage in gastric, intestinal, and fibroblastic cells exposed to ROS.
- To understand the role of cellular susceptibility in oxidative stress-induced damage.
Main Methods:
- In vitro co-culture of fMLP-stimulated human PMNs with gastric, intestinal, and fibroblastic cell lines.
- Measurement of ROS capture capacity by different cell types.
- Evaluation of cellular damage resulting from ROS exposure.
Main Results:
- Gastric, intestinal, and fibroblastic cell lines demonstrated differential ROS capture capacities.
- The degree of cellular damage correlated with the cell lines' capacity for ROS capture.
- Variations in cellular susceptibility to oxidative stress from stimulated PMNs likely explain the observed differences.
Conclusions:
- Cellular susceptibility to ROS varies significantly among different cell types.
- This differential susceptibility influences the extent of cellular damage during inflammatory processes.
- Understanding these variations is crucial for comprehending the pathogenesis of ROS-related diseases.
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