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[PRODUCTION OF REACTIVE OXYGEN SPECIES AND DEVELOPMENT OF APOPTOSIS IN BLOOD LEUKOCYTES IN EXPERIMENTAL
O Yaremchuk1, K Posokhova1, P Lykhatskyi1
11I. Horbachevsky Ternopil National Medical University, Ukraine.
Antiphospholipid syndrome (APS) in mice increases apoptosis and decreases reactive oxygen species (ROS) in blood cells. This suggests enhanced apoptosis and deficient ROS formation are key in APS development.
Area of Science:
- Immunology
- Pathobiology
Background:
- Antiphospholipid syndrome (APS) is an autoimmune disorder.
- Understanding cellular mechanisms in APS is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate apoptosis and reactive oxygen species (ROS) formation in blood cells of mice with experimental APS.
- To evaluate the impact of APS on leukocyte viability and population dynamics.
Main Methods:
- Flow cytometry was used to assess apoptosis (Annexin V/propidium iodide) and ROS levels (2',7'-dichlorofluorescein diacetate) in mouse blood leukocytes.
- Cell viability and light scattering (FS/SS) were analyzed to differentiate leukocyte populations.
Main Results:
- APS significantly reduced blood leukocyte viability compared to controls, partly due to apoptosis.
- A redistribution of leukocyte populations was observed, with an increase in granulocytes.
- Basal ROS production decreased in both granulocytes (27%) and agranulocytes (19%) in APS mice.
Conclusions:
- Enhanced apoptosis and deficient ROS formation are significant in the pathobiochemical mechanisms of experimental APS.
- These findings highlight potential therapeutic targets within cellular apoptosis and ROS pathways in APS.
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