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LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism
Published on: April 4, 2016
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Exogenous carbon monoxide prevents a decrease of mitochondrial membrane potential in lipopolysaccharide-stimulated
Tomiko Yakura1, Eri Nanizawa2, Yutaro Natsuyama1
1Department of Anatomy, Tokyo Medical University.
The Journal of Toxicological Sciences
|November 3, 2025
Summary
Carbon monoxide (CO) prevents lipopolysaccharide (LPS)-induced platelet activation by maintaining mitochondrial membrane potential (ΔΨm). This study shows CO inhibits inflammatory responses in platelets.
Area of Science:
- Biochemistry
- Immunology
- Cell Biology
Background:
- Acute inflammation involves lipopolysaccharide (LPS) and platelet activation.
- Carbon monoxide (CO) is an endogenous gas with known anti-inflammatory properties.
- CO interacts with mitochondria, influencing cellular processes.
Purpose of the Study:
- To investigate the effect of CO on mitochondrial membrane potential in LPS-activated human platelets.
- To elucidate the protective role of CO against LPS-induced platelet activation.
Main Methods:
- Human platelets were stimulated with LPS (10 μg/mL).
- Platelets were treated with CO or a CO-releasing molecule (CORM-2).
- Mitochondrial membrane potential (ΔΨm), lactate levels, and morphology were assessed.
Main Results:
- LPS treatment depolarized platelet mitochondrial membrane potential (ΔΨm) and increased lactate levels.
- CO and CORM-2 treatments prevented ΔΨm depolarization and lactate increase.
- LPS-induced morphological changes in platelets were inhibited by CO.
Conclusions:
- CO preserves platelet mitochondrial membrane potential (ΔΨm) against LPS-induced depolarization.
- CO effectively inhibits LPS-mediated platelet activation.
- CO represents a potential therapeutic agent for inflammatory conditions involving platelets.
