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Oxidative Stress Induced by Cortisol in Human Platelets.

Maria Grazia Signorello1, Silvia Ravera2, Giuliana Leoncini1

  • 1Biochemistry Laboratory, Department of Pharmacy, University of Genoa, 16132 Genova, Italy.

International Journal of Molecular Sciences
|April 13, 2024
PubMed
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Cortisol significantly increases oxidative stress in human platelets by stimulating reactive oxygen species (ROS) production and depleting antioxidant defenses. This hormonal effect is linked to thrombosis and cardiovascular disease risk.

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Area of Science:

  • Biochemistry
  • Hematology
  • Molecular Biology

Background:

  • Hypercortisolism impacts platelet function, but exogenous cortisol effects are poorly understood.
  • Existing research on cortisol's influence on human platelets yields conflicting results.

Purpose of the Study:

  • To investigate the impact of exogenous cortisol on oxidative stress markers in human platelets.
  • To elucidate the enzymatic pathways and ROS sources involved in cortisol-induced platelet oxidative stress.

Main Methods:

  • Analysis of reactive oxygen species (ROS) production, superoxide anion formation, and lipid peroxidation.
  • Measurement of glutathione (GSH) and membrane thiol (SH-group) content.
  • Assessment of enzyme involvement (src, syk, PI3K, AKT) and inhibition studies using specific pathway modulators (e.g., NADPH oxidase inhibitors, mitochondrial respiratory chain inhibitors).

Main Results:

  • Cortisol significantly elevated ROS production, superoxide anion formation, and lipid peroxidation in platelets.
  • Cortisol decreased platelet GSH and membrane SH-group content, indicating depletion of antioxidant defenses.
  • Involvement of src, syk, PI3K, and AKT enzymes was demonstrated; NADPH oxidase 1 activity and uncoupled oxidative phosphorylation were identified as key ROS sources.

Conclusions:

  • Exogenous cortisol potentiates oxidative stress in human platelets by enhancing ROS generation and impairing antioxidant capacity.
  • Cortisol-induced platelet oxidative stress involves NADPH oxidase 1 and mitochondrial complex I/III, but not complex II/IV.
  • This cortisol-mediated platelet oxidative stress may contribute to arterial and venous thrombosis, increasing cardiovascular disease risk.