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Related Experiment Video

Updated: May 11, 2026

Mitochondrial Preparation from Microglia for Glycan Analysis
06:40

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Published on: May 30, 2025

Glucocorticoids increase protein carbonylation and mitochondrial dysfunction.

V M Tang1, A H Young, H Tan

  • 1Department of Psychiatry, University of British Columbia, Vancouver, Canada.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|May 15, 2013
PubMed
Summary

Excessive glucocorticoids, like corticosterone, increase protein damage in brain cells by impairing mitochondrial function and reducing antioxidant defenses, specifically superoxide dismutase (SOD). This suggests a link between stress hormones and oxidative stress in psychiatric conditions.

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Published on: January 19, 2017

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Psychiatric illnesses are linked to prolonged glucocorticoid release, potentially harming neurons.
  • Oxidative stress, an imbalance between reactive oxygen species (ROS) and antioxidants, is implicated in psychiatric disorders.
  • Mitochondria and NADPH oxidase are key sources of ROS, while antioxidant enzymes like SOD and CAT combat oxidative damage.

Purpose of the Study:

  • To investigate the impact of glucocorticoids on oxidative damage in neuronal cells.
  • To assess effects on protein carbonylation, mitochondrial function, NADPH oxidase activity, and antioxidant capacity.

Main Methods:

  • Rat pheochromocytoma PC12 cells were treated with varying concentrations of corticosterone for 24 hours.
  • Assays were performed to measure protein carbonylation, mitochondrial complex I and III activity, NADPH oxidase activity, total antioxidant capacity, and SOD and catalase activity.

Main Results:

  • Corticosterone treatment elevated protein carbonylation.
  • Mitochondrial complex I activity decreased, while complex III and NADPH oxidase activities remained unchanged.
  • Total antioxidant capacity increased at the lowest dose, but SOD activity significantly decreased at the highest dose.
  • Catalase activity was unaffected.

Conclusions:

  • Glucocorticoids can induce oxidative damage to proteins in neuronal cells.
  • Inhibition of mitochondrial complex I and the antioxidant enzyme SOD may contribute to this damage.
  • Findings suggest a mechanism linking stress hormone excess to neuronal oxidative stress relevant to psychiatric illnesses.