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The effect of acute or/and chronic stress on the MnSOD protein expression in rat prefrontal cortex and hippocampus
Dragana Filipović1, Jelena Zlatković, Snezana B Pajović
1Laboratory of Molecular Biology and Endocrinology, Institute of Nuclear Sciences "Vinca", P.O.Box 522-090, 11001 Belgrade, Serbia. dragana@vinca.rs
Abstract:
Manganese superoxide dismutase (MnSOD) is the major antioxidant in mitochondria that protect brain from neuroendocrine stress. Although MnSOD is localized in the mitochondria, the immediate subcellular distribution of MnSOD protein level in the prefrontal cortex and hippocampus of Wistar male rats exposed to acute stressors immobilization or cold, chronic stress isolation or their combinations (acute/chronic) have not been studied. Western immunoblotting revealed that acute immobilization stress resulted in an increase in mitochondrial MnSOD protein level, whereas chronic isolation compromises MnSOD protein level. Chronically stressed animals exposed to novel acute stressors showed a significant decrease in mitochondrial MnSOD protein level and reciprocal increase in this protein in the cytosolic fraction. At the same time, a significant increase in serum corticosterone level was observed after acute stressors, whereas chronic isolation led to negligable changes and caused a reduced responsiveness to a novel acute stressors. Presence of cytochrome c in mitochondrial and cytosolic fraction of both brain structures was also confirmed. Results suggest that chronic stress isolation results in mitochondrial dysfunction and MnSOD release into the cytosol.
Insights
Chronic stress disrupts mitochondrial antioxidant defense in the brain. Manganese superoxide dismutase (MnSOD) levels decrease in mitochondria and increase in the cytosol, indicating dysfunction.
Area of Science:
- Neuroscience
- Biochemistry
- Stress Physiology
Background:
- Mitochondria are crucial for cellular energy and antioxidant defense.
- Manganese superoxide dismutase (MnSOD) is a key mitochondrial antioxidant protecting the brain.
- Subcellular distribution of MnSOD under various stress conditions is not well understood.
Purpose of the Study:
- To investigate the subcellular distribution of MnSOD in rat brain regions under acute and chronic stress.
- To assess the impact of different stress types (immobilization, cold, isolation) and combinations on MnSOD levels.
- To correlate MnSOD changes with serum corticosterone and mitochondrial integrity.
Main Methods:
- Western immunoblotting was used to quantify MnSOD protein levels.
- Experiments involved Wistar male rats exposed to acute immobilization, cold, chronic isolation, and combined stressors.
- Serum corticosterone levels were measured, and cytochrome c presence confirmed mitochondrial and cytosolic fractions.
Main Results:
- Acute immobilization stress increased mitochondrial MnSOD.
- Chronic isolation stress decreased mitochondrial MnSOD.
- Combined acute/chronic stress led to decreased mitochondrial MnSOD and increased cytosolic MnSOD.
- Serum corticosterone increased with acute stress but showed blunted response after chronic isolation.
Conclusions:
- Chronic stress, particularly isolation, impairs mitochondrial function.
- Stress-induced mitochondrial dysfunction leads to MnSOD release into the cytosol.
- This redistribution suggests a protective mechanism or a marker of cellular damage under chronic stress.
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