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Dopamine effect on the mitochondria potential in B lymphocytes of schizophrenic patients and normal controls
Ahmed M Elkashef1, Heba Al-Barazi, Dianne Venable
1Clinical Trials Branch, NIDA, Bethesda, MD 20892-9551, USA. ae8a@nih.gov
Abstract:
Brain metabolic abnormalities and aberrant dopamine (DA) metabolism have been reported in patients with schizophrenia. The authors hypothesized that mitochondria is a primary target of damage by increased free radical generation secondary to increased DA metabolism by monoamine oxidase (MAO). Epstein-Barr virus (EBV)-transformed human B-lymphocytes cell lines derived from patients with schizophrenia and normal controls were incubated in the absence or presence of DA, hydrogen peroxide (H2O2), or rotenone (Rot). The cells were then stained with rhodamine 123 (Rh 123) and analyzed for uptake using flow cytometry. Compared with untreated cells, DA significantly decreased Rh 123 uptake by the mitochondria. This effect was similar to the control cells treated with H2O2 or Rot. Nevertheless, there were no differences in Rh 123 uptake between the cells of schizophrenic patients and normal controls. This study shows that DA can impair the mitochondria membrane potential but that mechanism may not be evident in schizophrenia.
Insights
Dopamine (DA) impairs mitochondrial function in cell models, but this mechanism was not evident in schizophrenia patients. Further research is needed to understand brain metabolic abnormalities in schizophrenia.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Schizophrenia is associated with brain metabolic abnormalities and altered dopamine (DA) metabolism.
- Increased free radical generation from DA metabolism by monoamine oxidase (MAO) may damage mitochondria.
Purpose of the Study:
- To investigate the hypothesis that mitochondria are a primary target of damage in schizophrenia due to increased DA metabolism.
- To examine the effect of DA on mitochondrial membrane potential in Epstein-Barr virus (EBV)-transformed B-lymphocytes from schizophrenia patients and normal controls.
Main Methods:
- EBV-transformed B-lymphocytes from schizophrenia patients and controls were incubated with DA, H2O2, or rotenone (Rot).
- Mitochondrial membrane potential was assessed by rhodamine 123 (Rh 123) uptake using flow cytometry.
Main Results:
- DA significantly decreased Rh 123 uptake, indicating impaired mitochondrial membrane potential, similar to H2O2 or Rot treatment.
- No significant differences in Rh 123 uptake were observed between cells from schizophrenia patients and normal controls.
Conclusions:
- Dopamine can impair mitochondrial membrane potential.
- This specific mechanism of DA-induced mitochondrial dysfunction may not be directly evident or applicable in schizophrenia patients.