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Annals of Indian Academy of Neurology
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ORIGINAL ARTICLE
Year : 2021  |  Volume : 24  |  Issue : 4  |  Page : 506-512

Alteration of mitochondrial function in oxidative stress in parkinsonian neurodegeneration: A cross-sectional study


1 Department of Laboratory Medicine; Departments of Neurology, All India Institute of Medical Sciences, New Delhi, India
2 Department of Neurology, All India Institute of Medical Sciences, New Delhi, India
3 Jai Prakash Narayan Apex Trauma Centre, All India Institute of Medical Sciences, New Delhi, India
4 Department of Laboratory Medicine, All India Institute of Medical Sciences, New Delhi, India
5 Department of Laboratory Medicine, All India Institute of Medical Sciences, New Delhi; Department of Pathology, North DMC Medical College and Hindu Rao Hospital, Delhi, India

Correspondence Address:
Prof. Asok Kumar Mukhopadhyay
Department of Pathology, North DMC Medical College and Hindu Rao Hospital, Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aian.AIAN_392_20

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Context: Appropriate mitochondrial function and oxidative balance are critical to neuronal survival. Accumulation of reactive oxygen species leads to oxidative stress that can cause free radical damage to biomolecules of the cell components and the molecules in the cellular milieu that eventually lead to a variety of chronic diseases including neurodegenerative disorders. Mitochondrial dysfunction initiates neuronal apoptosis thereby leading to neurodegenerative diseases including Parkinson's disease (PD). Aim: To evaluate oxidative stress vis-a-vis mitochondrial function (Cytochrome C oxidase activity) in PD patients, Parkinson plus syndrome (PPS) patients in comparison with healthy controls (HCs). Settings and Design: Cross-sectional Study Methods: We assessed oxidative stress by chemiluminescence using luminol, and cytochrome c oxidase activity (CCO) by CCO kit using spectrophotometry in PD patients (n = 80), PPS patients (n = 40), and HCs (n = 40). Statistical Analysis: Data were presented as number (%) or mean ± SD/median as approximate. Quantitative baseline variables were compared among the groups using one-way ANOVA and qualitative variables were compared using Chi-square test. The difference in median was compared using Kruskal–Wallis test followed by Post-hoc Bonferronni correction. Results: Compared to HCs (Median 7.53 ± 15.58 RLU/sec/cell), ROS level in PD (14.13 ± 29.5), and PPS (17.43 ± 15.91) patients was significantly higher (P = 0.0029: HC vs, PD & P = 0.0500: HC vs. PPS). Also, ROS in PD patients (14.13 ± 29.5) was higher that PPS patients (17. 43 ± 15.91) but the difference was not statistically significant (P = 0.84). The CCO activity was found to be diminished in PD (Median: 0.025 ± 0.013 units/ml) and PPS patients (0.027 ± 0.008) in comparison to HCs (0.117 ± 0.049). Conclusion: Mitochondrial dysfunction and oxidative stress is associated with PD and PPS and may play an important role in etiopathogenesis. Though the cause–effect conundrum has not been comprehensively probed but addressing oxidative stress and mitochondrial damage may serve as an adjunctive therapy for PD and PPS. Iron metabolism as reflected in the red cell indices may aid in differentiating PD from PPS.


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