Modulation of the Mitochondrial ION Channel by Reactive Oxygen Species and Neurodegeneration
Journal Title: The 2nd Annual Meeting of International Center for Neuroscience Research - Year 2021, Vol 2, Issue 1
Abstract
Mitochondria serves as a vital transit point for the transports of ions and metabolites across its transmembrane. On the other hand, these ions and metabolites conduct a significant role in the regulation of normal neurophysiology or neuro-pathophysiology. Mitochondria are double membrane-bound organelle, anchoring a wide range of transport proteins. The outer mitochondrial membrane accommodates one of the most significant ion channels called Voltage-Dependent Anion Channel (VDAC). It has been reported that VDAC is modulated by various neuronal metabolites such as glutamate, dopamine, β-amyloid, α-synuclein, etc. Thus, VDAC can act as a decisive factor for neurological disorders like Alzheimer’s disease. HTL, a non-standard amino acid present in brain cells is toxic to neurons. However, the underlining mechanism of HTL’s action appears to be complicated and partially understood. Within this perspective, we proposed that VDAC could be one of the major plausible target proteins for HTL. It is of great significance to find out how HTL elicits its action on VDAC during neuronal oxidative stress. Our objective was to discover the impact of HTL on VDAC’s functional properties under oxidative stress using a bilayer lipid membrane (BLM) electrophysiology technique. Our experimental results suggest that HTL modulates VDAC in a concentration-dependent manner under normal conditions, and vice versa under oxidative stress. Based on our in vitro data, we propose a plausible interpretation of the role of HTL in the mitochondriamediated progression of neurodegeneration and hence, neurological disorders. However, the aforesaid proposed mechanism needs to be further substantiated by in vivo studies.
Authors and Affiliations
T. Daniel Tuikhang Koren* and Subhendu Ghosh
Keywords
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