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F92. ASSESSMENT OF CELLULAR HEALTH ON ETHANOL-INDUCED TOXICITY IN HUMAN NEURAL PRECURSOR CELLS
Alcohol use disorders (AUDs), including alcohol abuse and dependence, is one of the most common neuropsychiatric disorders. Nearly 5.1 % of the global burden of disease is attributable to alcohol consumption. In animal models, alcohol is known to disrupt neurogenesis. Bioenergetic maladaptation incl...
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Published in: | European neuropsychopharmacology 2024-10, Vol.87, p.254-254 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | Alcohol use disorders (AUDs), including alcohol abuse and dependence, is one of the most common neuropsychiatric disorders. Nearly 5.1 % of the global burden of disease is attributable to alcohol consumption. In animal models, alcohol is known to disrupt neurogenesis. Bioenergetic maladaptation including adverse effects on mitochondrial biogenesis is identified as one such mechanism involved in ethanol induced toxicity. However, the cellular and molecular mechanisms underlying AUD pathophysiology in the central nervous system still remain poorly understood. The current study aims to investigate the impact of in vitro ethanol exposure on cellular and mitochondrial health using human neural progenitor cells (NPCs).
Well characterized human male NPC line XCL-1 (XCell Science Inc) was used for the study. Dose-dependent alteration in cell viability of NPCs subjected to in vitro ethanol exposure for 48 hours was assayed by the MTT assay. Changes in reactive oxygen species (ROS) levels and mitochondrial biogenesis on in vitro ethanol exposure was analyzed in NPCs.
The cell viability was noted to be reduced across ethanol concentrations ranging from 20 mM to 500 mM. Cellular ROS detected by DCFDA assay showed higher ROS levels with in vitro exposure to ethanol (50mM and 200mM) in NPCs. Ethanol exposure to NPCs did not show significant alteration in mitochondrial DNA copy number.
Our primary motivation was to detect ethanol induced cellular and mitochondrial health abnormalities. And indeed, we find an increased level of cellular ROS in vitro exposure to ethanol. A potent link for the ROS and alterations in mitochondrial biogenesis would be further investigated on ethanol induced toxicity. In future experiments, I intend to investigate the alterations in mitochondrial membrane potential and cellular ATP, post in vitro exposure to ethanol in NPCs. |
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ISSN: | 0924-977X |
DOI: | 10.1016/j.euroneuro.2024.08.503 |