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Alcohol‐induced damage and death to developing and differentiated neurons.
Author(s) -
Carter Wayne,
Wijayamunige Buddhika,
Wijesekara Anusha
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.03933
Subject(s) - neural stem cell , programmed cell death , neurodegeneration , reactive oxygen species , progenitor cell , alcohol , viability assay , apoptosis , neurotoxicity , oxidative stress , retinoic acid , microbiology and biotechnology , chemistry , biology , biochemistry , stem cell , medicine , toxicity , disease , gene
Alcohol intoxication can induce foetal alcohol spectrum disorder after prenatal exposures, as well as damage neurons and contribute to neurodegeneration and cognitive decline in adults. The effect of alcohol on driving altered cellular mechanisms and post‐translational modification of proteins was investigated in both undifferentiated and differentiated human neural progenitor cells and SH‐SY5Y neuronal cells to mimic alcohol exposures during neuronal development and in adults. Human neural progenitor cells were differentiated into neuronal cells upon growth factor withdrawal, while all‐trans retinoic acid and brain‐derived nutrient factor were applied to differentiate SH‐SY5Y cells prior to a challenge with 0–200 mM alcohol for 3, 6, 12, or 24 hours. Alcohol exposure induced cell cytotoxicity in a concentration and time‐dependent fashion, with cell viability assessed using MTT, ATP, and LDH assays. Reactive oxygen species (ROS) generated in response to alcohol treatment were quantified using a dichlorofluorescin diacetate assay. The accumulation and quantitation of oxidatively damaged proteins was assessed by quantitation of protein carbonyl content and specific carbonyl group immuno‐blotting. In summary, at commonly encountered alcohol exposures, alcohol triggered cellular damage and death in developing as well as differentiated neurons. Support or Funding Information Commonwealth Scholarship Commission