Essential Amino Acid Starvation-Induced Oxidative Stress Causes DNA Damage and Apoptosis in Murine Osteoblast-like Cells

Intracellular nutrient metabolism, particularly the metabolism of essential amino acids (EAAs), is crucial for cellular functions, including energy production and redox homeostasis. An EAA deficiency can lead to cellular dysfunction and oxidative stress. This study explores the mechanisms underlying...

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Bibliographic Details
Published in:International journal of molecular sciences 2023-10, Vol.24 (20), p.15314
Main Authors: Li, Runbo, Kato, Hirohito, Fumimoto, Chihiro, Nakamura, Yurika, Yoshimura, Kimihiro, Minagawa, Emika, Omatsu, Keiju, Ogata, Chizuko, Taguchi, Yoichiro, Umeda, Makoto
Format: Article
Language:English
Subjects:
Acetylcysteine
Amino acids
Analysis
Antioxidants
Apoptosis
Cell cycle
Cell growth
DNA
DNA damage
essential amino acids
Gene expression
Glucose
Homeostasis
Metabolism
osteoblasts
Oxidative stress
Protein expression
Protein synthesis
Proteins
ROS
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Summary:Intracellular nutrient metabolism, particularly the metabolism of essential amino acids (EAAs), is crucial for cellular functions, including energy production and redox homeostasis. An EAA deficiency can lead to cellular dysfunction and oxidative stress. This study explores the mechanisms underlying cellular responses to EAA starvation, focusing on ROS-induced DNA damage and apoptosis. MC3T3-E1 cells were subjected to EAA starvation, and various assays were conducted to assess cell proliferation, survival, DNA damage, and apoptosis. The antioxidant N-acetylcysteine (NAC) was employed to block ROS formation and mitigate cellular damage. Gene expression and Western blot analyses were performed to elucidate molecular pathways. EAA starvation-induced ROS generation, DNA damage, and apoptosis in MC3T3-E1 cells. NAC administration effectively reduced DNA damage and apoptosis, highlighting the pivotal role of ROS in mediating these cellular responses during EAA deficiency. This study demonstrates that EAA starvation triggers ROS-mediated DNA damage and apoptosis, offering insights into the intricate interplay between nutrient deficiency, oxidative stress, and programmed cell death. NAC emerges as a potential therapeutic intervention to counteract these adverse effects.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms242015314