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Updated: Apr 26, 2026
Measuring Oxidative Stress Resistance of Caenorhabditis elegans in 96-well Microtiter Plates
Published on: May 9, 2015
Early-life redox perturbation programs intergenerational redox vulnerability through DAF-16/FOXO and SKN-1/Nrf2
Jingyimei Liang1, Yuxuan Zhao2, Yitong Xie3
1College of Food Science and Technology, Northwest University, Xi'an, 710069, China; Universidade de Vigo, Nutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty of Science, Ourense, 32004, Spain; Instituto de Agroecoloxía e Alimentación (IAA), Universidade de Vigo, Campus Auga, Ourense, 32004, Spain; Key Laboratory of Food Safety of Shaanxi Provincial Higher Education Institutions, Northwest University, Xi'an, 710069, China.
Abstract:
Early metabolic stress is a key factor influencing long term intergenerational adaptation in organisms. While excessive dietary methionine is known to disrupt one-carbon metabolism, it remains unclear whether early gestational methionine excess induces sustained epigenetic remodeling, thereby affecting redox stability in offspring. Using C. elegans as a model, we demonstrate that early gestational methionine excess in parental induces sustained metabolic stress in offspring, impairing their functional stability. This manifests as impaired motility, shortened lifespan, and elevated oxidative stress levels. Mechanistically, this intergenerational vulnerability is associated with metabolic reprogramming towards a serine-glycine-one-carbon axis. This leads to methyl donor imbalance and chromatin remodeling, characterized by SET-2/WDR-5.1 dependent H3K4 hypermethylation. Meanwhile, the stress response programs of DAF-16/FOXO and SKN-1/Nrf2 are restricted, thus affecting the redox adaptability of the offspring. Importantly, intervention with the dietary polyphenol epigallocatechin gallate (EGCG) can restore metabolic homeostasis and alleviate these chromatin and transcriptional restrictions. In summary, our findings reveal a metabolic and epigenetic framework by which early-life nutritional imbalances influence intergenerational redox resilience. We also emphasize that EGCG represents a potential nutritional strategy to alleviate metabolic stress caused by methionine excess.
