Chronic consumption of oxidatively modified rice bran protein accelerates aging process in C. elegans by suppressing DAF-16 and SKN-1 pathways

• Oxidized RBP shortened the lifespan and accelerated the aging process of C. elegans . • Oxidized RBP impaired mobility and induced oxidative damage of C. elegans . • The SKN-1 and DAF-16 participated in the shortened lifespan of C. elegans . Rice bran (RB), a promising source of premium protein, inevitably undergoes rancidity during rice milling, leading to oxidation of rice bran protein (RBP), along with changes in its structure and nutrition. Previous research has found that oxidatively modified RBP induces in vivo oxidative damage via oxidation-extent and consumption-period dependent patterns, but its accumulation effects of chronic consumption on aging progress remain unclear. Thus, Caenorhabditis elegans ( C. elegans ) was utilized to investigate the impacts of chronic exposure to oxidatively modified RBP on lifespan, healthspan, and related molecular pathways. Results demonstrated that chronic consumption of oxidatively modified RBP reduced the maximum and average lifespan in wild-type nematodes, with moderately and excessively oxidative-modified RBP shortening average lifespan by 9.46% and 18.40%, respectively. A 36-h treatment of oxidatively modified RBP exacerbated aging-related biomarkers, including lipofuscin accumulation, mobility decline, and oxidative stress. Furthermore, oxidatively modified RBP inhibited the transcription activity and nuclear translocation of DAF-16 and SKN-1, key regulators of stress resistance and longevity. The lifespan of daf-16 and skn-1 gene-deficient nematodes confirmed the essential role of DAF-16 and SKN-1 in oxidatively modified RBP shortening the lifespan of C. elegans. Results implied that chronic consumption of oxidatively modified RBP accelerated the aging and health-aging process, in which DAF-16 and SKN-1-mediated IIS and p38 MAPK pathways played significant role. This study systematically evaluated the health response of chronic consumption of oxidatively modified protein and mechanism involved, providing a theoretical basis for target nutritional guidelines.