Dietary L-Se-methylselenocysteine suppresses liver tumor progression via integrated antioxidant, immune, and apoptotic modulation in mice.

L-Se-methylselenocysteine (L-SeMC) is a naturally occurring organic selenium compound with superior bioavailability and safety compared to inorganic forms. Although proposed to possess antitumor potential, its efficacy in hepatic tumor prevention and intervention remains poorly characterized. This study investigated the long-term preventive and short-term interventional effects of L-SeMC on hepatic tumor development in a mouse model. Tumor progression, oxidative stress, cytokine profiles, apoptosis-related gene and protein expression, and tumor cell apoptosis were comprehensively assessed. L-SeMC significantly inhibited tumor growth, with inhibition rates reaching 66.63% in the high-dose preventive cohort and 73.56% in the preventive-acute continuous intervention cohort. These effects were attributed to the enhancement of antioxidant defenses, as evidenced by increased levels of SOD, CAT, GPx, and GSH, and decreased MDA levels. Additionally, cytokine modulation was observed, with upregulation of IL-4, IL-10, TNF-α, and IFN-γ. Furthermore, apoptotic signaling was activated, marked by elevated levels of Bax, caspase-8/9, and an increased Bax/Bcl-2 ratio, corroborated by TUNEL staining. Remarkably, L-SeMC demonstrated these advantages without causing toxicity or exerting any detrimental effects on body weight or immune organ indices. Overall, the findings highlight L-SeMC as a food-derived bioactive compound capable of integrating antioxidant, immunomodulatory, and apoptotic mechanisms to suppress hepatic tumor progression. This work provides an experimental basis for developing L-SeMC-enriched functional foods and dietary strategies for hepatic tumor prevention.