Galactose-specific lectin from bean sprouts induces oxidative stress, inflammation, and apoptosis in the mouse liver

BS-Gal, a galactose-specific lectin isolated from bean sprouts and highly resistant to digestive degradation, caused significant hepatocellular and hepatobiliary injury in BALB/c mice after 20 days of oral exposure. Plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and bilirubin were markedly elevated, indicating impaired liver function. Antioxidant defences were disrupted, with reduced activities of superoxide dismutase (SOD) and catalase (CAT) and compensatory increases in glutathione peroxidase (GPx) and glutathione reductase (GR), accompanied by elevated hepatic hydrogen peroxide (H 2 O 2 ), nitric oxide (NO), and malondialdehyde (MDA), reflecting pronounced oxidative and nitrosative stress. This oxidative imbalance was associated with strong activation of nuclear factor kappa B (NF-κB) and increased production of proinflammatory cytokines IL-6, IL-1β, and TNF-α. Moreover, BS-Gal shifted apoptotic signalling toward cell death by upregulating proapoptotic proteins BAD and BAX and downregulating the antiapoptotic protein Bcl-2. Collectively, these findings demonstrate that BS-Gal induces coordinated oxidative, inflammatory, and apoptotic hepatic damage, emphasising potential health risks linked to the consumption of raw bean sprouts containing biologically active lectins.