Dietary plant-derived lectins induce oxidative stress, metabolic dysfunction, apoptosis and neuroinflammation in mice brain

<b>Background:</b> Lectins are carbohydrate-binding proteins found in plants and animals. While they serve essential biological functions, certain plant-derived lectins-especially from legumes-may exert neurotoxic effects through the gut-brain axis. The growing intake of raw plant-based foods, including lectin-rich sprouts, raises safety concerns.<b>Objective:</b> To evaluate the neurotoxic potential of a galactose-specific lectin (BS-Gal) isolated from bean sprouts, with a focus on oxidative stress, energy metabolism, and neuroinflammation in mice.<b>Methods:</b> Mice were chronically administered BS-Gal orally. Brain regions (substantia nigra, cerebellum, brainstem) were analyzed for oxidative markers, metabolic enzymes, apoptotic signals, and inflammatory mediators using biochemical assays and immunoblotting.<b>Results:</b> BS-Gal significantly increased hydrogen peroxide, nitric oxide, and malondialdehyde levels, alongside reduced antioxidant enzyme activities, indicating oxidative damage. Glycolytic and citric acid cycle enzymes were suppressed, suggesting disrupted cellular metabolism. Apoptotic analysis revealed elevated pro-apoptotic markers (Bad, Bax) and reduced anti-apoptotic proteins (Bcl-2, Bcl-xL). Neuroinflammation was evident via NF-κB activation, increased proinflammatory cytokines (TNF-α, IL-6, IL-1β), and decreased anti-inflammatory markers (IκB-α, IL-4, IL-10, TGF-β).<b>Conclusion:</b> Chronic oral exposure to BS-Gal induces oxidative stress, metabolic dysfunction, and neuroinflammation in key mouse brain regions. These findings suggest potential neurotoxic risks associated with dietary intake of lectin-rich plant foods like bean sprouts.