Selenium-carrageenan modulates arsenic bioaccessibility in simulated gastrointestinal bio-fluids: Dual mechanisms of gastric promotion and intestinal inhibition

Inorganic arsenic (As) exposure via oral ingestion poses significant carcinogenic risks, with bioaccessibility in the gastrointestinal tract critical for risk assessment. Selenium (Se), an essential micronutrient, exhibits paradoxical effects on As toxicity, yet its mechanistic role in modulating As bioavailability during digestion remains poorly understood. This study investigates the dual-phase impact of selenated carrageenan (Se-car), a cost-effective organic Se supplement, on As bioaccessibility using an in vitro simulated digestion model. Results show that Se-car (50 g/L) enhances total As, As(III), and As(V) bioaccessibility by 22.28 %, 20.00 %, and 22.53 % during gastric digestion (pH 1.5, 1 h), driven by competitive adsorption of Se-car's anionic groups on hematite surfaces, proton dissociation, and pepsin-mediated reductive dissolution. Conversely, in intestinal digestion (pH 6.5, 8 h), Se-car suppresses total As, As(III), and As(V) bioaccessibility release by 8.51 %, 9.08 %, and 4.71 % through molecular entanglement, enzyme encapsulation, and reduced Fe(II) solubility. Elevated NaCl concentrations (0.01–1 M) synergistically inhibit As release by 7.28 % (gastric) and 2.47 % (intestinal), attributable to ionic shielding-induced Se-car chain contraction. Mechanistic insights indicate gastricization relies on acidic dissolution and Se-car–pepsin interactions, while intestinal inhibition stems from Se-car-trypsin binding and surface passivation. Health risk assessments demonstrate Se-car exacerbates gastric-phase THQ values of As (children: 5.20 → 16.97) but mitigates intestinal-phase risks (children: 9.14 → 3.99). This work elucidates pH- and ionic strength-dependent Se-car behaviors, offering novel insights for optimizing dietary Se interventions in As-endemic regions. The dual-phase regulatory mechanism highlights the importance of digestive-phase-specific risk management and provides a foundation for developing polysaccharide-based As antagonists targeting complex gastrointestinal environments.