Food-borne carbon dots (FCDs) are ubiquitous nanoparticles in food thermal processing, which might co-occur with persistent environmental pollutants and pose potential health risks. Cadmium (Cd) is a common harmful heavy metal pollutant in the environment. However, the interaction between FCDs and Cd and the biotoxic effects of the resultant complexes (FCDs-Cd) on organisms remain almost entirely unexplored. Herein, TEM, FTIR, XPS, and ITC were utilized to analyze the interaction between FCDs and Cd. Based on this, zebrafish and mice were employed as model animals to explore the exposure of FCDs-Cd. The results illustrated that FCDs spontaneously interacted with Cd to form FCDs-Cd. Furthermore, exposure to FCDs-Cd caused 2.73-fold higher mortality in zebrafish and exacerbated developmental abnormalities. Moreover, accumulation of FCDs-Cd was found in the liver, kidney, and intestine of mice, which led to redox homeostasis imbalance and reactive oxygen species overproduction. Furthermore, FCDs-Cd caused 4-fold higher Cd accumulation in the colon than the Cd group, resulting in more pronounced damage. Transcriptome analysis further revealed that the FCDs-Cd may induce colonic injury in mice via activating the Syk/Btk/NF-κB pathway. This study provides novel perspectives for assessing the health risks of endogenous nanoparticles and heavy metals.

Epicatechin (EC) was used in this study to antagonize the cognitive dysfunction caused by lead (Pb) exposure in mice. Eight-week-old male Kunming mice were treated with PbCl₂ (20 mg/kg) and/or EC (50 mg/kg) by gavage administration for 4 weeks. Morris water maze test showed that EC could improve memory dysfunction induced by Pb. EC antagonized Ca²⁺ overload, activated Nrf2 signaling pathway and reduced the accumulation of Pb in the brain and serum, which suggested that EC might alter Pb distribution in mice. In vitro, spectroscopic analysis, potentiometric titration and docking studies were applied to inquiry into the interaction between bovine serum albumin (BSA) and Pb²⁺ in presence or absence of EC. EC was proved to chelate Pb²⁺ and reduced the interaction between BSA and Pb²⁺. In summary, EC might protect Pb-induced cognitive impairment by activating Nrf2 signaling pathway, and suppressing Pb accumulation via interference on the binding of Pb to albumin.