AIM: Studying the mechanism of protective role of metallothionein (MT) in hypoxic preconditioning(HPC) of cultivated rat cardiomyocytes. METHODS: Using the model of hypoxia/reoxygenation of cultivated rat cardiomyocytes. Determing the contents of MT, malonyldialdehyde (MDA) - metabolism product of lipid peroxidation and the activities of Na+ - K+ ATPase, Ca2+ - Mg2+ ATPase of cardiomyocytes 24 h after HPC, the determining the relevant changes after using MT antibody. RESULTS: After 24 h in HPC, the contents of MT and activities of Na+ - K+ ATPase, Ca2+ - Mg2+ ATPase were obviously higher than those in the control and hypoxia/reoxygenation(P＜ 0. 05 ), and the contents of MDA were decreased remarkedly (P ＜ 0.01 ). Then after using MT antibody, the activities of two enzyme were progressively decreased and the contents of MDA were significanily higher than those in the control and MT antibody - free groups(P ＜ 0.01 ). CONCLUSION: HPC may induce excessive synthesis of MT, and MT can protect myocardial reoxygenation injury by eliminating lipid peroxidation and rising the activities of Na+ - K+ ATPase and Ca2+ - Mg2+ ATPase.

Background The affinity between placental transporters and perfluoroalkyl substances (PFAS) could affect the placental transport and toxicity of PFAS, while the study on the interaction between PFAS and placental transporters is limited. Objective To explore interactions between PFAS and placental transporters using molecular docking, and to provide a theoretical basis for PFAS toxicity prediction and fetal health risk assessment. Methods Fifteen PFAS compounds, each conformationally sampled and energy-minimized, and 16 placental transporters, represented by their 3D structures, were imported into a molecular docking software (MOE 20140901). For each PFAS, 30 distinct conformations were generated and docked into the active pockets of the transporters using a semi-flexible docking mode. Docking poses were primarily scored and ranked based on their calculated binding free energy (ΔG, kcal·mol⁻¹), with additional consideration given to hydrogen bonding interactions and the ligand's root mean square deviation (RMSD) at the binding site; the top 20 poses for each complex were subsequently output. Optimal binding configurations were identified as those exhibiting a relatively low binding free energy (ΔG ranging from −3 to −10 kcal·mol⁻¹), well-defined hydrogen bonds, and an RMSD ≤ 2.0 Å. The binding capabilities of the PFAS to the placental transporters were then evaluated based on these optimal docking results. Results The PFAS could bind to the placental transporters, with structural specificity. For example, the binding capabilities increased as the carbon chain length of PFAS increased, and it was also higher for PFOS alternatives than for PFOS. Besides, the binding capabilities of sulfonic PFAS with the same carbon chain length was also stronger than that of carboxylic PFAS. For example, the binding capabilities of PFOS (C8) to 15 placental transporters was higher than that of PFOA (C8), except for glucose transporter 1 (PFOS vs. PFOA: −4.14 vs. −4.14). Further, PFAS might be bound to the placental transporter through hydrogen, ionic, and hydrophobic interactions. Conclusion PFAS are able to bind the placental transporters, and its toxicity and exposure risk can’t be ignored.