Persulfates activation by carbon nanotubes (CNT) has been evidenced as nonradical systems for oxidation of organic pollutants. Peroxymonosulfate (PMS) and peroxydisulfate (PDS) possess discrepant atomic structures and redox potentials, while the nature of their distinct behaviors in carbocatalytic activation has not been investigated. Herein, we illustrated that the roles of nitrogen species in CNT-based persulfate systems are intrinsically different. In PMS activation mediated by nitrogen-doped CNT (N-CNT), surface chemical modification (N-doping) can profoundly promote the adsorption quantity of PMS, consequently elevate potential of derived nonradical N-CNT–PMS* complexes, and boost organic oxidation efficiency via an electron-transfer regime. In contrast, PDS adsorption was not enhanced upon incorporating N into CNT due to the limited equilibrium adsorption quantity of PDS, leading to a relatively lower oxidative potential of PDS/N-CNT system and a mediocre degradation rate. However, with equivalent persulfate adsorption on N-CNT at a low quantity, PDS/N-CNT exhibited a stronger oxidizing capacity than PMS/N-CNT because of the intrinsic higher redox potential of PDS than PMS. The oxidation rates of the two systems were in great linearity with the potentials of carbon–persulfate* complexes, suggesting N-CNT activation of PMS and PDS shared the similar electron-transfer oxidation mechanism. Therefore, this study provides new insights into the intrinsic roles of heteroatom doping in nanocarbons for persulfates activation and unveils the principles for a rational design of reaction-oriented carbocatalysts for persulfate-based advanced oxidation processes.

Carbon-driven advanced oxidation processes are appealing in wastewater purification because of the metal-free feature of the carbocatalysts. However, the regime of the emerging nonradical pathway is ambiguous because of the intricate carbon structure. To this end, this study was dedicated to unveil the intrinsic structure-performance relationship of peroxydisulfate (PDS) activation by carbon nanotubes (CNTs) toward nonradical oxidation of organics such as phenol (PE) via electron transfer. Eighteen analogical CNTs were synthesized and functionalized with different categories and contents of oxygen species. The quenching tests and chronopotentiometry suggest that an improved reactivity of surface-regulated CNTs was attributed to the reinforced electron-transfer regime without generation of free radicals and singlet oxygen. The quantitative structure–activity relationships were established and correlated to the Tafel equation, which unveils the nature of the nonradical oxidation by CNT-activated PDS complexes (CNT-PDS*). First, a decline in the concentration of oxygen groups in CNTs will make the zeta potential of the CNT become less negative in neutral solutions, which facilitated the adsorption of PDS because of weaker electrostatic repulsion. Then, the metastable CNT-PDS* was formed, which elevated the oxidation capacity of the CNT. Finally, PE would be oxidized over CNT-PDS* via electron transfer to fulfill the redox cycle. Moreover, the nonradical oxidation rate was uncovered to be exponentially related with the potential of the complexes, suggesting that the nonradical oxidation by the CNT-PDS* undergoes a mechanism analogous to anodic oxidation.

Hepatocellular carcinoma (HCC) is a fatal disease and patients with HCC frequently die from metastasis. The mechanisms of HCC metastasis are not completely understood. In the present study, in vitro and in vivo data showed that HCC cells promoted cancer cell proliferation and lung metastases formation in a paracrinal/endocrinal way. We found that HCC-derived exosomes mediated this phenomenon and observed enhanced cell adhesion in the presence of these malignant exosomes. We further identified that reactive oxygen species (ROS) regulated the adhesive molecules. Intriguingly, attached HCC cells released exosomes containing both SMAD Family Member 3 (SMAD3) protein and mRNA, which were delivered to detached HCC cells and facilitated their adhesion. These exosomes induced enhanced SMAD3 signaling in the recipient HCC cells and increased their adhesive ability. In addition, we showed that SMAD3-abundant exosomes existed in the peripheral blood of patients with HCC, and their levels correlated with disease stage and the SMAD3 expression of primary tumors. Our study suggested a possible mechanism by which primary HCC supported metastases formation and revealed the role of SMAD3 in the exosomes-mediated crosstalk between primary and circulating HCC cells.