Reduced sulfur accelerates Fe(III)/Fe(II) recycling in FeS2 surface for enhanced electro-Fenton reaction.

FeS2 is well-known for its role in redox reactions. However, the mechanism within heterogeneous electron-Fenton (Hetero-EF) systems remains unclear. In this study, a novel FeS2 based three-dimensional system (GF/Cu-FeS2) with self-generation of H2O2 was investigated for Hetero-EF degradation of sulfamethazine (SMZ). The results revealed that SMZ could be completely removed in 1.5 h, accompanying with the mineralization efficiency of 96% within 4 h. This system performed excellent stability, evidenced by consistently eliminated 100% of SMZ within 2 h over 4 cycles. The generated Reactive Oxygen Species (ROS) of •OH and •O2- in every degradation cycle were quantitatively measured to confirm the stability of the GF/Cu-FeS2 system. Additionally, the redox reaction mechanism on the surface of FeS2 was thoroughly analyzed in detail. The accelerated reduction of Fe(III) to Fe(II), triggered by S22- on the surface of FeS2, promoted the iron cycling, thereby quickening the Fenton process. Density Functional Theory (DFT) results illustrated the process of S22- to be oxidized to in detail. Therefore, this work provides deeper insight into the mechanistic role of S22- in FeS2 for environmental remediation.

Regulatory effects of non-steroidal anti-inflammatory drugs on cardiac ion channels Nav1.5 and Kv11.1.

Non-steroidal Anti-inflammatory Drugs (NSAIDs) are widely used because of their excellent anti-inflammatory and analgesic effects. However, NSAIDs could cause certain cardiac side effects, such as myocardial infarction, heart failure, atrial fibrillation, arrhythmia and sudden cardiac death. Therefore, meloxicam, nimesulide, piroxicam, and diclofenac were selected and the whole cell patch clamp technique was used to investigate the electrophysiological regulatory effects of them on the sodium channel hNav1.5 and potassium channel hKv11.1, which were closely associated to the biotoxicity of cardiac, and to explore the potential cardiac risk mechanism. The results showed that the four NSAIDs could inhibit the peak currents of hNav1.5 and hKv11.1. Furthermore, the four NSAIDs could affect both the activation and inactivation processes of hNav1.5 with I-V curves left-shifted to hyperpolarized direction in activation phase. These data indicate that the inhibition effects of Nav1.5 and Kv11.1 by meloxicam, nimesulide, piroxicam, and diclofenac might contribute to their potential cardiac risk. These findings provide a basis for the discovery of other potential cardiac risk targets for NSAIDs.