Electronic and electrical products have deeply permeated all aspects of life, bringing a lot of convenience to individuals. However, the generation of e-waste after their end-of-life has resulted in serious risks both to the ecological environment and human health due to a lack of scientific and effective recycling and treatments. As two major types of components in e-waste, heavy metals and plastics can not only directly enter the human body via inhalation, ingestion, and skin absorption, but also accumulate in the human body indirectly through the food chain. E-waste is full of resources such as valuable metals like gold, silver, and copper that are often discarded incorrectly. Environmental and health risks derived from unregulated e-waste dismantling activities may be finally addressed through the application of advanced e-waste recycling technology, policy support of governments, legislation on recycling laws and regulations, and the improvement of public environmental protection awareness. This review gives a brief overview of the history, current situation, and future development of e-waste in China, which may provide novel thinking and approaches to e-waste management in the world.

Exposure to high ambient temperatures can cause significant damage to the gastrointestinal tract; however, the therapeutic potential of fecal microbiota transplantation (FMT) in this context remains largely unexplored. We investigated whether FMT could alleviate heat-induced colonic injury in C57BL/6J mice. Mice were randomly divided into four groups: normal control (22°C only), normal-FMT (NF, 22 °C+ FMT), heat exposure (HE, 39°C only), and HE-FMT (HF, 39°C + FMT). The HE and HF groups were exposed to 39°C for 2 hours daily over 15 consecutive days. FMT (100 µL/day) was administered by oral gavage to the NF and HF groups for 15 days, starting after the first HE. Our results showed that FMT significantly modulated gut microbiota composition, increasing the relative abundance of Alistipes , Citrobacter , Parasutterella , Bifidobacterium, Lachnospiraceae_UCG-001 , Raoultella , Woeseia , Prevotellaceae_UCG-001, and Christensenellaceae, while decreasing Clostridium_sensu_stricto_1 , Eubacterium_xylanophilum_group , Clostridioides , Bilophila , GCA-900066575, and Peptococcus . Notably, FMT markedly restored epithelial integrity and enhanced mucus production, as shown by hematoxylin-eosin and periodic acid-Schiff staining. Moreover, FMT attenuated heat-induced epithelial cell apoptosis, evidenced by reduced apoptotic cells and downregulation of mitochondrial apoptotic markers, including Bax, Bak, cleaved Caspase-3, cleaved Caspase-9, and the phospho-P53/P53 ratio. In addition, FMT mitigated oxidative stress induced by HE, indicated by decreased 3-nitrotyrosine levels and normalization of antioxidant-related proteins, such as Nrf2 , Sod1 , Cat , and Gpx4 . Collectively, these findings demonstrate that FMT alleviates heat-induced colonic injury by restoring mucosal barrier integrity, inhibiting apoptosis, and reducing oxidative stress, highlighting its potential as a promising therapeutic strategy for heat-related gastrointestinal disorders. IMPORTANCE: This study is the first to demonstrate the protective role of fecal microbiota transplantation (FMT) against heat-induced colonic injury in a mouse model. We show that FMT mitigates colonic damage by restoring gut microbiota balance, preserving mucosal barrier integrity, inhibiting epithelial cell apoptosis, and reducing oxidative stress. These findings underscore the essential role of the gut microbiota in maintaining intestinal homeostasis under heat stress and highlight the therapeutic potential of microbiota-targeted strategies, such as FMT, in preventing or treating heat-related intestinal injury.

Diet and gut microbiota alterations are key contributors to metabolic syndrome (MetS). As the Dietary Index for Gut Microbiota (DI-GM) captures diet–

6:2 chlorinated polyfluorinated ether sulfonate (F-53B, also known as 6:2 Cl-PFESA) is a major alternative to perfluorooctane sulfonate (PFOS) and a widespread environmental pollutant with potential public health hazards. However, its nephrotoxic effects and underlying molecular mechanisms remain poorly understood. This study investigated renal injury induced by environmentally relevant concentrations of F-53B and delineated the mechanistic cascade using a mouse model combined with quantitative proteomic and molecular biological approaches. Male C57BL/6 mice were exposed to 0, 4, 40, and 400 μg/L F-53B for 4 weeks. F-53B exposure led to significant renal dysfunction, histopathological damage, elevated renal injury biomarkers, and pronounced oxidative stress in a dose-dependent manner. A proteomic comparison of the 0 μg/L versus 400 μg/L groups identified 276 differentially expressed proteins that were strongly enriched in oxidative phosphorylation, autophagy, and apoptosis pathways, with cytochrome c oxidase subunit 7b (Cox7b) serving as a core downregulated hub molecule. Further validation confirmed that F-53B triggered overt mitochondrial structural damage, impaired respiratory chain complex assembly, aberrant ATP production, and disturbed mitochondrial dynamics. Consequently, excessive autophagy activation and mitochondrial-mediated apoptosis were simultaneously stimulated in renal tissues. Notably, although statistically significant, the alterations induced by F-53B were generally mild in magnitude. Collectively, our findings demonstrate that F-53B induces nephrotoxicity through a sequential pathological cascade. This study provides novel mechanistic insights into F-53B-elicited renal injury and highlights the potential health risks of this emerging per- and polyfluoroalkyl substance (PFAS) alternative.