![]() The results of this study provided insights into the joint toxicity evaluation of NPs and marine algae toxins. the DNA replication, in which one double stranded DNA is replicated into two. WGCNA highlighted enrichment in the Fanconi anemia pathway and MAPK signaling pathway and identified that IER3 was the hub gene in PS and OA co-exposed AGS cells. being my personal Java trainer and food-shopping-assistant Thanks to. Moreover, the high concentration of PS significantly enhanced the toxicity of OA. In addition, co-exposure to PS and OA caused cellular damage by activating PI3K/AKT, ERK/c-FOS and caspase-3/caspase-9 signaling pathways. Our data indicated that the joint toxicity of PS and OA to AGS cells was mainly characterized by a decrease in cell viability, depolarization of mitochondrial membrane potential, and a decrease in IL10 and p53 protein activity, accompanied by an increase in intracellular ROS production and calcium and IL8 levels in comparison with single contaminants. AGS cells were exposed to 20 nm PS (0.5, 8 μg mL −1) or/and OA (5, 10 ng mL −1), and their cytotoxicity was assessed by measuring relevant indicators, transcriptomics, and weighted gene co-expression network analysis (WGCNA). In this study, the joint toxic effects and mechanisms of polystyrene (PS) NPs and okadaic acid (OA) were investigated on human gastric adenocarcinoma (AGS) cells. However, the joint toxic effects of marine algae toxins and NPs on human health remain unknown. NPs and marine algae toxins are found in marine organisms and both can enter the human body through the food chain. last couple of years, not least to move crude oil stranded in Cushing and around. ![]() The coexistence of nanoplastics (NPs) and various pollutants in the marine environment has become a problem that cannot be ignored.
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