Possible toxification mechanisms of acute and chronic pentachlorophenol to Montipora digitata: Limitation of energy supply and immunotoxicity.

Pentachlorophenol (PCP) is widely found in coastal environments and has various adverse effects, and its potential impact on coral reef ecosystems concerning. The scleractinian coral Montipora digitata was used for PCP stress experiments in this study. Phenotypes, physiological indicators, microbial diversity analysis and RNA sequencing were used to investigate the mechanisms underlying the responses of corals to acute and chronic PCP exposure. After 96 h of acute exposure, coral bleaching occurred at 1000 µg/LPCP and there was a significant decrease in Symbiodiniaceae density, Fv/Fm, and chlorophyll a content. Exposure to different concentrations of PCP significantly increased the content of malondialdehyde (MDA), leading to oxidative stress in corals. Chronic PCP exposure resulted in bleaching at 60 days, with the Fv/Fm significantly reduced to 0.461. Microbial diversity analysis revealed an increase in the abundance of potential pathogens, such as Vibrio, during acute PCP exposure and the emergence of the degrading bacterium Delftia during chronic PCP exposure. Transcriptional analysis showed that PCP exposure caused abnormal carbohydrate and amino acid metabolism in zooxanthella, which affected energy supply, induced immune responses, and disrupted symbiotic relationships. Corals respond to injury by boosting the expression of genes associated with signal transduction and immune response. Additionally, the expression of genes associated with environmental adaptation increased with chronic PCP exposure, which is consistent with the results of the microbial diversity analysis. These results indicate that PCP exposure might affect the balance of coral- zooxanthellae symbiosis in the stony coral M. digitata, impairing coral health and leading to bleaching.

Inactivation of Heterosigma akashiwo under UV/peroxydisulfate advanced disinfection system in marine waters.

Heterosigma akashiwo (H. akashiwo) is recognized as a harmful algal bloom (HABs) species with a global distribution, capable of posing significant threats to marine ecosystems, particularly when spread through ship ballast water. This investigation focused on elucidating the inactivation kinetics and underlying mechanism of H. akashiwo through a combined ultraviolet irradiation and peroxydisulfate (UV/PDS) process. The results demonstrated a strong synergistic effect within the UV/PDS system, resulting in an inactivation of 0.78-ln and 2.67-ln within 40 min of UV and UV/PDS processes. The principal agents accountable for inactivation were identified as sulfate radicals (•SO4-) and hydroxyl radical (•OH), which exhibited a synergistic effect in the UV/PDS process. Furthermore, the study observed a negatively impact of seawater pH and salinity on the efficiency of inactivation. UV/PDS caused oxidative stress on algal cells, initially involving the participation of antioxidant enzymes in counteracting cellular damage, but this protective mechanism diminished as the reaction duration extended. The UV/PDS treatment not only inflicted damage upon H. akashiwo's photosynthetic system but also caused the extracellular release of DNA and algal organic matter (AOM) due to damaged cell membranes. Transcriptome analysis provided a molecular biology perspective on the cellular inactivation process. Upregulation of genes linked to photosynthesis and oxidative phosphorylation suggested a potential elevation in energy metabolism. In contrast, genes associated with cellular and metabolic processes, including glycolysis and the tricarboxylic acid cycle (TCA cycle), exhibited downregulation. Moreover, this treatment exerted an inhibitory influence on RNA polymerase and protein synthesis, resulting in the reduced expression of genetic information.

USP7, negatively regulated by miR-409-5p, aggravates hypoxia-induced cardiomyocyte injury.

Hypoxia-induced apoptosis is linked to the pathogenesis of myocardial infarction (MI) and heart failure. Ubiquitin-specific peptidase 7 (USP7) is related to catabolic/pro-apoptotic signaling. However, its role in cardiomyocyte injury is unclear. In this study, we aimed to investigate the role and the underlying regulatory mechanism of USP7 in MI. H9c2 cardiomyocytes were cultured in hypoxia to establish an in vitro model of myocardial hypoxic/ischemic injury. Sprague-Dawley (SD) rats were used to establish animal models with MI. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays were performed to evaluate the expression levels of miR-409-5p, USP7, and p53, respectively. After USP7 and miR-409-5p were selectively regulated in H9c2 cells, the inflammatory response, apoptosis, and cell viability were detected by ELISA, flow cytometry, and MTT assay, respectively. The interaction between USP7 and miR-409-5p was determined by bioinformatics analysis, qRT-PCR, Western blot, and dual-luciferase reporter assay. LVEF, LVIDd, and LVIDs of rats after MI were also measured. USP7 expression was markedly elevated while miR-409-5p expression was significantly down-regulated in H9c2 cells under hypoxic culture. Augmentation of USP7 expression led to a dramatic promotion of hypoxia-induced apoptosis of cardiomyocytes, accompanied by an increase in the secretion of the cytokines IL-1ß, TNF-α, and IL-6. Myocardial injury markers LDH, cTnI, and CK-MB expressions were also increased. Besides, overexpression of USP7 aggravated left ventricular remodeling and decreased left ventricular function of the rats. Conversely, the up-regulation of miR-409-5p expression protected H9c2 cells from apoptosis and inhibited the release of cytokines and myocardial injury. Left ventricular remodeling and left ventricular function were also improved by miR-409-5p overexpression. Furthermore, USP7 was identified as a target of miR-409-5p and the overexpression of miR-409-5p reversed the effects of USP7 on H9c2 cells. USP7 exacerbates myocardial ischemic injury by promoting inflammation and apoptosis of cardiomyocytes, and the up-regulation of its expression is partly caused by the down-regulation of miR-409-5p expression.