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Sediments provide habitat and food for benthos, and phthalates (PAEs) have been detected in numerous river and marine sediments as a widely used plastic additive. PAEs in sediments is not only toxic to benthos, but also poses a threat to pelagic fish and human health through the food chain, so it is essential to comprehensively assess the contamination of sediments with PAEs. This paper presents a critical evaluation of PAEs in sediments, which is embodied in the analysis of the sources of PAEs in sediments from multiple perspectives. Biological production is indispensable, while artificial synthesis is the most dominant, thus the focus was on analyzing the industrial and commercial sources of synthetic PAEs. In addition, since the content of PAEs in sediments varies, some factors affecting the content of PAEs in sediments are summarized, such as the properties of PAEs, the properties of plastics, and environmental factors (sediments properties and hydrodynamic conditions). As endocrine disruptors, PAEs can produce toxicity to its direct contacts. Therefore, the effects of PAEs on benthos immunity, endocrinology, reproduction, development, and metabolism were comprehensively analyzed. In addition, we found that reciprocal inhibition and activation of the systems lead to genotoxicity and apoptosis. Finally, the paper discusses the feasible measures to control PAEs in wastewater and leachate from the perspective of source control, and summarizes the in-situ treatment measures for PAEs contamination in sediments. This paper provides a comprehensive review of PAEs contamination in sediments, toxic effects and removal strategies, and provides an important reference for reducing the contamination and toxicity of PAEs to benthos., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Perfluorooctane sulfonate (PFOS) is an increasingly important environmental pollutant that is pervasive in the environment. A number of studies have focused on the toxicological effects of PFOS on model fish species (zebrafish and medaka), but little is known about the impact of PFOS on commercially important marine fish. Thus, the present study examined transcriptome responses to PFOS exposure in the liver of juvenile Cynoglossus semilaevis, an important farmed flatfish in China. Then, in response to PFOS challenges, 1695 and 5244 genes were identified as significantly increased and depressed, respectively. Significant expression changes were observed in immune‐related genes (cytokine–cytokine receptor interaction, T‐helper [Th]17 cell differentiation, and the chemokine nuclear factor‐kappa B and T‐cell receptor signaling pathways), indicating that immunotoxicity is a key aspect of the effects of PFOS on C. semilaevis. Exposure to PFOS also altered the gene expression levels of hormones (inhibin, insulin, somatostatin, and glucagon), which could lead to severe metabolic and endocrine dysfunction. As expected from previous studies, several phase I and phase II detoxification enzymes were significantly up‐regulated, which could facilitate the biotransformation and detoxification of PFOS in C. semilaevis. The present study provides new insights into the molecular toxicology of PFOS in a commercially important fish species. Environ Toxicol Chem 2020;39:556–564. © 2019 SETAC [ABSTRACT FROM AUTHOR]

• ODP exposure reduced sperm motility in adult male zebrafish. • Long-term exposure to ODP increased the release of proinflammatory mediators. • ODP exposure reduced testosterone levels in male zebrafish. • The environmental concentration of ODP delayed the hatching time of zebrafish embryos. Wastewater and organic oxygen-demanding pollutants (ODPs) are produced by various factories in China, the United States and other countries. However, whether ODP affects reproductive health remains unclear. To investigate the impact of environmental concentrations of ODP exposure on reproductive health, adult male zebrafish were used to evaluated the effects ODP exposure on the fertility in this study. We found that exposure to ODP reduced the sperm motility of adult male zebrafish. Similarly, the testosterone content of the experimental zebrafish was obviously decreased. Transcription of immune response-related genes, including tumor necrosis factor (tnf)-α, il-1β, and il-8 , was upregulated upon exposure to ODP. Mating experiments indicated that the hatching time of the offspring embryos was clearly prolonged upon ODP exposure, but the embryo fertilization rate was not different. These results assumed that exposure to ODP at ambient concentrations visibly affected the sperm motility in adult zebrafish maybe due to the expression of immune response-related genes in the zebrafish male gonads and the release of pro-inflammatory mediators. Therefore, we assumed that the impact of ODP on the reproductive health of aquatic organisms cannot be ignored. [ABSTRACT FROM AUTHOR]

• Exposure to aphantoxins induced hepatic pro- and anti-inflammatory responses in zebrafish. • The observed hyperemia and HSI increases reflected hepatic tissue inflammation and damage. • Increased levels of TNF-α, IL-1β, IL-6, and IL-8 suggested pro-inflammatory reactions. • Upregulation of IL-10 and TGF-β indicated anti-inflammatory induction. • The hyperemia, HSI, and inflammatory factor induction results showed that exposure aphantoxins caused hepatic immunotoxicity. Blooms of the dominant cyanobacterium Aphanizomenon flosaquae are frequently encountered in natural waters, and their secretion of neurotoxic paralytic shellfish toxins called aphantoxins threatens environmental safety and human health worldwide. The liver is the primary detoxification organ in animals, and its pro- and anti-inflammatory responses are important functions in the detoxification of toxins. Therefore, we investigated the response of these inflammatory factors to aphantoxins in the liver of zebrafish (Danio rerio). A. flosaquae DC-1 was sampled during blooms in Dianchi Lake, China and cultured, and the toxin was extracted and analyzed using high performance liquid chromatography. The primary constituents were gonyautoxins 1 (34.04%) and 5 (21.28%) and neosaxitoxin (12.77%). Zebrafish were injected intraperitoneally with 5.3 μg (low dose) or 7.61 μg (high dose) of saxitoxin equivalents [equivalents (eq.)]/kg body weight of A. flosaquae DC-1 aphantoxins. Hyperemia, the hepatosomatic index (HSI), and physiological and molecular responses of pro- and anti-inflammatory cytokines in the zebrafish liver were investigated at different time points 1–24 h post-exposure. Aphantoxins significantly enhanced hepatic hyperemia and altered the HSI 3–24 h post-exposure, suggesting that inflammation caused morphological changes. Subsequent investigations using the enzyme-linked immunosorbent assay showed that the pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β (IL-1β), IL-6, and IL-8 and anti-inflammatory cytokines IL-10 and transforming growth factor β were higher in the liver of zebrafish exposed to aphantoxins, which indicated physiological inflammatory responses. Further analysis by real-time fluorescence quantitative polymerase chain reaction demonstrated upregulated mRNA expression of these cytokines, suggesting molecular inflammatory responses in the zebrafish liver. These changes showed dose- and time-dependent patterns. These results indicated that aphantoxins induced hyperemia and altered the HSI, and subsequently increased the levels of proinflammatory cytokines TNF-α, IL-1β, IL-6 and IL-8 to induce physiological inflammatory responses. These changes activated the anti-inflammatory cytokines IL-10 and TGF-β to suppress inflammatory damage. The induced changes were the result of upregulated mRNA expression of these inflammatory cytokines caused by aphantoxins. Aphantoxins resulted in hepatic immunotoxicity and response by inducing pro-inflammatory cytokines. Zebrafish liver in turn suppressed the inflammatory damage by upregulating the activities of anti-inflammatory cytokines. In the future, these pro- and anti-inflammatory cytokines in the zebrafish liver may be prove to be useful biomarkers of aphantoxins and blooms in nature. [ABSTRACT FROM AUTHOR]

In this study, the acute toxicity of paraquat (PQ) in common carp was determined. Then, the contents and mRNA levels of the cytokines interleukin-1β (IL-1β), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) were evaluated following subacute exposure to PQ. The results show that the LC50 of PQ for common carp at 72 and 96 h was 15.962 and 15.106 mg/L, respectively. Moreover, after 7 days of subacute PQ exposure, the IL-1β content in the fish liver and kidney increased, although it decreased in spleen. However, changes in the IFN-γ content showed an irregular trend. The TNF-α content increased in the liver and spleen but decreased in the kidney. Additionally, PQ exposure also induced alterations in the mRNA levels of IL-1β, IFN-γ, and TNF-α. These results suggest that PQ exposure may result in suppression or excessive activation of the immune system in treated fish and lead to immune dysfunction and reduced immunity., (© 2014 Wiley Periodicals, Inc.)

To evaluate the immunotoxicity of trichloroethylene (TCE), we conducted a cross-sectional molecular epidemiology study in China of workers exposed to TCE. We measured serum levels of IL-6, IL-10, and TNF-α, which play a critical role in regulating various components of the immune system, in 71 exposed workers and 78 unexposed control workers. Repeated personal exposure measurements were taken in workers before blood collection using 3 M organic vapor monitoring badges. Compared to unexposed workers, the serum concentration of IL-10 in workers exposed to TCE was decreased by 70% (P = 0.001) after adjusting for potential confounders. Further, the magnitude of decline in IL-10 was >60% and statistically significant in workers exposed to <12 ppm as well as in workers with exposures ≥ 12 ppm of TCE, compared to unexposed workers. No significant differences in levels of IL-6 or TNF-α were observed among workers exposed to TCE compared to unexposed controls. Given that IL-10 plays an important role in immunologic processes, including mediating the Th1/Th2 balance, our findings provide additional evidence that TCE is immunotoxic in humans., (© 2013 Wiley Periodicals, Inc.)