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      Acute Toxicity of an Emerging Insecticide Pymetrozine to Procambarus clarkii Associated with Rice-Crayfish Culture (RCIS)

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          Abstract

          This study aims to evaluate the acute toxicity of pymetrozine to juvenile Procambarus clarkii. Two 96-h toxicity tests were conducted to assess the lethal concentration 50 (LC 50) values, behaviors, and histopathology (at 50% of the 96 h LC 50) after pymetrozine exposure. The results showed high toxicity of pymetrozine to juvenile P. clarkii in a dose and time dependent manner, with a decreasing LC 50 from 1.034 mg/L at 24 h to 0.479 mg/L at 96 h. The maximum allowable concentration (MAC) of pymetrozine for P. clarkii was 0.106 mg/L. Behavioral abnormalities were observed in pymetrozine-treated crayfish, such as incunabular hyperexcitability, subsequent disequilibrium, lethargy, and increased defecation. Significant lesions were observed in all pymetrozine-treated tissues, including: (1) in gill, hemocytic infiltration and 33.27% of epithelial cells lesions; (2) in perigastric organs, 64.37%, 29.06%, and 13.99% of tubules with lumen atrophy, vacuolation, and cell lysis, respectively; (3) in heart, 2.5%, 8.55% and 7.74% of hemocytic infiltration, vacuolization, and hyperplasia, respectively; (4) in stomach, 80.82%, 17.77%, 6.98%, 5.24% of cuticula swelling, vacuolization, muscle fragmentation, hemocytic infiltration, respectively; (5) in midgut, 7.45%, 10.98%, 6.74%, and 13.6% of hyperplasia, tissue lysis and vacuolation, hemocytic infiltration, muscle fracture; and (6) in abdominal muscle, 14.09% of myofiber fracture and lysis. This research demonstrates that pymetrozine is highly toxic to juvenile P. clarkii, with significant effects on mortality, behavior and histopathology at concentrations of ≤1.1 mg/L, while the estimated practical concentration of pymetrozine in rice-crayfish culture water was around 20 times lower than the calculated MAC.

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          Developmental toxicity and alteration of gene expression in zebrafish embryos exposed to PFOS.

          Perfluorooctanesulfonate (PFOS) is a persistent organic pollutant, the potential toxicity of which is causing great concern. In the present study, we employed zebrafish embryos to investigate the developmental toxicity of this compound. Four-hour post-fertilization (hpf) zebrafish embryos were exposed to 0.1, 0.5, 1, 3 and 5 mg/L PFOS. Hatching was delayed and hatching rates as well as larval survivorship were significantly reduced after the embryos were exposed to 1, 3 and 5 mg/L PFOS until 132 hpf. The fry displayed gross developmental malformations, including epiboly deformities, hypopigmentation, yolk sac edema, tail and heart malformations and spinal curvature upon exposure to PFOS concentrations of 1 mg/L or greater. Growth (body length) was significantly reduced in the 3 and 5 mg/L PFOS-treated groups. To test whether developmental malformation was mediated via apoptosis, flow cytometry analysis of DNA content, acridine orange staining and TUNEL assay was used. These techniques indicated that more apoptotic cells were present in the PFOS-treated embryos than in the control embryos. Certain genes related to cell apoptosis, p53 and Bax, were both significantly up-regulated upon exposure to all the concentrations tested. In addition, we investigated the effects of PFOS on marker genes related to early thyroid development (hhex and pax8) and genes regulating the balance of androgens and estrogens (cyp19a and cyp19b). For thyroid development, the expression of hhex was significantly up-regulated at all concentrations tested, whereas pax8 expression was significantly up-regulated only upon exposure to lower concentrations of PFOS (0.1, 0.5, 1 mg/L). The expression of cyp19a and of cyp19b was significantly down-regulated at all exposure concentrations. The overall results indicated that zebrafish embryos constitute a reliable model for testing the developmental toxicity of PFOS, and the gene expression patterns in the embryos were able to reveal some potential mechanisms of developmental toxicity.
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            Time- and Oil-Dependent Transcriptomic and Physiological Responses to Deepwater Horizon Oil in Mahi-Mahi (Coryphaena hippurus) Embryos and Larvae.

            The Deepwater Horizon (DWH) oil spill contaminated the spawning habitats for numerous commercially and ecologically important fishes. Exposure to the water accommodated fraction (WAF) of oil from the spill has been shown to cause cardiac toxicity during early developmental stages across fishes. To better understand the molecular events and explore new pathways responsible for toxicity, RNA sequencing was performed in conjunction with physiological and morphological assessments to analyze the time-course (24, 48, and 96 h post fertilization (hpf)) of transcriptional and developmental responses in embryos/larvae of mahi-mahi exposed to WAF of weathered (slick) and source DWH oils. Slick oil exposure induced more pronounced changes in gene expression over time than source oil exposure. Predominant transcriptomic responses included alteration of EIF2 signaling, steroid biosynthesis, ribosome biogenesis and activation of the cytochrome P450 pathway. At 96 hpf, slick oil exposure resulted in significant perturbations in eye development and peripheral nervous system, suggesting novel targets in addition to the heart may be involved in the developmental toxicity of DHW oil. Comparisons of changes of cardiac genes with phenotypic responses were consistent with reduced heart rate and increased pericardial edema in larvae exposed to slick oil but not source oil.
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              Toxicity of selected insecticides to Trichogramma chilonis: Assessing their safety in the rice ecosystem

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                Author and article information

                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                14 May 2018
                May 2018
                : 15
                : 5
                : 984
                Affiliations
                [1 ]State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, 7 South Donghu Road, Wuhan 430072, Hubei, China; jxyu001@ 123456126.com (J.Y.); liwei@ 123456ihb.ac.cn (W.L.); jinshiyu@ 123456ihb.ac.cn (S.J.); yuanting@ 123456ihb.ac.cn (T.Y.); jsliu@ 123456ihb.ac.cn (J.L.); zhongjie@ 123456ihb.ac.cn (Z.L.)
                [2 ]College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China
                [3 ]Department of Chemical Engineering, McGill University, Montreal, QC H3A 0C5, Canada; genbo.xu@ 123456mail.mcgill.ca
                Author notes
                [* ]Correspondence: tlzhang@ 123456ihb.ac.cn ; Tel.: +86-027-6878-0369
                Article
                ijerph-15-00984
                10.3390/ijerph15050984
                5982023
                29757963
                d0060300-eb0f-44e5-bb18-d8e387ff10f0
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 23 March 2018
                : 26 April 2018
                Categories
                Article

                Public health
                pesticide,aquatic toxicology,behavioral effects,histopathology,freshwater crayfish
                Public health
                pesticide, aquatic toxicology, behavioral effects, histopathology, freshwater crayfish

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