Dietary diisononylphthalate contamination induces hepatic stress: a multidisciplinary investigation in gilthead seabream (Sparus aurata) liver.

In this study, adult gilthead seabream (Sparus aurata) were exposed for 21 days to Di-iso-nonylphthalte (DiNP at 15 and 1500 µg kg-1 bw day-1) via the diet. This plastic additive has been recently introduced to replace the di-(2-ethylhexyl)phthalate, the toxicity of which has been demonstrated conclusively both in vivo and in vitro trials. An analysis of a set of biomarkers involved in stress and immune response provides evidence of hepatic toxicity by DiNP in the present study. Both hsp70 and gr mRNA levels were upregulated significantly by DiNP, while plasma cortisol increased only in fish fed with the lowest DiNP dose. The oxidative stress markers g6pdh, glut red, gpx1 and CAT were upregulated by DiNP; gst mRNA was induced by the high dose and gck mRNA was downregulated significantly by the low dose. The mRNA levels of genes involved in the immune response, such as pla2, 5-lox, tnfa and cox2, were upregulated significantly only by the high dose of DiNP, while il1 mRNA increases in both doses. These molecular evidences were complemented with features obtained by Fourier Transform Infrared Imaging (FTIRI) analysis regarding the hepatic distribution of the main biological macromolecules. The FTIRI analysis showed an alteration of biochemical composition in DiNP samples. In particular, the low dose of DiNP induced an increase of saturated and unsaturated lipids and phosphorylated proteins, and a decrease of glycogen levels. The levels of caspase did not change significantly in the study, suggesting that DiNP does not activate apoptosis. Finally, the results also suggested the onset of hepatic oxidative stress and the activation of immune response, adding new knowledge to the already described hepatic DiNP toxicity.

An integrated approach to evaluate port sediment quality: From chemical characterization to multispecies bioassays.

Management of dredged sediments results in an environmental and social cost. Based on their level of contamination, they can be intended for beach nourishment or for alternative uses. Sediment quality is established considering their specific chemical contamination level and setting up bioassays to evaluate their toxic effects on living organisms. The integration of these different Line of Evidence (LOE) generates toxicity indexes, the Hazard Chemical Quotient (HQc), and the Hazard Ecotoxicological Quotient (HQe), which are further elaborated using the SediQualSoft software, finally providing evidence on the levels of sediment contamination. In this study, four different dredged sediments were analysed. Except for one, which was sampled in a reference area, the others were assigned to the same class of toxicity, despite they presented different levels of chemical and ecotoxicological toxicity. As a novelty, this study introduces transcriptomics as a new LOE, to provide a new tool to better categorize sediment toxicity. C. gigas embryos were exposed to sediment elutriates, sampled at 5 and 18 h post-fertilization (hpf), and the expression of a set of genes involved in immune and stress response (hsp70, gpx, sod, dehf1, galectin, lysozyme, tg) was analysed by Real-time PCR. Molecular results suggested that the 18 hpf stage represents a sensitive window of exposure during development and can be suggested as a critical time point for ecotoxicity studies. Finally, by multivariate statistical analysis, integrating the well-established LOEs with molecular data, it was demonstrated that transcriptomics could be a useful and novel LOE with the ability to provide greater accuracy in the assessment of sediment toxicity.