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Simple Summary: Due to the global increase in pesticide applications, aquatic animals are constantly subjected to their action in natural reservoirs. Terbuthylazine and malathion, two commonly detected pesticides in water and soil samples elsewhere, have been shown to have a significant negative impact on zebrafish, even at environmentally realistic concentrations. They can induce oxidative stress, mitochondrial and lysosomal destabilization, leading to immune toxicity, cytotoxicity, and DNA damage. All of these adverse outcomes might severely impact the health status of fish before being translated into an effect on the population. The present study should emphasize the importance of paying attention to pesticide traces in the environment, which can have devastating effects on biota even at low concentrations. Our research sought to determine the molecular and biochemical effects of environmentally relevant exposure to commonly used chloro-s-triazine herbicide terbuthylazine and organophosphate insecticide malathion on zebrafish. To this aim, mature zebrafish were exposed to 2 and 30 µg L−1 terbuthylazine and 5 and 50 µg L−1 malathion alone and in combination for 14 days. Aside from the accumulation of TBARS and protein carbonyls, a decrease in antioxidants and succinate dehydrogenase activity, an increase in oxidized glutathione, and enhanced apoptosis via Caspase-3 and BAX overexpression were observed. Furthermore, terbuthylazine and malathion induced mitochondrial swelling (up to 210% after single exposure and up to 470% after co-exposure) and lactate dehydrogenase leakage (up to 268% after single exposure and up to 570% after co-exposure) in a concentration-dependent manner. Significant upregulation of ubiquitin expression and increased cathepsin D activity were characteristics that appeared only upon terbuthylazine exposure, whereas the induction of IgM was identified as the specific characteristic of malathion toxicity. Meanwhile, no alterations in the zebrafish hypothalamic-pituitary-thyroid axis was observed. Co-exposure increased the adverse effects of individual pesticides on zebrafish. This study should improve the understanding of the mechanisms of pesticide toxicity that lead to fish impairment and biodiversity decline. [ABSTRACT FROM AUTHOR]

Zinc oxide nanoparticles are released into marine environments from industrial, medical and consumer uses sparking concerns about their potential ecotoxicological effects. Ecological hazard assessment of nZnO in marine ecosystems is hindered by the lack of understanding of the potential interactive effects of nZnO toxicity with other common abiotic stressors, such as salinity fluctuations, in marine organisms. To close this gap in our knowledge, we carried out a comprehensive biomarker-based assessment of the combined effects of salinity and nZnO in a sentinel marine bivalve, the blue mussels Mytilus edulis. The mussels were exposed for 21 days to clean seawater (control), an environmentally relevant concentration (100 μg Zn l−1) of nZnO or dissolved Zn (to identify the toxic effects attributable to Zn2+ toxicity) under the normal (15), low (5) and fluctuating (5–15) salinity regimes. The selected molecular and biochemical markers focused on the oxidative stress, apoptosis, detoxification system and inflammation in the gills and the digestive gland of the mussels. Biomarker analysis showed different effects of nZnO and dissolved Zn on biomarkers of oxidative stress, xenobiotic detoxification and apoptosis but similar effects of both pollutants on the levels of metallothioneins and inflammatory markers. Exposure to nZnO led to elevated levels of lipid peroxidation, upregulation of p53 and p38 stress kinases and apoptosis-related genes, most notably in the gills. Exposure to dissolved Zn led to accumulation of protein carbonyls and activated redox-sensitive detoxification enzymes (NADPH-P450 reductase and glutathione-S-transferase) in the mussels. The ambient salinity had significant effects the cellular adverse effects of nZnO in the mussels. The nZnO-induced cellular stress was detectable under the normal (15) and fluctuating (5–15) salinity conditions in the studied brackish water population of the mussels. At low salinity (5), nZnO toxicity signal was almost completely dampened. These findings indicate that chronic osmotic stress close to the tolerance limits of M. edulis prevails over the effects of the environmentally relevant nZnO and dissolved Zn concentrations in combined exposures. These stressor interactions might ameliorate the cellular toxicity of nZnO in the mussels but limit applicability of cellular stress biomarkers for detecting the toxic effects of nanopollutants in low salinity habitats. [Display omitted] • Salinity regime affects the molecular stress response to nZnO in mussels. • nZnO exposure induces lipid peroxidation and upregulates stress kinases. • Dissolved Zn exposure induces protein carbonylation and activates detoxification. • Low salinity dampens the molecular nZnO toxicity signal. [ABSTRACT FROM AUTHOR]

Nanoparticle toxicity is a growing concern in freshwater habitats. However, understanding of the nanoparticle effects on aquatic organisms is impeded by the lack of the studies of the nanoparticles effects in the environmentally relevant context of multiple stress exposures. Zinc oxide nanoparticles (n-ZnO) are widely used metal-based nanoparticles in electronics and personal care products that accumulate in aquatic environments from multiple non-point sources. In this study, we evaluated the effects of n-ZnO in a model organism, a mussel Unio tumidus , and the potential modulation of these effects by common co-occurring environmental stressors. Male U. tumidus were exposed for 14 days to n-ZnO (3.1 μM), Zn 2+ (3.1 μM), Ca-channel blocker nifedipine (Nfd 10 μM), combinations of n-ZnO and Nfd or n-ZnO and thiocarbamate fungicide Tattoo (Ta, 91 μg L −1 ) at 18 °C, and n-ZnO at 25 °C (n-ZnO + t °). Total and metallothionein-bound Zn levels as well as levels of metallothioneins (MT), cellular stress responses and cytotoxicity biomarkers were assessed in the mussels. The key biomarkers that showed differential responses to different single and combined stressors in this study were activities of caspase-3 and lysosomal cathepsin D, as well as protein carbonyl content. At 18 °C, exposures to n-ZnO, organic pollutants and their combinations led to a prominent up-regulation of MT levels (by ∼30%) and oxidative stress response including up-regulation of superoxide dismutase activity, an increase in oxyradical production, and a 2–3-fold decrease in the levels of protein carbonyls in all exposures except nZnO + Ta. Expos ure to n-ZnO in the absence of other stressors also led to a strong (∼7-fold) elevation of cathepsin D activity. Cellular responses to Zn 2+ and n-ZnO were different indicating that n-ZnO was not due exclusively to Zn release. Ca-channel blocker Nfd affected intracellular Zn distribution (reflected in the prominent elevation of Zn-MT levels) and caused reductive stress indicated by elevated levels of reduced glutathione levels and an increase in lactate/pyruvate ratio (reflecting higher NADH/NAD ratio). Elevated temperature (25 °C) abolished most of the typical responses to n-ZnO and induced oxidative injury, DNA fragmentation and caspase-3 mediated apoptosis in n-ZnO-exposed mussels. DNA fragmentation was also induced by exposure to organic toxins (alone and in combination with n-ZnO) but not by n-ZnO alone. These data indicate that n-ZnO toxicity to freshwater organisms is modulated by organic pollutants and enhanced by elevated temperatures. [ABSTRACT FROM AUTHOR]

Abstract: The main goal of this study was to evaluate the ability of fish Carassius auratus tissues to release cobalt (Co) and zinc (Zn) cations present in the applied Co- and Zn-containing nanoscale composites (NCs). Male fish was subjected to 14day long action of Co- and Zn-NCs, as well as of Co2+ and Zn2+ or polymeric substance (PS) used for the NC preparation and derived from the vinylpyrrolidone. 50μg∙L−1 of Co and 100μg∙L−1 of Zn were applied either as a salt or a nanocomposite. Both Co and Co-NC increased (3.1 and 2.3 times, respectively) concentration of total Co, metallothionein-related Co (3.7 and 6.6 times, respectively) and thiols (by 71 and 95%, respectively), and caspase-3 activity (2.2 and 3.7 times, respectively) in the fish liver. At the same time, Co and Co-NC decreased glutathione level (1.8 and 1.9 times, respectively) and activated vitellogenesis (5.1 and 9.9 times, respectively) in the fish liver. Both Zn and Zn-NC increased markedly concentrations of metallothionein-related Zn (2.4 and 2.9 times, respectively) and Cu (2.8 and 3.2 times, respectively), and decreased metallothionein-related thiol (2.5 and 4.2 times, respectively), oxyradical (by 30.4 and 44.2%, respectively), and caspase-3 (3.0 and 5.3 times, respectively) levels in the fish liver. These peculiarities are common for metal and metal-NC and witness a release of metal from NS in fish organism. The differences in the levels of DNA strand breaks, biotransformation enzymes and total Zn levels in the liver were dependent on the kind of exposure. [Copyright &y& Elsevier]

• Toxicity of central European cyanobacterial strains was assessed with biomarkers. • The studied strains produce no cylindrospermopsin (CYN) or microcystin (MC). • Bioactive compounds of the studied strains are toxic to zebrafish. • Toxic mechanisms of different strains are different and distinct from CYN or MC. • Assessment of cyanobacterial toxicity cannot solely rely on known toxin detection. The global increase in cyanobacterial blooms poses environmental and health threats. Selected cyanobacterial strains reveal toxicities despite a lack of synthesis of known toxic metabolites, and the mechanisms of these toxicities are not well understood. Here we investigated the toxicity of non-cylindrospermopsin and non-microcystin producing Aphanizomenon gracile and Raphidiopsis raciborskii of Central European origin to zebrafish exposed for 14 days to their extracts. Toxicological screening revealed the presence of anabaenopeptins and a lack of anatoxin-a, ß-methylamino-L-alanine or saxitoxins in examined extracts. The responses were compared to 20 μg L−1 of common cyanobacterial toxins cylindrospermopsin (CYN) and microcystin-LR (MC-LR). The expression of the marker genes involved in apoptosis (caspase 3a and 3b, Bcl-2, BAX, p53, MAPK, Nrf2), DNA damage detection and repair (GADD45, RAD51, JUN, XPC), detoxification (CYP1A, CYP26, EPHX1), lipid metabolism (PPARa, FABP1, PLA2), phosphorylation/dephosphorylation (PPP6C, PPM1) and cytoskeleton (actin, tubulin) were examined using targeted transcriptomics. Cellular stress and toxicity biomarkers (oxidative injury, antioxidant enzymes, thiol pool status, and lactate dehydrogenase activity) were measured in the liver, and acetylcholinesterase activity was determined as an index of neurotoxicity in the brain. The extracts of three cyanobacterial strains that produce no known cyanotoxins caused marked toxicity in D. rerio , and the biomarker profiles indicate different toxic mechanisms between the bioactive compounds extracted from these strains and the purified cyanotoxins. All studied cyanobacterial extracts and purified cyanotoxins induced oxidative stress and neurotoxicity, downregulated Nrf2 and CYP26B1, disrupted phosphorylation/dephosphorylation processes and actin/tubulin cytoskeleton and upregulated apoptotic activity in the liver. The tested strains and purified toxins displayed distinctively different effects on lipid metabolism. Unlike CYN and MC-LR, the Central European strain of A. gracile and R. raciborskii did not reveal a genotoxic potential. These findings help to further understand the ecotoxicological consequences of toxic cyanobacterial blooms in freshwater ecosystems. [Display omitted] [ABSTRACT FROM AUTHOR]

Biofouling causes massive economical losses in the maritime sector creating an urgent need for effective and ecologically non-harmful antifouling materials. Zinc oxide (ZnO) nanorod coatings show promise as an antifouling material; however, the toxicity of ZnO nanorods to marine organisms is not known. We compared the toxicity of suspended ZnO nanorods (NR) with that of ZnO nanoparticles (NP) and ionic Zn2+ in a marine bivalve Mytilus edulis exposed for two weeks to 10 or 100 μg Zn L−1 of ZnO NPs, NRs or Zn2+, or to immobilized NRs. The multi-biomarker assessment included bioenergetics markers (tissue energy reserves, activity of mitochondrial electron transport system and autophagic enzymes), expression of apoptotic and inflammatory genes, and general stress biomarkers (oxidative lesions, lysosomal membrane stability and metallothionein expression). Exposure to ZnO NPs, NRs and Zn2+ caused accumulation of oxidative lesions in proteins and lipids, stimulated autophagy, and led to lysosomal membrane destabilization indicating toxicity. However, these responses were not specific for the form of Zn (NPs, NR or Zn2+) and showed no monotonous increase with increasing Zn concentrations in the experimental exposures. No major disturbance of the energy status was found in the mussels exposed to ZnO NPs, NRs, or Zn2+. Exposure to ZnO NPs and NRs led to a strong induction of apoptosis- and inflammation-related genes, which was not seen in Zn2+ exposures. Based on the integrated biomarker response, the overall toxicity as well as the pro-apoptotic and pro-inflammatory action was stronger in ZnO NPs compared with the NRs. Given the stability of ZnO NR coatings and the relatively low toxicity of suspended ZnO NR, ZnO NR coating might be considered a promising low-toxicity material for antifouling paints. Unlabelled Image • Toxicity of ZnO nanoparticles (NPs) and nanorods (NRs) have been studied in marine mussels. • ZnO NPs and NRs induce autophagy and overexpression of apoptosis- and inflammation-related genes. • ZnO NRs are less toxic than NPs at the same concentration. • Toxicity mechanisms of nano-ZnO differ from those of ionic Zn. • Apoptosis-related biomarkers can detect and differentiate effects of nano-ZnO from Zn2+. [ABSTRACT FROM AUTHOR]