This study aimed at evaluating the interactive effects of acetaminophen (AC; 400 mg kg−1) and silicon dioxide nanomaterial (nano-SiO2;3 mg kg−1) on soil-grown barley. After 14 days of growth, plant growth, evaluated in terms of fresh and dry weight, was greatly inhibited by AC, independently of being or not co-treated with nano-SiO2. Plants growing under high levels of AC did not show any increase in malondialdehyde (MDA) nor thiols contents, though levels of superoxide anion (O2.-) and hydrogen peroxide (H2O2) were increased in leaves and roots, respectively. When plants were co-treated with nano-SiO2, reactive oxygen species (ROS) content remained unchanged, but lipid peroxidation (LP) was diminished and the thiol redox network was up-regulated in roots. The evaluation of the response of the antioxidant system showed that AC affected both non-enzymatic and enzymatic components in an organ-specific manner: proline levels and superoxide dismutase (SOD) activity were enhanced, whilst catalase (CAT) activity decreased in leaves; ascorbate content and CAT activity were diminished in roots. In response to the nano-SiO2 co-treatment, this pattern was not vastly altered, despite for ascorbate peroxidase (APX), whose activity was greatly enhanced in both organs. Overall, combining biometric, biochemical and molecular approaches, this study revealed that, although AC impaired plant growth and development, it did not trigger a harsh oxidative stress condition. Maybe by this reason, the ameliorating potential of nano-SiO2 was not so evident; yet, nano-SiO2 was able to reduce LP and to stimulate thiol content and APX activity, possibly as a defense mechanism against AC-induced stress.

Several monitoring studies have shown that benzoylecgonine (BE) is the main illicit drug residue commonly measured in the aquatic system worldwide. Few studies have investigated the potential toxicity of this molecule towards invertebrate and vertebrate aquatic non-target organisms focusing on effects at low levels of the biological organization, but no one has assessed the consequences at higher ones. Thus, the present study was aimed at investigating the toxicity of a 48-h exposure to two concentrations of BE, similar to those found in aquatic ecosystems (0.5 μg/L and 1.0 μg/L), on the cladoceran Daphnia magna at different levels of the ecological hierarchy. We relied on a multi-level approach focusing on the effects at biochemical/biomolecular (biomarkers), individual (swimming activity) and population (reproduction) levels. We measured the amount of reactive oxygen species and of the activity of antioxidant (SOD, CAT, and GPx) and detoxifying (GST) enzymes to assess if BE exposure can alter the oxidative status of D. magna specimens, while the lipid peroxidation (TBARS) was measured as a marker of oxidative damage. Moreover, we also measured the acetylcholinesterase (AChE) activity because it is strictly related to behavioral changes in aquatic organisms. Changes in swimming behavior were investigated by a video tracking analysis, while the consequences on reproduction were assessed by a chronic toxicity test. Our results showed that BE concentrations similar to those found in aquatic ecosystems induced oxidative stress and inhibited AChE activity, affecting swimming behavior and the reproduction of Daphnia magna individuals.

Microplastics are widespread emerging contaminants that have been found globally in the marine and freshwater ecosystem, but there is limited knowledge regarding its impact on coral reef ecosystem and underpinning mechanism. In the present study, using Pocillopora damicornis as a model, we investigated cytological, physiological, and molecular responses of a scleractinian coral to acute microplastic exposure. No significant changes were observed in the density of symbiotic zooxanthellae during the entire period of microplastic exposure, while its chlorophyll content increased significantly at 12 h of microplastic exposure. We observed significant increases in the activities of antioxidant enzymes such as superoxide dismutase and catalase, significant decrease in the detoxifying enzyme glutathione S-transferase and the immune enzyme alkaline phosphatase, but no change in the other immune enzyme phenoloxidase during the whole experiment period. Transcriptomic analysis revealed 134 significantly up-regulated coral genes at 12 h after the exposure, enriched in 11 GO terms mostly related to stress response, zymogen granule, and JNK signal pathway. Meanwhile, 215 coral genes were significantly down-regulated at 12 h after exposure, enriched in 25 GO terms involved in sterol transport and EGF-ERK1/2 signal pathway. In contrast, only 12 zooxanthella genes exhibited significant up-regulation and 95 genes down-regulation at 12 h after the microplastic exposure; genes regulating synthesis and export of glucose and amino acids were not impacted. These results suggest that acute exposure of microplastics can activate the stress response of the scleractinian coral P. damicornis, and repress its detoxification and immune system through the JNK and ERK signal pathways. These demonstrate that microplastic exposure can compromise the anti-stress capacity and immune system of the scleractinian coral P. damicornis, despite the minimal impact on the abundance and major photosynthate translocation transporters of the symbiont in the short term.

Due to the activities inherent to medical care units, the hospital effluent released contains diverse contaminants such as tensoactives, disinfectants, metals, pharmaceutical products and chemical reagents, which are potentially toxic to the environment since they receive no treatment or are not effectively removed by such treatment before entering the drain. They are incorporated into municipal wastewater, eventually entering water bodies where they can have harmful effects on organisms and can result in ecological damage. To determine the toxicological risk induced by this type of eflluents, eight metals and 11 pharmaceuticals were quantified, in effluent from a hospital. Developmental effects, teratogenesis and oxidative stress induction were evaluated in two bioindicator species: Xenopus laevis and Lithobates catesbeianus. FETAX (frog embryo teratogenesis assay–Xenopus) was used to obtain the median lethal concentration (LC50), effective concentration inducing 50% malformation (EC50), teratogenic index (TI), minimum concentration to inhibit growth (MCIG), and the types of malformation induced. Twenty oocytes in midblastula transition were exposed to six concentrations of effluent (0.1, 0.3, 0.5, 0.7, 0.9, 1%) and negative and positive (6-aminonicotinamide) controls. After 96 h of exposure, diverse biomarkers of oxidative damage were evaluated: hydroperoxide content, lipid peroxidation, protein carbonyl content, and the antioxidant enzymes superoxide dismutase and catalase. TI was 3.8 in X. laevis and 4.0 in L. catesbeianus, both exceed the value in the FETAX protocol (1.2), indicating that this effluent is teratogenic to both species. Growth inhibition was induced as well as diverse malformation including microcephaly, cardiac and facial edema, eye malformations, and notochord, tail, fin and gut damage. Significant differences relative to the control group were observed in both species with all biomarkers. This hospital effluent contains contaminants which represents a toxic risk, since these substances are teratogenic to the bioindicators used. The mechanism of damage induction may be associated with oxidative stress.

Given that cadmium (Cd) uptake by plants is linked to transpiration rate and activity of antioxidant enzymes and further that silicon (Si) can regulate them, it was hypothesized that improved Si nutrition could reduce Cd concentration in plants. Thus, present study was carried out to elucidate the positive effect of Si nutrition on the growth, activities of antioxidant enzymes and tissue cadmium (Cd) concentration in Cd-tolerant (Iqbal-2000) and Cd-sensitive wheat (Triticum aestivum L.) cultivars. Fifteen days after seedling transplantation, 15 μM Cd stress alone and in combination with 0.6 mM Si was applied. Silicon application improved root and shoot dry matter of Cd-sensitive cultivar Sehar-2006 while the effect was non-significant in Cd-tolerant cultivar Iqbal-2000. Silicon-treated Cd-sensitive cultivar showed marked improvements in chlorophyll content and photosynthesis, while stomatal conductance and transpiration rate decreased by Si application. Silicon treatment enhanced the activities of enzymatic antioxidants including catalase, ascorbate peroxidase, guaiacol peroxidase and superoxide dismutase and the increase was higher for Cd-tolerant cultivar Iqbal-2000. Although Si nutrition depressed malondialdehyde (MDA) content in both Cd-stressed cultivars, the response was more evident in Cd-sensitive Sehar-2006. Lower lipid peroxidation was related to Si-induced increase in antioxidant activities only in Cd-sensitive cultivar. Silicon application decreased Cd accumulation in the roots and shoots of both the cultivars. The decrease in shoot Cd was associated with a decrease in Cd uptake by roots and Cd translocation from roots to shoots. Overall, it is concluded that Si suppressed Cd contents by decreasing transpiration rate in Cd-sensitive cultivar and by increasing antioxidant activity in Cd-tolerant cultivar.

Chlorinated polyfluorinated ether sulfonate (Cl-PFESA) is a novel alternative compound for perfluorooctane sulfonate (PFOS), with its environmental risk not well known. The bioaccumulation and toxic effects of Cl-PFESA in the freshwater alga is crucial for the understanding of its potential hazards to the aquatic environment. Scenedesmus obliquus was exposed to Cl-PFESA at ng L⁻¹ to mg L⁻¹, with the exposure regime beginning at the environmentally relevant level. The total log BAF of Cl-PFESA in S. obliquus was 4.66, higher than the reported log BAF of PFOS in the freshwater plankton (2.2–3.2). Cl-PFESA adsorbed to the cell surface accounted for 33.5–68.3% of the total concentrations. The IC50 of Cl-PFESA to algal growth was estimated to be 40.3 mg L⁻¹. Significant changes in algal growth rate and chlorophyll a/b contents were observed at 11.6 mg L⁻¹ and 13.4 mg L⁻¹ of Cl-PFESA, respectively. The sample cell membrane permeability, measured by the fluorescein diacetate hydrolyzation, was increased by Cl-PFESA at 5.42 mg L⁻¹. The mitochondrial membrane potential, measured by Rh123 staining, was also increased, indicating the hyperpolarization induced by Cl-PFESA. The increasing ROS and MDA contents, along with the enhanced SOD, CAT activity, and GSH contents, suggested that Cl-PFESA caused oxidative damage in the algal cells. It is less possible that current Cl-PFESA pollution in surface water posed obvious toxic effects on the green algae. However, the bioaccumulation of Cl-PFESA in algae would contribute to its biomagnification in the aquatic food chain and its effects on membrane property could potentially increase the accessibility and toxicity of other coexisting pollutants.

Pesticide contamination is more often found as a mixture of different pesticides in water bodies rather than individual compounds. However, regulatory risk evaluation is mostly based on the effects of individual pesticides. In the present study, we aimed to investigate the individual and joint toxicities of triazophos (TRI) and imidacloprid (IMI) to the zebrafish (Danio rerio) using acute indices and various sublethal endpoints. Results from 96-h semi-static test indicated that the LC₅₀ values of TRI to D. rerio at multiple life stages (embryonic, larval, juvenile and adult stages) ranged from 0.49 (0.36–0.71) to 4.99 (2.06–6.81) mg a.i. L⁻¹, which were higher than those of IMI ranging from 26.39 (19.04–38.01) to 128.9 (68.47–173.6) mg a.i. L⁻¹. Pesticide mixtures of TRI and IMI displayed synergistic response to zebrafish embryos. Activities of carboxylesterase (CarE) and catalase (CAT) were significantly changed in most of the individual and joint exposures of pesticides compared with the control group. The expressions of 26 genes related to oxidative stress, cellular apoptosis, immune system, hypothalamic-pituitary-thyroid and hypothalamic-pituitary-gonadal axis at the mRNA level revealed that zebrafish embryos were affected by the individual or joint pesticides, and greater changes in the expressions of six genes (Mn-sod, CXCL-CIC, Dio1, Dio2, tsh and vtg1) were observed when exposed to joint pesticides compared with their individual pesticides. Taken together, the synergistic effects indicated that it was highly important to incorporate joint toxicity studies, especially at low concentrations, when assessing the risk of pesticides.

The main objective of the present study was to investigate possible links between sub-individual and supra-individual levels (i.e. population level) biomarkers in D. magna exposed to sublethal concentrations of the insecticide chlorpyrifos (CPF). To achieve the aim, 8-day old individuals were exposed for 96 h to two environmentally relevant concentrations of CPF (50 and 250 ng/L). Sub-individual level effects were investigated by measuring the activity of antioxidant (SOD, CAT, and GPx) and detoxifying (GST) enzymes, as well as by measuring the acetylcholinesterase (AChE) inhibition. In addition, the effects at supra-individual level were assessed by using a video-tracking system and analyzing changes in swimming capabilities (i.e. percentage of activity time, distance moved, and velocity). Our data have shown that daphnids exposed to both CPF concentrations were in a condition of stress which was highlighted by changes in both sub- and supra-individual biomarkers. Moreover, our results highlighted that the lowest tested CPF concentration did not modulate the antioxidant and detoxifying enzymes, whereas, an inhibition of AChE and a decrease of some parameters related to swimming behaviour (distance moved and velocity) were noted. On the contrary, significant changes in all the sub-individual biomarkers were measured at the highest tested concentration. In addition, organisms recovered the movement capability (distance moved) and also activate a mechanism of avoidance (increased swimming velocity). On the other hand, a reduction in the percent of active time was measured and this was attributed to the energy spent by organisms to activate antioxidant and detoxifying enzymes and the mechanism of avoidance. Based on these results, our study suggests the existence of a link between sub- and supra-individual levels, as the activation or non-activation in the antioxidant and detoxifying enzymes activities can led to different modifications of the swimming behaviour in D. magna.

Heavy metal tolerance of microorganisms is the basis of heavy metal removal by growing cells. In this study, a cross-protection effect generated by salt stress significantly enhanced the cadmium tolerance of multi-stress-tolerant Pichia kudriavzevii. Comparative transcriptome analysis using RNA-Seq linked with physiological and biochemical observation was used to elucidate the underlying mechanisms of the improved cadmium tolerance. The expression of cadmium transport related genes (GSTY2, GLR1, GLO2, YCF1 and YOR1), GSH content and GST activity were elevated by salt stress, suggesting enhanced cadmium conjugation and detoxification in yeast cells. The inhibited cadmium uptake by ZRT1 and enhanced cadmium efflux by YOR1 contributed to the decrease in the intracellular cadmium concentration. The improved expression of antioxidant enzyme genes (SOD1, SOD2, SOD6, CAT1 and PRXIID), along with the enhanced activities of antioxidant enzymes (SOD, CAT and POD) resulted in a decrease in cadmium-induced ROS production, protein carbonylation, lipid peroxidation and cell death. The abundant expression of heat shock protein genes (HSP12, HSP10 and SSC1) and genes related to trehalose synthesis (TPS1 and TSL1) induced by salt stress protected yeast cells against complex stress conditions, contributing to the improved cadmium tolerance. These findings will be useful to develop cadmium-tolerant yeasts for cadmium removal by growing cells.

Fluralaner is a novel isoxazoline insecticide which shows high insecticidal activity against parasitic, sanitary and agricultural pests, but there is little information about the effect of fluralaner on non-target organisms. This study reports the acute toxicity, bioconcentration, elimination and antioxidant response of fluralaner in zebrafish. All LC50 values of fluralaner to zebrafish were higher than 10 mg L⁻¹ at 24, 48, 72 and 96 h. To study the bioconcentration and elimination, the zebrafish were exposed to sub-lethal concentrations of fluralaner (2.00 and 0.20 mg L⁻¹) for 15 d and then held 6 d in clean water. The results showed medium BCF of fluralaner with values of 12.06 (48 h) and 21.34 (144 h) after exposure to 2.00 and 0.20 mg L⁻¹ fluralaner, respectively. In the elimination process, a concentration of only 0.113 mg kg⁻¹ was found in zebrafish on the 6th day after removal to clean water. After exposure in 2.00 mg L⁻¹ fluralaner, the enzyme activities of SOD, CAT, and GST, GSH-PX, CarE and content of MDA were measured. Only CAT and CarE activities were significantly regulated and the others stayed at a stable level compared to the control group. Meanwhile, transcriptional expression of CYP1C2, CYP1D1, CYP11A were significantly down-regulated at 12 h exposed to 2.00 mg L⁻¹ of fluralaner. Except CYP1D1, others CYPs were up-regulated at different time during exposure periods.Fluralaner and its formulated product (BRAVECTO®) are of low toxicity to zebrafish and are rapidly concentrated in zebrafish and eliminated after exposure in clean water. Antioxidant defense and metabolic systems were involved in the fluralaner-induced toxicity. Among them, the activities of CAT and CarE, and most mRNA expression level of CYPs showed fast response to the sub-lethal concentration of fluralaner, which could be used as a biomarker relevant to the toxicity.