International audience | Climate warming is expected to impact the response of species to insecticides. Recent studies show that this interaction between insecticides and temperature can depend on other factors. Here, we tested for the influence of transgenerational effects on the Insecticide x Temperature interaction in the crop pest moth Spodoptera littoralis. Specifically, we analysed reaction norms among experimental clutches based on a split-plot design crossing the factors temperature, insecticide and clutch. The study was performed on 2280 larvae reared at four temperatures (23, 25, 27 and 29°C), and their response to the insecticide deltamethrin (three concentrations and a control group) was tested. Temperature had a global influence with effects on larval survival, duration of development, pupal body mass, and significant reaction norms of the clutches for temperature variations of only 2°C. In addition to the expected effect of deltamethrin on mortality, the insecticide slightly delayed the development of S. littoralis, and the effects on mortality and development differed among the clutches. Projection models integrating all the observed responses illustrated the additive effects of deltamethrin and temperature on the population multiplication rate. Variation in the response of the clutches showed that transgenerational effects influenced the impact of insecticide and temperature. Although no evidence indicated that the Insecticide x Temperature interaction depended on transgenerational effects, the studies on the dependence of the Insecticide x Temperature interaction on other factors continue to be crucial to confidently predict the combined effects of insecticides and climate warming.

International audience | Environmental contamination is one of the major factors or cofactors affecting amphibian populations. Since 2000, the number of studies conducted in laboratory conditions to understand impacts of chemical exposures increased. They aimed to characterize biological effects on amphibians. This review proposes an overview of biological responses reported after exposures to metals, phytopharmaceuticals or emerging organic contaminants and focuses on endpoints relating to reproduction and development. Due to amphibian peculiar features, these periods of their life cycle are especially critical to pollutant exposures. Despite the large range of tested compounds, the same model species are often used as biological models and morphological alterations are the most studied observations. From the results, the laboratory-to-field extrapolation remained uneasy and exposure designs have to be more elaborated to be closer to environmental conditions. Few studies proposed such experimental approaches. Lastly, gametes, embryos and larvae constitute key stages of amphibian life cycle that can be harmed by exposures to freshwater pollutants. Specific efforts have to be intensified on the earliest stages and notably germ cells.

Under laboratory conditions, the effects of thiamethoxam were investigated in larvae, pupae and emerging honey bees after exposure at larval stages with different concentrations in the food (0.00001 ng/µL, 0.001 ng/µL and 1.44 ng/µL). Thiamethoxam reduced the survival of larvae and pupae and consequently decreased the percentage of emerging honey bees. Thiamethoxam induced important physiological disturbances. It increased acetylcholinesterase (AChE) activity at all developmental stages and increased glutathione-S-transferase (GST) and carboxylesterase para (CaEp) activities at the pupal stages. For midgut alkaline phosphatase (ALP), no activity was detected in pupae stages, and no effect was observed in larvae and emerging bees. We assume that the effects of thiamethoxam on the survival, emergence and physiology of honey bees may affect the development of the colony. These results showed that attention should be paid to the exposure to pesticides during the developmental stages ofthe honey bee. This study represents the first investigation of the effects of thiamethoxam on the development of A. mellifera following larval exposure.

Populations of plants and animals, including humans, living in close proximity to abandoned uranium mine sites are vulnerable to uranium exposure through drainage into nearby waterways, soil accumulation, and blowing dust from surface soils. Little is known about how the environmental impact of uranium exposure alters the health of human populations in proximity to mine sites, so we used developmental zebrafish (Danio rerio) to investigate uranium toxicity. Fish are a sensitive target for modeling uranium toxicity, and previous studies report altered reproductive capacity, enhanced DNA damage, and gene expression changes in fish exposed to uranium. In our study, dechorionated zebrafish embryos were exposed to a concentration range of uranyl acetate (UA) from 0 to 3000 μg/L for body burden measurements and developmental toxicity assessments. Uranium was taken up in a concentration-dependent manner by 48 and 120 h post fertilization (hpf)-zebrafish without evidence of bioaccumulation. Exposure to UA was not associated with teratogenic outcomes or 24 hpf behavioral effects, but larvae at 120 hpf exhibited a significant hypoactive photomotor response associated with exposure to 3 μg/L UA which suggested potential neurotoxicity. To our knowledge, this is the first time that uranium has been associated with behavioral effects in an aquatic organism. These results were compared to potential metal co-contaminants using the same exposure paradigm. Similar to uranium exposure, lead, cadmium, and iron significantly altered neurobehavioral outcomes in 120-hpf zebrafish without inducing significant teratogenicity. Our study informs concerns about the potential impacts of developmental exposure to uranium on childhood neurobehavioral outcomes. This work also sets the stage for future, environmentally relevant metal mixture studies. Summary Uranium exposure to developing zebrafish causes hypoactive larval swimming behavior similar to the effect of other commonly occurring metals in uranium mine sites. This is the first time that uranium exposure has been associated with altered neurobehavioral effects in any aquatic organism.

The present study investigated the effects of dietary iron (Fe) exposure on physiological performance and homeostatic regulation of trace metals during development (5–28 days post-fertilization; dpf) in zebrafish (Danio rerio). The results demonstrated that whole body Fe content was increased in 14 dpf larvae fed a high Fe diet. Cumulative mortality was also significantly elevated during exposure to the high Fe diet. Using droplet digital PCR, we observed that high Fe-exposed larvae exhibited an increase in mRNA levels of the Fe-storage protein ferritin, which appeared to be associated with the elevated level of whole body Fe content. Further, the results indicated that dietary Fe exposure induced transient changes in the mRNA expression levels of various metal transporters, including the iron transporter dmt1, and the zinc transporters zip8 and zip14. The expression of the epithelial Ca²⁺ channels (i.e., ecac) was also found to increase by high dietary Fe. Overall, our findings suggest that larval fish during the early nutritional transition period are sensitive to the effects of dietary Fe.

Microplastic has been ubiquitously detected in freshwater ecosystems. A variety of freshwater organisms were shown to ingest microplastic particles, while a high potential for adverse effects are expected. However, studies addressing the effect of microplastic in freshwater species are still scarce compared to studies on marine organisms. In order to gain further insights into possible adverse effects of microplastic particles on freshwater invertebrates and to set the base for further experiments we exposed the mud snail (Potampoyrgus antipodarum) to a large range of common and environmentally relevant non-buoyant polymers (polyamide, polyethylene terephthalate, polycarbonate, polystyrene, polyvinylchloride). The impact of these polymers was tested by performing two exposure experiments with irregular shaped microplastic particles with a broad size distribution in a low (30%) and a high microplastic dose (70%) in the food.First, possible effects on adult P. antipodarum were assessed by morphological and life-history parameters. Second, the effect of the same mixture on the development of juvenile P. antipodarum until maturity was analyzed.Adult P. antipodarum showed no morphological changes after the exposure to the microplastic particles, even if supplied in a high dose. Moreover, although P. antipodarum is an established model organism and reacts especially sensitive to endocrine active substances no effects on embryogenesis were detected. Similarly, the juvenile development until maturity was not affected.Considering, that most studies showing effects on marine and freshwater invertebrates mostly exposed their experimental organisms to very small (≤20 μm) polystyrene microbeads, we anticipate that these effects may be highly dependent on the chemical composition of the polymer itself and the size and shape of the particles. Therefore, more studies are necessary to enable the identification of harmful synthetic polymers as some of them may be problematic and should be declared as hazardous whereas others may have relatively moderate or no effects.

Deciphering the potential mechanism of chemical-induced toxicity enables us to alleviate the cellular and organismal dysfunction. The environmental presence of nonylphenol (endocrine disruptor) has a major health concern due to its widespread usage in our day-to-day life. The current study establishes a novel functional link among nonylphenol-induced oxidative stress, Heat shock protein 27 (Hsp27, member of stress protein family), and Ecdysone receptor (EcR, a nuclear receptor), which eventually coordinates the nonylphenol-induced sub-cellular and organismal level toxicity in a genetically tractable model Drosophila melanogaster. Drosophila larvae exposed to nonylphenol (0.05, 0.5 and 5.0 μg/mL) showed a significant decrease in Hsp27 and EcR mRNA levels in the midgut. In concurrence, reactive oxygen species (ROS) levels were increased with a corresponding decline in glutathione (GSH) level and Thioredoxin reductase (TrxR) activity. Increased lipid peroxidation (LPO), protein carbonyl (PC) contents, and cell death were also observed in a correlation with the nonylphenol concentrations. Sub-cellular toxicity poses a negative organismal response, which was evident by delayed larval development and reduced Drosophila emergence. Subsequently, a positive genetic correlation (p < 0.001) between EcR and Hsp27 revealed that nonylphenol-dependent EcR reduction is a possible link for the downregulation of Hsp27. Further, Hsp27 overexpression in midgut cells showed a reduction in nonylphenol-induced intracellular ROS, LPO, PC content, and cell death through the TrxR mediated regenerative pathway and reduced GSH level improving the organismal response to the nonylphenol exposure. Altogether, the study elucidates the potential EcR-Hsp27 molecular interactions in mitigating the nonylphenol-induced cellular and organismal toxicity.

The effect of microplastics (MP) exposure on the chironomid species Chironomus riparius Meigen, 1804 was investigated using the OECD sediment and water toxicity test. Chironomid larvae were exposed to an environmentally relevant low microplastics concentration (LC), a high microplastics concentration (HC) and a control (C). The LC was 0.007 g m⁻² on the water surface + 2 g m⁻³ in the water column + 8 g m⁻² in the sediment, and the HC was 10 X higher than this for each exposure. The size of the majority of the manufactured microplastic pellets varied between 20 and 100 μm. The MP mixture consisted of: polyethylene-terephtalate (PET), polystyrene (PS), polyvinyl-chloride (PVC) and polyamide (PA) in a ratio of 45%: 15%: 20%: 20%, respectively, for the sediment exposure; 100% polyethylene for the water column exposure; and 50% polyethylene: 50% polypropylene for the water surface exposure. Different endpoints were monitored, including morphological changes in the mandibles and mentums of 4th instar larvae, morphological changes in the wings, mortality, emergence ratio, and developmental time. A geometric morphometric analysis showed a tendency toward widening of the wings, elongation of the mentums and changing the shape of the mandibles in specimens exposed to both concentrations of microplastics. The development time of C. riparius was significantly prolonged by the MP treatment: 13.8 ± 0.5; 14.4 ± 0.6; and 15.3 ± 0.4 days (mean ± SD) in the C, LC, and HC, respectively. This study indicates that even environmentally relevant concentrations of MP mixture have a negative influence on C. riparius, especially at the larval stage.

Lambda-cyhalothrin (LCT) is a widely used broad-spectrum pyrethroid insecticide and is expected to cause deleterious effects on the male reproductive system. However, the effects of LCT on Leydig cell development during puberty are unclear. The current study addressed these effects. Twenty-eight-day-old male Sprague Dawley rats orally received LCT (0, 0.25, 0.5 or 1 mg/kg body weight/day) for 30 days. The levels of serum testosterone, luteinizing hormone, and follicle-stimulating hormone, Leydig cell number, and its specific gene and protein expression were determined. LCT exposure lowered serum testosterone levels at doses of 0.5 and 1 mg/kg and luteinizing hormone levels at a dose of 1 mg/kg, but increased follicle-stimulating hormone levels at doses of 0.5 and 1 mg/kg. LCT lowered Star and Hsd3b1 mRNA or their protein levels at a dose of 1 mg/kg. Immature Leydig cells were purified from pubertal rats and treated with different concentrations of LCT for 24 h and medium androgen levels, Leydig cell mRNA and protein levels, the mitochondrial membrane potential (△Ψm), and the apoptotic rate of immature Leydig cells were investigated. LCT inhibited androgen production at 5 μM and downregulated Scarb1 at 0.05 μM, Hsd3b1 and Hsd11b1 at 0.5 μM, and Cyp11a1 at 5 μM. LCT also decreased △Ψm at 0.5 and 50 μM. In conclusion, LCT can influence the function of Leydig cells.