Carbendazim is a widely used broad spectrum benzimidazole fungicide; however, its effects to non-target aquatic organisms are poorly studied. The aim of this study was to investigate the toxic effects of carbendazim to zebrafish early life stages at several levels of biological organization, including developmental, biochemical and behavioural levels. The embryo assay was done following the OECD guideline 236 and using a concentration range between 1.1 and 1.8mg/L. Lethal and developmental endpoints such as hatching, edemas, malformations, heart beat rate, body growth and delays were assessed in a 96h exposure. A sub-teratogenic range (from 0.16 to 500μg/L) was then used to assess effects at biochemical and behavioural levels. Biochemical markers included cholinesterase (ChE), glutathione-S-transferase (GST), lactate dehydrogenase (LDH) and catalase (CAT) and were assessed at 96h. The locomotor behaviour was assessed using an automated video tracking system at 120h. Carbendazim (96h-LC50 of 1.75mg/L) elicited several developmental anomalies in zebrafish embryos with EC50 values ranging from 0.85 to 1.6mg/L. ChE, GST and LDH activities were increased at concentrations equal or above 4μg/L. The locomotor assay showed to be extremely sensitive, detecting effects in time that larvae spent swimming at concentrations of 0.16μg/L and thus, being several orders of magnitude more sensitive that developmental parameters or lethality. These are ecological relevant concentrations and highlight the potential of behavioural endpoints as early warning signs for environmental stress. Further studies should focus on understanding how the behavioural disturbances measured in these types of studies translate into fitness impairment at the adult stage.

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During the last century the increase in the mean global temperatures has been shown to impact on freshwater physicochemical parameters such as pH, dissolved oxygen, or ultraviolet (UV) light abundance. Changes in these parameters could modify the toxicity of environmental pollutants. Therefore, in the present study, the authors studied the tolerance (survival and sublethal endpoints) of zebrafish (Danio rerio) embryos to variations in pH (3-12), dissolved oxygen (3.9-237 μmol/L) and UV intensity (55-467 mW/m ) using selected endpoints. Sublethal endpoint assessment included the quantification of hatching success, developmental delay, reduction of body length, frequency of edema, and morphological abnormalities. Median lethal concentrations (LC50s; 96-h) of 3.68 and 10.21 were determined for acid and alkaline pH, respectively. Embryo survival appeared to be relatively resistant to oxygen depletion with a 96-h LC50 of 0.42 mg/L. However, concentrations of 6 mg/L and below caused edema and developmental retardations. Continuous exposure to UV radiation affected zebrafish development by reducing survival and hatching rate and triggering a series of developmental abnormalities such as pericardial edema and deformities. A 72-h LC50 of 227 mW/m was derived from intensity-response modeling. By generation of concentration-response parameters the authors' data provide a basis for the subsequent assessment of combined effect of environmental stress parameters and chemicals. Environ Toxicol Chem 2017;36:682-690. © 2016 SETAC.

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The relative body size at which predators are willing to attack prey, a key trait for predator-prey interactions, is usually considered invariant. However, this ratio can vary widely among individuals or populations. Identifying the range and origin of such variation is key to understanding the strength and constraints on selection in both predators and prey. Still, these sources of variation remain largely unknown. We filled this gap by measuring the genetic, maternal and environmental variation of the maximum prey-to-predator size ratio (PPSRmax) in juveniles of the wolf spider Lycosa fasciiventris using a paternal half-sib split brood design, in which each male was paired with two different females and the offspring reared in two different food environments: poor and rich. Each juvenile spider was then sequentially offered crickets of decreasing size and the maximum prey size killed was determined. We also measured body size and body condition of spiders upon emergence and just before the trial. We found low, but significant heritability (h2=0.069) and dominance and common environmental variance (d2+4c2=0.056). PPSRmax was also partially explained by body condition (during trial) but there was no effect of the rearing food environment. Finally, a maternal correlation between body size early in life and PPSRmax indicated that offspring born larger were less predisposed to feed on larger prey later in life. Therefore, PPSRmax, a central trait in ecosystems, can vary widely and this variation is due to different sources, with important consequences for changes in this trait in the short and long terms.

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