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Non-target organisms in aquatic environments may experience lethal or sublethal effects following exposure to contaminants. Most protocols and regulations, however, are designed to provide protection from lethal effects and are thus based on conventional estimates of population lethality. The relative lack of reliable behavioral endpoints makes it challenging to implement regulations that are similarly protective against sublethal toxicity. The objective of this study was to quantify the avoidance behavior of Hyalella azteca when exposed to three insecticides—bifenthrin (B), chlorpyrifos (C), and permethrin (P)—at a range of estimated lethal concentrations. A two-choice behavioral arena was used for each chemical to quantify H. azteca activity and time spent in either uncontaminated sediment or sediment spiked at concentrations reflecting estimated 48-h lethal concentrations (LC 50 , LC 25 , and LC 10). For all three insecticides, naïve H. azteca demonstrated a preference for the uncontaminated sediment over the contaminated sediment at the LC 50 (B: 312 ng/g OC ; C: 1265 ng/g OC ; P: 5042 ng/g OC) and LC 25 (B: 230 ng/g OC ; C: 859 ng/g OC ; P: 3817 ng/g OC), spending significantly more time in the uncontaminated side of the arena. H. azteca did not avoid sediment at LC 10 (B: 204 ng/g OC ; C: 609 ng/g OC ; P: 1515 ng/g OC) levels, indicating the existence of a potential threshold of detection. Despite the lack of substrate preference at this exposure level, H. azteca were nevertheless more active (i.e., increased zone-switching) when exposed to bifenthrin at the LC 10 , suggesting a possible irritation response (e.g., movement after exposure) to this chemical. Our results provide evidence that H. azteca exhibit innate avoidance responses to sediments contaminated with common insecticides at concentrations below those represented by traditional toxicological endpoints (e.g., LC 50). The sensitivity and ease with which this behavioral endpoint can be assayed demonstrates the potential utility of behavioral endpoints in toxicological assessments using model organisms. [Display omitted] • Avoidance behavior is a sensitive endpoint with population-level consequences. • Hyalella azteca avoided insecticides in sediment at and below the LC 50 and LC 25. • Avoidance was not detected at insecticide concentrations equal to the LC 10. • Increased activity at the bifenthrin LC 10 suggest a threshold of detection. • We advocate for the utility of avoidance as an informative behavioral endpoint. [ABSTRACT FROM AUTHOR]

The frequent detection of progestins in various aquatic environments and their potential endocrine disruptive effects in fish have attracted increasing attention worldwide. However, data on their effects on thyroid function and neurotoxicity in fish are limited, and the underlying mechanisms remain unclear. Here, the effects of gestodene (GES, a common progestin) on the thyroid endocrine and nervous systems of mosquitofish (Gambusia affinis) were studied. Adult female fish were exposed to GES at environmentally relevant concentrations (4.4–378.7 ng/L) for 60 days. The results showed that exposure to 378.7 ng/L GES caused a significant decrease in fish growth compared with the control and a marked reduction in the total distance traveled (50.6%) and swimming velocity (40.1–61.9%). The triiodothyronine (T3) levels were significantly increased by GES in a dose-dependent manner, whereas those of tetraiodothyronine (T4) were significantly decreased only at the G500 concentration. The acetylcholinesterase (AChE) activity was decreased significantly in the 4.42 ng/L GES treatments, but increased significantly at 378.67 ng/L. In the brain, a strong increase in the transcriptional levels of bdnf , trh , and dio2 was observed in fish after the 378.7 ng/L treatment. In addition, chronic exposure to GES caused colloid depletion with a concentration-dependent manner in the thyroid, and angiectasis, congestion, and vacuolar necrosis in the brain. These findings provide a better understanding of the effects of GES and associated underlying mechanisms in G. affinis. [Display omitted] • The effects of gestodene exposure on thyroid endocrine disruption and neurotoxicity were investigated in G. affinis. • The levels of thyroid hormone T3 was increased, while T4 was decreased in G. affinis. • Gestodene caused colloid depletion in the thyroid, and angiectasis, congestion and vacuolar necrosis in the cerebellum. [ABSTRACT FROM AUTHOR]

Aquatic animals are exposed to various cyanobacterial products released concomitantly to the environment by decaying blooms. Although there exist results on the toxicity of cyanobacterial extracts little is known on the influence of pure oligopeptides or their mixtures and elucidated mechanisms of behavioral toxicity in zooplanktonic organisms. Therefore, the aim of the present study was to assess the effects of single and mixed pure cyanobacterial oligopeptides: microginin FR-1 (MG-FR1), anabaenopeptin-A (ANA-A) and microcystin-LR (MC-LR) at various concentrations on the swimming behavior and catecholamine neurotransmitter activity, muscular F-actin structure, DNA nuclear content and cell viability of a model rotifer Brachionus calyciflorus. Swimming behavior was analyzed with the use of video digital analysis. Fluorescent microscopy imaging was used to analyze neuromotoric biomarkers in the whole organisms: neuromediator release (by staining with EC517 probe), muscle F-actin filaments (by staining with blue phalloidin dye). DNA content and cytotoxicity was also determined by Hoechst 34580 and propidium iodide double staining, respectively. The results showed that single oligopeptides inhibited all the tested endpoints. The binary mixtures induced synergistic interaction on swimming speed except for MG-FR1 +MC-LR which was nearly additive. Both binary and ternary mixtures also synergistically degraded F-actin and triggered cytotoxic effects visible in the whole organisms. Antagonistic inhibitory effects of all the binary mixtures were found on catecholamine neurotransmitter activity, however the ternary mixture induced additive toxicity. Antagonistic effects of both binary and ternary mixtures were also noted on nuclear DNA content. The results of the study suggest that both depression of neurotransmission and impairment of muscle F-actin structure in muscles may contribute to mechanisms of Brachionus swimming speed inhibition by the tested single cyanobacterial oligopeptides and their mixtures. The study also showed that natural exposure of rotifers to mixtures of these cyanobacterial metabolites may result in different level of interactive toxicity with antagonistic, additive synergistic effects depending on the variants and concentrations present in the environment. [Display omitted] • Microginin-FR-1, anabaenopeptin-A-, microcystin-LR affect Brachionus calyciflorus. • Synergistic decrease of swimming speed, muscular F-actin degradation by cyanopeptides. • Antagonistic DNA degradation, decreased neurotransmitter activity by cyanopeptides. • Peptide behavioral toxicity results from neurotransmitter and muscle disorders. [ABSTRACT FROM AUTHOR]

The present study investigated the developmental neurotoxicity of an early exposure to α-HBCDD through the ingestion of contaminated hen's egg in pregnant and lactating Wistar female rats. Hens were given α-HBCDD-contaminated feed (40 ng/g fresh matter) for 5 and 10 days, which produced eggs with HBCDD content of 33 and 102 ng/g lipid weight, respectively. Female rats were administered daily p.o. with an appropriate volume of the whole egg from the day of fertilization (GD0) to the weaning day for pups (PND21). Fetuses and pups were thus exposed continuously to α-HBCDD via the dam over a whole 42-day period that included both gestation and lactation. The administered egg volume was calculated on the basis of daily egg consumption in humans (0.7 egg/person/day) and duration of gestation and lactation in both species, which led animals to be exposed to α-HBCDD at levels of 22 and 66 ng/kg/day, respectively. Neurobehavioral development of pups was investigated from PND3 to PND25 using various tasks including the righting reflex (PND4), the grasping reflex (PND5), the negative geotaxis (PND9), the forelimb grip strength test (PND10) and the locomotor coordination test (PND20). Pup ultrasonic vocalizations were also recorded daily from PND4 to PND14. After weaning, behaviors related to spontaneous locomotor activity and anxiety were examined in the open-field (PND25) and in an elevated-plus maze (PND26), respectively. The results showed a significant decrease in body weight of pups exposed to the lower HBCDD level from PND3 to PND28, whereas the weight of rat pups given 66 ng/kg/day of HBCDD was not different from controls. During the first 3 weeks of life, impairments in motor maturation of pups were observed in a dose-dependent manner depending on the test, whereas no significant differences were reported between male and female pups. At PND26, the anxiety level of female rats exposed to the lowest dose of HBCDD (22 ng/kg/day) was significantly reduced whereas it remained unchanged in males. No significant variations were measured in rats exposed to the higher level of HBCDD (66 ng/kg/day). These results suggest the potent developmental neurotoxicity of an early chronic exposure to the HBCDD α-isomer through the ingestion of hen's eggs contaminated with this pollutant and question the long-lasting consequences of this exposure on behavior abilities and brain functioning in adulthood. [ABSTRACT FROM AUTHOR]

Humans are increasingly and consistently exposed to a variety of endocrine disrupting chemicals (EDCs), chemicals that have been linked to neurobehavioral disorders such as ADHD and autism. Many of such EDCs have been shown to adversely influence brain mesocorticolimbic systems raising the potential for cumulative toxicity. As such, understanding the effects of developmental exposure to mixtures of EDCs is critical to public health protection. Consequently, this study compared the effects of a mixture of four EDCs to their effects alone to examine potential for enhanced toxicity, using behavioral domains and paradigms known to be mediated by mesocorticolimbic circuits (fixed interval (FI) schedule controlled behavior, novel object recognition memory and locomotor activity) in offspring of pregnant mice that had been exposed to vehicle or relatively low doses of four EDCs, atrazine (ATR – 10 mg/kg), perfluorooctanoic acid (PFOA – 0.1 mg/kg), bisphenol-A (BPA – 50 μg/kg), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD – 0.25 μg/kg) alone or combined in a mixture (MIX), from gestational day 7 until weaning. EDC-treated males maintained significantly higher horizontal activity levels across three testing sessions, indicative of delayed habituation, whereas no effects were found in females. Statistically significant effects of MIX were seen in males, but not females, in the form of increased FI response rates, in contrast to reductions in response rate with ATR, BPA and TCDD, and reduced short term memory in the novel object recognition paradigm. MIX also reversed the typically lower neophobia levels of males compared to females. With respect to individual EDCs, TCDD produced notable increases in FI response rates in females, and PFOA significantly increased ambulatory locomotor activity in males. Collectively, these findings show the potential for enhanced behavioral effects of EDC mixtures in males and underscore the need for animal studies to fully investigate mixtures, including chemicals that converge on common physiological substrates to examine potential mechanisms of toxicity with full dose effect curves to assist in interpretations of relevant mechanisms. [ABSTRACT FROM AUTHOR]

Abstract: Exposure of iminodipropionitrile (IDPN) to rodents produces permanent behavioral syndrome characterized by repetitive head movements, circling and back walking. Other synthetic nitriles of industrial importance such as crotonitrile and allylnitrile are also able to produce similar motor deficits in experimental animals. However, due to the well-defined behavioral deficits and their easy quantification, IDPN-induced behavioral syndrome is a preferential animal model to test the interaction of various agents with synthetic nitriles. This study reports the effect of non-specific nitric oxide synthase inhibitor, N-nitro-l-arginine (NARG) on IDPN-induced neurobehavioral toxicity in adult male Wistar rats. Four groups of animals were given i.p. injections of IDPN (100mg/kg) for 6 days. These rats were treated with oral administration of NARG in the doses of 0 (IDPN alone group), 50, 150 and 300mg/kg, 60min before IDPN, respectively. Control rats received vehicle only, whereas another group was treated with 300mg/kg of NARG alone (without IDPN). The results showed that NARG significantly exacerbated the incidence and intensity of IDPN-induced dyskinetic head movements, circling and back walking. The histology of inner ear showed massive degeneration of the sensory hair cells in the crista ampullaris of rats receiving the combined treatment with IDPN and NARG, suggesting a possible role of nitric oxide in IDPN-induced neurobehavioral syndrome in rats. [Copyright &y& Elsevier]

Abstract: Cadmium selenium (CdSe) quantum dots (QDs) are semiconductor nanocrystals that hold wide range of applications and substantial production volumes. Due to unique composition and nanoscale properties, their potential toxicity to aquatic organisms has increasingly gained a great amount of interest. However, the impact of CdSe QDs exposure on zebrafish embryo and larvae remains almost unknown. Therefore, the lab study was performed to determine the developmental and behavioral toxicities to zebrafish under continuous exposure to low level CdSe QDs (0.05–31.25mgL−1) coated with mercaptopropionic acid (MPA). The results showed MPA–CdSe exposure from embryo to larvae stage affected overall fitness. Our findings for the first time revealed that: (1) The 120h LC50 of MPA–CdSe for zebrafish was 1.98mgL−1; (2) embryos exposed to MPA–CdSe resulted in malformations incidence and lower hatch rate; (3) abnormal vascular of FLI-1 transgenic zebrafish larvae appeared after exposure to MPA–CdSe including vascular junction, bifurcation, crossing and particle appearance; (4) larvae behavior assessment showed during MPA–CdSe exposure a rapid transition from light-to-dark elicited a similar, brief burst and a higher basal swimming rate; (5) MPA–CdSe induced embryos cell apoptosis in the head and tail region. Results of the observations provide a basic understanding of MPA–CdSe toxicity to aquatic organisms and suggest the need for additional research to identify the toxicological mechanism. [Copyright &y& Elsevier]

Abstract: CdTe quantum dots (QDs) are nanocrystals of unique composition and properties that have found many new commercial applications; therefore, their potential toxicity to aquatic organisms has become a hot research topic. The lab study was performed to determine the developmental and behavioral toxicities to zebrafish under continuous exposure to low concentrations of CdTe QDs (1–400nM) coated with thioglycolic acid (TGA). The results show: (1) the 120h LC50 of 185.9nM, (2) the lower hatch rate and body length, more malformations, and less heart beat and swimming speed of the exposed zebrafish, (3) the brief burst and a higher basal swimming rate of the exposed zebrafish larvae during a rapid transition from light-to-dark, and (4) the vascular hyperplasia, vascular bifurcation, vascular crossing and turbulence of the exposed FLI-1 transgenic zebrafish larvae. [Copyright &y& Elsevier]

Abstract: This paper provides a summary of the “state of knowledge” regarding behavioral impacts of domoic acid exposure on fish. Initial studies by authors of this paper suggested that fish are behaviorally impacted by domoic acid in the same way that birds and mammals are impacted during toxic Pseudo-nitzschia blooms. However, subsequent research and field observations have contradicted that hypothesis and provide evidence that fish are more tolerant to domoic acid under ecologically relevant exposure conditions than their piscivorous predators. This is an important distinction as more attention has been drawn to domoic acid producing algal blooms and the potential for domoic acid to cause fish kills. Currently available data indicate that domoic acid producing algal blooms do not cause fish kills or neuroexcitotoxic behaviors in fish. Neuroexcitatory behavioral effects have been documented in fish in laboratory studies when fish were intraceolomically (IC) injected with domoic acid. In fact, with IC injection as the mode of exposure all fish, bird, and mammal species tested to date show a similar neurologic sensitivity to domoic acid in terms of behavioral excitotoxicity as quantified by a 50% effective concentration (EC50) metric. However, IC injection is not an ecologically relevant mode of exposure. Dietary consumption during toxic blooms is the route of exposure for fish. Results from oral exposure experiments and observations from multiple highly toxic bloom events have provided strong evidence that fish are not behaviorally affected by domoic acid during natural bloom conditions, even though fish regularly contain high levels of the toxin and act as vectors to seabirds and marine mammals. Collectively, the data presented in this review suggest that fish are not significantly impacted by domoic acid during typical toxigenic Pseudo-nitzschia blooms. [Copyright &y& Elsevier]

Abstract: This study investigated the possible effects of a commonly used foliar herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) formulation on medulla spinalis of lebistes. Fish were exposed to 2,4-D (15, 30, 45mgL−1), behavioral changes were monitored. Fish were fixed, histopathological examination was carried out on sections taken from the upper parts of the fish body. Histopathology showed increase in neuronal loss, swelling indicating formation of intracellular edema, vacuolization noticed as the formation of vacuoles within or adjacent to cells, deformation in the Nissl granules, pyknosis and gliosis in medulla spinalis. Behavioral changes were decreased general activity, grouping, shortness in breath, sudden rotations and jumping, loss of equilibrium and colour. In conclusion, this commercial formulation of 2,4-D is considerably neurotoxic to lebistes. Fish constitute the last link in the chain of the feeding cycle in aquatic eco-system, number of studies investigating acute and chronic neurotoxicity of various herbicides in fish should be increased. [Copyright &y& Elsevier]

Abstract: Pregnant rhesus monkeys (Macaca mulatta) were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at 30 and 300ng/kg by subcutaneous injection at gestational day 20, followed by additional injections of TCDD (1.5 and 15ng/kg, respectively) every 30 days till 90 days after parturition. The offspring delivered from these experimentally TCDD-exposed mothers were subjected to a series of behavioral tests after the weaning at 12–14 months old (MO): a finger maze learning task (12–15MO), encounter tests between two monkeys (at 12–15 and 24–27MO), and an eye-contact test (23–26MO) to estimate learning ability, social interaction with a peer subject, and interest or hostility to a human observer, respectively. TCDD exposure had no significant effect on learning ability or interest/hostility to an observer. It did, however, significantly affect behavioral characteristics in the encounter tests. In the first encounter test, monkeys exposed to TCDD showed more visual exploration and mutual proximity but less stereotypy behavior compared to control monkeys. In the second encounter test, these differences seemed to disappear, suggesting that the behavioral effects of TCDD exposure in the encounter tests might disappear as the monkey develops. This study produced evidence of the behavioral toxicity of TCDD in social interactions using non-human primates. [Copyright &y& Elsevier]

In this study two indices of swimming behavior (horizontal and vertical swimming activity) in a gammaridean amphipod (Gammarus lawrencianus) were examined for their sensitivity to Cd exposure. G. lawrencianus were exposed for 72 h to a variety of Cd concentrations [background (∼12), 62, 125, 250 and 500 μg l-1] at 20 ppt. Subsequent to exposure, video surveillance of survivors held within grooved rings or clear boxes was used to assess horizontal swimming activity (percentage of time mobile) and vertical swimming activity (number of surfacings), respectively. Results show that control amphipods were quite active, being mobile ∼61% of the time, with horizontal swimming activity decreasing (P < 0.01) to ∼0.3% between a Cd exposure concentration of 125 and 500 μg l-1. Vertical swimming activity in amphipods was also impacted by Cd exposure (P < 0.001), with the greatest decrease occurring between background (∼12 μg l-1) and 62 μg l-1 (60 versus ∼26 surfacings, respectively), which is approximately four-fold lower than the estimated 72 h LC50 (250 μg l-1) for G. lawrencianus. Based on fluid dynamic considerations, it is speculated that of the two behaviors, vertical swimming activity is more sensitive to Cd exposure because of the presumed greater energetic costs associated with producing enough thrust to attain the lift required to make a vertical ascent into the water. [Copyright &y& Elsevier]

Carbamate pesticides (CMs) and organophosphorus pesticides (OPs) have been widely used in agriculture and toxicologically affect non-target organisms. Although there are many reports about their toxicities, the combined behavioral toxicities of CM/OP mixtures on Caenorhabditis elegans have rarely been studied. In this study, body bend inhibition (BBI), head thrash inhibition (HTI), and swimming speed inhibition (SSI) by CMs and OPs were chosen as the toxicity endpoints. The locomotion behavioral toxicities of individual pesticides (carbofuran (CAR), methomyl (MET), chlorpyrifos (CPF), and triazophos (TAP)) and their binary mixtures on C. elegans were determined systematically and the toxicological interaction profiles of various CM/OP mixture rays constructed using the combination index. It was shown that four pesticides and their binary mixture rays have significant inhibitory effects on the locomotion behavior of C. elegans ; that is, they produce locomotion behavioral toxicities and the toxicity of two OPs is higher than those of two CMs. The toxicological interactions in the binary CM and OP mixtures are different from each other. For example, one mixture ray (CAR-MET-R1) in the CM system on the SSI endpoint exhibits synergism at all concentration levels, another ray (CAR-MET-R3) displays low-dose synergism and high-dose additive action on BBI and HTI endpoints, and weak synergism at high-dose on SSI, and other rays perform additive action. Two rays (CPF-TAP-R1 and CPF-TAP-R2) in the OP mixture system display low-dose additive action and high-dose antagonism on the three endpoints. Another ray (CPF-TAP-R3) shows the additive action at all concentration levels. It can be concluded that it is not sufficient to evaluate the combined toxicity of binary CM/OP mixtures using only one concentration ratio ray and that it is necessary to examine multiple concentration ratios. Unlabelled Image • Chlorpyrifos and triazophos (OPs) are more toxic than CMs (carbofuran and methomyl). • CAR-MET-R1 on swimming speed inhibition endpoint exhibits synergism. • CAR-MET-R3 exhibits partial synergism on all three endpoints. • CPF-TAP-R1 and CPF-TAP-R2 display low-dose additive action and high-dose antagonism. • Three endpoints show the similar toxicity rule in four pesticides and binary mixture. [ABSTRACT FROM AUTHOR]

The literature has largely shown the toxicity of petroleum-based PLA biomicroplastics (PLABioMPs) and encouraged the production of alternative materials to replace their use, such as biopolymers. However, knowledge concerning the effects of biopolymers on aquatic organisms remains under development. The hypothesis that the acute exposure (five days) to polylactic acid (PLA) biopolymers may lead to behavioral and biochemical changes and to their accumulation in Danio rerio larvae was tested. Based on the results, PLA biomicroplastics (PLA BioMPs) at concentration of 3 and 9 mg/L decreased swimming distance and speed of larvae in the open field test. This outcome suggests effects on animals' locomotor and exploration activities. Larvae's longer immobility time and greater permanence in the peripheral zone of the apparatus is indicative of anxiety-like behavior caused by the exposure to PLA BioMPs. Zebrafish larvae accumulated PLA BioMPs and their acetylcholinesterase activity was inhibited by their presence, which reinforces the accumulative potential of biopolymers and their direct or indirect role as anxiogenic agents, even at sublethal concentrations. The decreased activity of acetylcholinesterase reinforces the neurotoxic action in groups exposed to PLA BioMPs. The current study has confirmed the initial hypothesis and is an insight about the toxicity of these biopolymers in D. rerio larvae, since it deepens the discussion about the environmental risk of these substances in freshwater ecosystems. ga1 • Polylactic acid bioplastic alters locomotor activity of Danio rerio larvae. • Anxiety-like behavior is observed in D. rerio larvae exposed to PLA bioplastics. • PLA bioplastics causes change in acetylcholinesterase enzyme activity. • PLA bioplastics can be dangerous to larval development. [ABSTRACT FROM AUTHOR]

Nowadays, silica nanoparticles (SiNPs) as one of the most productive nano-powder, has been extensively applied in various filed. The potential harm of SiNPs has previously received severe attention. A bulk of researches have proven the adverse effect of SiNPs on the health of ecological organisms and human. However, neurotoxic impacts of SiNPs, still remain in the stage of exploration. The potential neurotoxic effects of SiNPs need to be further explored. And the toxic mechanism needs comprehensive clarification. Herein, the neurotoxicity of SiNPs of various concentrations (100, 300, 1000 μg/mL) on adult zebrafish was determined by behavioral phenotyping and confirmed by molecular biology techniques such as qPCR. Behavioral phenotype revealed observable effects of SiNPs on disturbing light/dark preference, dampening exploratory behavior, inhibiting memory capability. Furthermore, the relationship between neurotoxic symptom and the transcriptional alteration of autophagy- and parkinsonism-related genes was preliminarily assessed. Importantly, further investigations should be carried out to determine the effects of SiNPs to cause neurodegeneration in the brain as well as to decipher the specific neurotoxic mechanisms. In sum, this work comprehensively evaluated the neurotoxic effect of small-sized SiNPs on overall neurobehavioral profiles and indicated the potential for SiNPs to cause Parkinson's disease, which will provide a solid reference for the research on the neurotoxicity of SiNPs. • Neurobehavioral toxicity of SiNPs was comprehensively determined. • SiNPs caused anxiety behavior and suppressed exploratory behavior. • SiNPs inhibited memory capability. • SiNPs disturbed autophagy- and parkinsonism-related genes expression in the brain. [ABSTRACT FROM AUTHOR]