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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]

Mercury (Hg) is a ubiquitous environmental contaminant and potent neurotoxin. In aquatic environments, Hg can be transformed into methylmercury (MeHg), which bioaccumulates in aquatic food webs, including fish. Methylmercury has been shown to transfer from female fish to developing eggs; however, relatively little is known regarding the effects of maternally transferred MeHg on fish embryos. The present study evaluated the effects of maternally transferred MeHg on fathead minnow ( Pimephales promelas) embryos. Embryos were collected from adult fatheads exposed for 30 d to 1 of 3 diets spiked with MeHg: a control diet (0.02 ppm Hg dry wt), a low diet (0.87 ppm Hg dry wt), or a high diet (5.5 ppm Hg dry wt). No effects on spawning frequency, clutch size, or total egg output were observed. In embryos, Hg concentration was a function of female diet and the duration (number of days) of female exposure. Compared with controls, embryos from the low-diet treatment displayed altered embryonic movement patterns (hyperactivity) and decreased time to hatch. Embryos from the high-diet treatment had delayed hatching and increased mortality compared with the other treatments. Collectively, these results suggest that maternally transferred Hg may impact survival, behavior, and developmental milestones of the embryo-larval stages of fish. Environ Toxicol Chem 2016;35:1436-1441. © 2015 SETAC [ABSTRACT FROM AUTHOR]

BSTRACT Cadmium, a toxic heavy metal with various applications in technology, can affect people both by environmental (foodborne) and occupational (inhalation) exposure and can cause nervous system damage. To model this, rats were subacutely treated either with CdCl2 solution per os (3.0 mg kg−1 b.w.) or nanoparticulate CdO2 (particle size ca 65 nm) by intratracheal instillation (0.04 mg kg−1 b.w.) alone or in sequential combination. Nervous system effects were observed at different levels of function (open field behavior, cortical electrical activity, nerve action potential) and some general toxicological indicators were also measured. Three weeks of oral plus one week of intratracheal exposure caused significant reduction of body weight gain and open field motility. Lengthening of latency of sensory evoked potentials, observed in all treated rats, was also the most significant in the group receiving oral plus intratracheal treatment. Conduction velocity of the tail nerve was likewise decreased in all treated groups. Several of the effects pointed to a potentiating interaction between the two forms of Cd. Modeling environmental and occupational Cd exposure by oral and intratracheal application in rats was feasible, with results suggesting serious negative health effects in humans suffering such a combined exposure. [ABSTRACT FROM AUTHOR]

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]

The effects of 6 weeks of oral exposure to propoxur (PR; at doses of 0.851 and 8.51 mg/kg body wt.), methylparathion (MP; at doses of 0.218 and 0.872 mg/kg body wt.), and their combinations were investigated in male Wistar rats. Measurement endpoints of the investigation were certain general toxicological parameters (body weight gain, organ weights), plaque-forming cell (PFC) count from the spleen, open field (OF) behavior, auditory startle response (ASR), prepulse inhibition (PPI), rotarod performance, somatosensory and auditory cortical evoked potentials, and peripheral nerve conduction velocity. The treated rats did not show any sign of acute intoxication during the 6 weeks of exposure. The higher dose of PR, but not of MP, significantly decreased the relative liver weight. Both agents produced a significant dose-dependent increase of OF activity, with larger expression after 2 weeks than after 6 weeks. The number of ASR responses and the ASR amplitude increased. The amplitude after PPI was increased by MP but only minimally altered by PR and the combinations. There was a small, but with high-dose PR significant, increase in the latency of the somatosensory evoked potentials. Neither of the two substances alone had any effect on the PFC response. The effect of the combination of high-dose PR and low-dose MP was significantly different from that of high-dose PR alone on the liver weight, on the ASR amplitude, and on the PFC/106 cell and PFC/spleen counts. With high-dose MP and low-dose PR, no such interaction was observed. According to the results, the noneffective dose of MP can influence the toxicity of the effective dose of PR in a combined exposure situation. [Copyright &y& Elsevier]

The potential for neurotoxic effects was evaluated in rat offspring after exposure in utero and/or during the neonatal period to a recombinant subunit vaccine of gp120 prepared from the MN strain of HIV-1 (MN rgp120/HIV-1). Thirty pregnant female rats were given MN rgp120/HIV-1 with alum adjuvant, and 30 rats were given vehicle, once every 3 days from Day 1 of presumed gestation until parturition. One pup/sex/litter from treated and control group dams were given a daily subcutaneous injection, from Day 1 through Day 22 postpartum (PP) of vehicle, MN rgp120/HIV-1, MN rgp120/HIV-1 with alum, or MN rgp120/HIV-1 with OS-21 adjuvant. Neurobehavioral and physical development were evaluated (preweaning reflex and development, sexual maturation, motor activity, acoustic startle, passive avoidance, functional observational battery, and water M-maze testing), and tissues were processed for anatomical examination (whole and regional brain weights, and neuropathology). Administration of MN rgp120/HIV-1, with or without adjuvant, to pups did not cause any persistent effect on any parameter evaluated. Neurohistological examination did not reveal any pathological effects related to treatment. Thus, MN rgp120/HIV-1 alone or formulated as a vaccine does not cause neurotoxicity or developmental toxicity in neonatal rats after exposure in utero and/or during the neonatal period. [ABSTRACT FROM PUBLISHER]

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]