18 resultados para Risk of exposure to pesticides

em Chinese Academy of Sciences Institutional Repositories Grid Portal


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In the present study, we examined the effects of exposure to an extremely low-frequency magnetic field of 1 mT intensity on learning and memory in Lohmann brown domestic chicks using detour learning task. These results show that 20 h/day exposure to a low

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We examined breeding behavior responses of male root votes (Microtus oeconomus) to temporal risk of predation by using acute and chronic exposure to predator odor. The 2 series of exposure experiments provided 2 types of temporal patterns of risk: continuous safety with a brief period of risk and Sustained risk with a brief period of safety. Male root votes that were acutely exposed to predator odor for I h suppressed their breeding behavior, but bred immediately after exposure to control odor for I h. Those chronically exposed to predator odor for 20 days maintained behavioral suppression during the 1-h period of exposure to control odor. Acutely exposed males did not change their physiological patterns of breeding, but those chronically exposed to predator odor had reduced testosterone concentration and epididymis index. Our results indicate that breeding behavior in a given situation depends on the overall patterns of risk experienced by male root votes, and the acute and chronic stress responses that affect reproduction are responsible for different behavioral responses to the 2 types of temporal patterns of risk. We also discuss the reasons for conflicting results about breeding suppression of votes between previous studies in the laboratory and the field.

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Antipsychotic treatment during pregnancy is indicated when risk of drug exposure to the fetus is outweighed by the untreated psychosis in the mother. Although increased risk of congenital malformation has not been associated with most available antipsycho

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Acute stressful events enhance plasma corticosterone release and profoundly affect synaptic functions, which are involved in the development of stress-related cognitive and mental disorders. However, how exposure to stressful context immediately after str

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We investigated memory impairment in newly hatched chicks following in ovo exposure to a 50-Hz magnetic field (MF) of 2 mT (60 min/day) on embryonic days 12-18. Isolated and paired chicks were used to test the effect of stress during training, and memory retention was tested at 10, 30, and 120 min, following exposure to a bitter-tasting bead (100% methylanthranilate). Results showed that memory was intact at 10 min in both isolated and paired chicks with or without MF exposure. However, while isolated chicks had good memory retention levels at 30 and 120 min, those exposed to MF did not. The results suggest a potential disruption of memory formation following in ovo exposure to MF, with this effect only evident in the more stressed, isolated chicks. Bioelectromagnetics 31:150-155, 2010. (C) 2009 Wiley-Liss. Inc.

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Thyroid hormones (THs) play an important role in the normal development and physiological functions in fish. Environmental chemicals may adversely affect thyroid function by disturbing gene transcription. Perfluorooctane sulfonate (PFOS), a persistent compound, is widely distributed in the aquatic environment and wildlife. In the present study, we investigated whether PFOS could disrupt the hypothalamic-pituitary-thyroid (HPT) axis. Zebrafish embryos were exposed to various concentrations of PFOS (0, 100, 200 and 400 mu g L-1) and gene expression patterns were examined 15 d post-fertilization. The expression of several genes in the HIPT system, i.e., corticotropin-releasing factor (CRF), thyroid-stimulating hormone (TSH), sodium/iodide symporter (NIS), thyroglobulin (TG), thyroid peroxidase (TPO), transthyretin (TTR), ioclothyronine deiodinases (Dio1 and Dio2) and thyroid receptor (TR alpha and TR beta), was quantitatively measured using real-time PCR. The gene expression levels of CRF and TSH were significantly up-regulated and down-regulated, respectively, upon exposure to 200 and 400 mu g L-1 PFOS. A significant increase in NIS and Diol gene expression was observed at 200 mu g L-1 PFOS exposure, while TG gene expression was down-regulated at 200 and 400 mu g L-1 PFOS exposure. TTR gene expression was down-regulated in a concentration-dependent manner. Up-regulation and down-regulation of TR alpha and TR beta gene expression, respectively, was observed upon exposure to PFOS. The whole body thyroxine (T-4) content remained unchanged, whereas triiodothyronine (T-3) levels were significantly increased, which could directly reflect disrupted thyroid hormone status after PFOS exposure. The overall results indicated that PFOS exposure could alter gene expression in the HPT axis and that mechanisms of disruption of thyroid status by PFOS could occur at several steps in the synthesis, regulation, and action of thyroid hormones. (C) 2009 Elsevier Ltd. All rights reserved.

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Fluorotelomer alcohols (FTOHs) have shown estrogenic activity in vitro and in vivo, but the mechanism of this activity is not known. In this study, 18-week-old zebrafish (Danio rerio) were exposed to 0, 0.03, 0.3 and 3.0 mg/l 1H, 1H, 2H, 2H-perfluorooctan-1-ol (6:2 ETCH) for 7 days, and the effects on plasma sex hormone levels were measured followed by use of real-time PCR to examine selected gene expression in hypothalamic-pituitary-gonadal (HPG) axis and liver. Exposure to 6:2 FTOH significantly increased plasma estradiol (E2) and testosterone (T) levels in both males and females. Furthermore, the ratio of T/E2 was reduced in females while increased in males. In females, the increase of E2 was accompanied by up-regulated hepatic estrogenic receptor alpha (ER alpha) and vitellogenin (VTG1 and VTG3) expression. In males, the elevation of the T level is consistent with the up-regulation of cytochrome P450 c17 alpha-hydroxylase, 17, 20-lase (CYP17) and the down-regulation of cytochrome P450 aromatase A (CYP19A). The present study demonstrated that waterborne exposure to 6:2 FTOH alter plasma sex hormone levels and the ratio of T/E2, as well as the transcriptional profiles of some genes in the HPG axis and liver. The results suggested that FTOHs may disturb fish reproduction through endocrine disrupted activity. (C) 2009 Elsevier B.V. All rights reserved.

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This study was designed to determine cytotoxic effects of PBDE-47 and HBCDs individually or with a mixture of both compounds exposure to Hep G2 cells. The results showed PBDE-47 and HBCDs induced increase of nitric oxide synthase (NOS) activity, release of NO. dissipation of mitochondria membrane potential and cell apoptosis. Exposure to HBCDs induced ROS formation. Moreover, preincubation with PTIO (NO scavanger) and N-acetylcysteine (ROS scavanger) partially reversed cytotoxic effects of these compounds. The possible mechanism is that PBDE-47 and HBCDs could boost generation of NO and/or ROS, impact mitochondria, and result in start-ups of apoptosis program. Cells exposed to mixture of both compounds and each of them showed non-apoptotic rate significant difference, but the combination of them caused more adverse effects on cells. These results Suggest that PBDE-47 and HBCDs in single and complex exposure have the cytotoxic activity of anti-proliferation and induction of apoptosis in tumor cells in vitro. (C) 2008 Elsevier B.V. All rights reserved.

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Toxicity of many waterborne organic contaminants to aquatic organisms is mediated through oxidative damages resulting from the production of reactive oxygen species (ROS). Using duroquinone as a model ROS inducer, we carried out in vitro and in vivo experiments to test the hypothesis that reproduction in common carp (Cyprinus carpio) can be impaired through oxidative damage of their spermatozoa. In vitro exposure of fish spermatozoa to 0, 12.5, 25, 50, 100 and 200 mu M duroquinone for 2 h showed a significant increase in the level of ROS in a dose-dependant manner. Sperm motility was significantly reduced in all exposure groups, but lipid peroxidation (LPO) and DNA strand break (measured by comet assay) were only enhanced at 50 mu M and above. A significant decrease in subsequent hatching rate was recorded in all the exposure groups, despite fertilization rate was not affected. In the in vivo experiment, spermatozoa were collected 24 and 72 h after fish received intra-peritoneal injections of 1.0 and 10 mg kg(-1) body weight duroquinone. DNA damage was clearly evident in spermatozoa of all treatment groups after 72 h exposure, and ROS was significantly enhanced in the high concentration group. LPO however, remained unchanged in both treatment groups. The overall results of both our in vitro and in vivo experiments demonstrated that duroquinone can induce ROS production in spermatozoa, which may impair sperm quality and subsequently reproductive success through oxidative stress. (c) 2006 Elsevier B.V. All rights reserved.

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Mature female and male zebrafish were separated and exposed to nonylphenol (NP) at 0.1, 1, 10, 50, 100 and 500 mu g/L, respectively, for 3 weeks. Gonadosomatic index (GSI) in both sexes and vitellogenin (VTG) induction in males was measured as the bioindicators for the impairment to the parents. The results indicated that 50 mu g/L of NP was the non-observed effect concentration (NOEC) for GSI and VTG induction. Afterwards, the 50 mu g/L NP exposed females and males, and the control females and males were cross-wise pair-bred in the control water for one week to examine the reproductive effects. The embryonic cathepsin D (CAT D) activity, eggshell thickness, fecundity, hatching rate and malformation (vertebral column flexure) rate of offspring were determined in the four pair-bred groups. While endpoints remained unchanged in the groups with exposed males, prenatal exposure of females to 50 mu g/L of NP resulted in the impairment of reproduction in groups with exposed females including inhibition of CAT D activity (P < 0.05), decrease of eggshell thickness (by 23.6%) and elevation of malformation rate (P < 0.001). These results suggested NP could induce reproductive damage to zebrafish at NOEC for parents. The results also imply that alterations of CAT D activity and eggshell thickness may be more sensitive biomarkers to indicate the reproductive effects caused by endocrine disrupting chemicals. (c) 2005 Elsevier Inc. All rights is reserved.

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Silver carp (Hypophthalmichthys molitrix) samples were collected from five selected sites that represent diverse levels of downgraded persistent organic pollutants (POPs) contamination in Ya-Er Lake in October 1999. Hepatic ethoxyresorufin-O-deethylase (EROD) and UDP glucuronosyltransferase (UDPGT) activities, hepatosomatic index (HSI), hepatic retinoids, serum thyroid hormones were measured. It was found that hepatic retinol and serum free 3,5,3'- tetraiodothyronine (FT3) significantly increased (P < 0.01) when both hepatic EROD and UDPGT activities significantly declined (P < 0.01) from pond 1 to 5 with decrease in the degree of pollution. This significant negative correlation (P < 0.01) suggests that the persistent organochlorinated contaminants could induce hepatic EROD and UDPGT activities, alter retinoid and thyroid hormone homeostasis, and finally lead to the reduction of retinol and FT3, the two biologically active forms of retinoids and thyroid hormone in silver carp of Ya-Er Lake. (C) 2002 Elsevier Science Ltd. All rights reserved.

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Thyroid hormones (THs) play an important role in the normal development and physiological functions in fish. Environmental chemicals may adversely affect thyroid function by disturbing gene transcription. Perfluorooctane sulfonate (PFOS), a persistent compound, is widely distributed in the aquatic environment and wildlife. In the present study, we investigated whether PFOS could disrupt the hypothalamic– pituitary–thyroid (HPT) axis. Zebrafish embryos were exposed to various concentrations of PFOS (0, 100, 200 and 400 lg L 1) and gene expression patterns were examined 15 d post-fertilization. The expression of several genes in the HPT system, i.e., corticotropin-releasing factor (CRF), thyroid-stimulating hormone (TSH), sodium/iodide symporter (NIS), thyroglobulin (TG), thyroid peroxidase (TPO), transthyretin (TTR), iodothyronine deiodinases (Dio1 and Dio2) and thyroid receptor (TRa and TRb), was quantitatively measured using real-time PCR. The gene expression levels of CRF and TSH were significantly up-regulated and down-regulated, respectively, upon exposure to 200 and 400 lg L 1 PFOS. A significant increase in NIS and Dio1 gene expression was observed at 200 lg L 1 PFOS exposure, while TG gene expression was down-regulated at 200 and 400 lg L 1 PFOS exposure. TTR gene expression was down-regulated in a concentration-dependent manner. Up-regulation and down-regulation of TRa and TRb gene expression, respectively, was observed upon exposure to PFOS. The whole body thyroxine (T4) content remained unchanged, whereas triiodothyronine (T3) levels were significantly increased, which could directly reflect disrupted thyroid hormone status after PFOS exposure. The overall results indicated that PFOS exposure could alter gene expression in the HPT axis and that mechanisms of disruption of thyroid status by PFOS could occur at several steps in the synthesis, regulation, and action of thyroid hormones.