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  • Rats  (10)
  • Chemistry
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  • 1
    Language: English
    In: Environmental Toxicology and Chemistry, 2001, Vol.20(9), p.2088
    Description: We studied the chronic effects of 4-nonylphenol (4-NP) on reproductive status of medaka (Oryzias latipes) over two generations of continuous exposure. The exposure study of the parental (F0) medaka was begun on embryos within 24 h post-fertilization and continued with monitoring through embryological development, hatching, posthatch survival, growth, sexual differentiation, and reproduction under flow-through exposures to mean measured 4-NP concentrations of 4.2, 8.2, 17.7, 51.5, and 183 µg/litre for up to 104 d. Eggs spawned from the F0 fish at 102 and 103 d posthatch were also examined for hatchability, survival after hatching, growth, and sexual differentiation until 60 d posthatch. The 183-µg/litre treatment significantly reduced the embryo survival and swim-up success of the F0 fish. The cumulative mortality after swim-up of the F0 fish exposed to 17.7 and 51.5 µg/litre were significantly higher than the control mortality. No concentration-related effect of 4-NP was observed on the growth of surviving F0 fish at 60 d posthatch. However, the sex ratio estimated from the appearance of their secondary sex characteristics was skewed toward female in the 51.5-µg/litre treatment. Additionally, gonadal histology showed that 20% of the fish in the 17.7-µg/litre treatment and 40% in the 51.5-µg/litre treatment had testis-ova, indicating that 4-NP affects the gonadal development and survival of medaka at similar concentrations in juveniles. The sex ratio of the F0 fish in the 51.5-µg/litre treatment was completely skewed toward female; subsequently, the effects on fecundity and fertility in this generation were monitored at mean measured concentrations of 4.2, 8.2, and 17.7 µg/litre from 71 to 103 d posthatch. Fecundity was unaffected by any of the treatments examined. The mean fertility in the 17.7-µg/litre treatment was reduced to 76% of that in the controls, although no statistically significant differences were determined. Overall, these results indicate that the lowest-observed-effect concentration (LOEC) and no-observed-effect concentration (NOEC) of 4-NP through the life cycle of the F0 medaka were 17.7 and 8.2 µg/litre, respectively. In the F1 medaka, no significant effects were observed on hatching success, posthatch mortality, or growth, but sexual differentiation at 60 d posthatch was affected. Induction of testis-ova in the gonads of the F1 fish was observed in both the 8.2- and the 17.7-µg/litre concentrations. The results indicate that 4-NP can have significant effects on reproductive potential of medaka at concentrations as low as 17.7 µg/litre.
    Keywords: Aquatic Animals ; Aquatic Organisms ; Embryonic Development ; Embryos ; Growth ; Mortality ; Nontarget Effects ; Ovaries ; Reproduction ; Sex Differentiation ; Survival ; Testes ; Toxic Substances ; Toxicity ; Toxicology ; Aquatic Species ; Death Rate ; Embryo Development ; Embryo Growth ; Nonylphenols ; Poisons ; Testicles ; Oryzias Latipes ; Oryzias ; Adrianichthyidae ; Beloniformes ; Osteichthyes ; Fishes ; Vertebrates ; Chordata ; Animals ; Eukaryotes;
    ISSN: 0730-7268
    E-ISSN: 1552-8618
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  • 2
    Language: English
    In: Environmental Toxicology and Chemistry, September 1999, Vol.18(9), pp.1948-1955
    Description: The study aims to evaluate the impact of insecticides associated with rainfall‐induced surface runoff from arable land on macroinvertebrate populations. These effects of insecticides were distinguished from the hydraulic stress also associated with surface runoff. Transient increase in discharge and insecticide contamination (maximum 6 μg/L parathion‐ethyl in stream water, 302 μg/L fenvalerate in suspended particulates) was observed in a headwater stream subsequent to surface runoff from arable land. In the aquatic macroinvertebrate community, eight of the eleven abundant species disappeared, and the remaining three were reduced significantly in abundance following the insecticide‐contaminated runoff. Recovery within 6 months was observed for four species and recovery within 11 months for nine species. Two species remained at a low population density for over a year. The effects of insecticides were distinguished from other parameters, such as hydraulic stress associated with surface runoff, as well. The causal connection between insecticide contamination and biological response was established by eliminating increased hydraulic stress during surface runoff using in‐parallel bypass microcosms containing the dominant species and . The mortality of these species was similar to that of the same species in the stream. Additional microcosms, disconnected from the stream during runoff events, served as a control. Thus, the toxic potential of the runoff water is considered to be responsible for the observed effect on the macroinvertebrates. It is concluded that agricultural insecticide input may alter the dynamics of macroinvertebrate communities in streams.
    Keywords: Pesticides ; Headwater Stream ; Macroinvertebrates ; Recovery ; Microcosm
    ISSN: 0730-7268
    E-ISSN: 1552-8618
    Source: John Wiley & Sons, Inc.
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  • 3
    Language: English
    In: The Journal of biological chemistry, 22 October 2010, Vol.285(43), pp.32878-87
    Description: The corticotropin-releasing factor receptor type 2a (CRF(2(a))R) belongs to the family of G protein-coupled receptors. The receptor possesses an N-terminal pseudo signal peptide that is unable to mediate targeting of the nascent chain to the endoplasmic reticulum membrane during early receptor biogenesis. The pseudo signal peptide remains uncleaved and consequently forms an additional hydrophobic receptor domain with unknown function that is unique within the large G protein-coupled receptor protein family. Here, we have analyzed the functional significance of this domain in comparison with the conventional signal peptide of the homologous corticotropin-releasing factor receptor type 1 (CRF(1)R). We show that the presence of the pseudo signal peptide leads to a very low cell surface receptor expression of the CRF(2(a))R in comparison with the CRF(1)R. Moreover, whereas the presence of the pseudo signal peptide did not affect coupling to the G(s) protein, G(i)-mediated inhibition of adenylyl cyclase activity was abolished. The properties mediated by the pseudo signal peptide were entirely transferable to the CRF(1)R in signal peptide exchange experiments. Taken together, our results show that signal peptides do not only influence early protein biogenesis. In the case of the corticotropin-releasing factor receptor subtypes, the use of conventional and pseudo signal peptides have an unexpected influence on signal transduction.
    Keywords: Protein Sorting Signals ; Adenylyl Cyclases -- Metabolism ; Gtp-Binding Protein Alpha Subunits, Gi-Go -- Metabolism ; Gene Expression Regulation -- Physiology ; Receptors, Corticotropin-Releasing Hormone -- Biosynthesis ; Signal Transduction -- Physiology
    E-ISSN: 1083-351X
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 4
    Language: English
    In: BBA - Biomembranes, September 2013, Vol.1828(9), pp.2121-2133
    Description: The cell-toxic bile salt glycochenodeoxycholic acid (GCDCA) and taurochenodeoxycholic acid (TCDCA) are responsible for hepatocyte demise in cholestatic liver diseases, while tauroursodeoxycholic acid (TUDCA) is regarded hepatoprotective. We demonstrate the direct mitochondrio-toxicity of bile salts which deplete the mitochondrial membrane potential and induce the mitochondrial permeability transition (MPT). The bile salt mediated mechanistic mode of destruction significantly differs from that of calcium, the prototype MPT inducer. Cell-toxic bile salts initially bind to the mitochondrial outer membrane. Subsequently, the structure of the inner boundary membrane disintegrates. And it is only thereafter that the MPT is induced. This progressive destruction occurs in a dose- and time-dependent way. We demonstrate that GCDCA and TCDCA, but not TUDCA, preferentially permeabilize liposomes containing the mitochondrial membrane protein ANT, a process resembling the MPT induction in whole mitochondria. This suggests that ANT is one decisive target for toxic bile salts. To our knowledge this is the first report unraveling the consecutive steps leading to mitochondrial destruction by cell-toxic bile salts.
    Keywords: Mitochondria ; Bile Salts ; Cholestasis ; Mitochondrial Permeability Transition ; Liver ; Chemistry
    ISSN: 0005-2736
    E-ISSN: 1879-2642
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  • 5
    Language: English
    In: The Journal of biological chemistry, 25 August 2006, Vol.281(34), pp.24910-21
    Description: The corticotropin-releasing factor receptor type 2a (CRF(2(a)) receptor) belongs to the family of G protein-coupled receptors. The receptor possesses a putative N-terminal signal peptide that is believed to be cleaved-off after mediating the endoplasmic reticulum targeting/insertion process, like the corresponding sequence of the homologous CRF(1) receptor. Here, we have assessed the functional significance of the putative signal peptide of the CRF(2(a)) receptor and show that it is surprisingly completely incapable of mediating endoplasmic reticulum targeting, despite meeting all sequence criteria for a functional signal by prediction algorithms. Moreover, it is uncleaved and forms part of the mature receptor protein. Replacement of residue Asn(13) by hydrophobic or positively charged residues converts the sequence into a fully functional and cleaved signal peptide demonstrating that conventional signal peptide functions are inhibited by a single amino acid residue. Deletion of the domain leads to an increase in the amount of immature, intracellularly retained receptors demonstrating that the sequence has adopted a new function in receptor trafficking through the early secretory pathway. Taken together, our results identify a novel hydrophobic receptor domain in the family of the heptahelical G protein-coupled receptors and the first pseudo signal peptide of a eukaryotic membrane protein. Our data also show that the extreme N termini of the individual CRF receptor subtypes differ substantially.
    Keywords: Receptors, Corticotropin-Releasing Hormone -- Chemistry
    ISSN: 0021-9258
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 6
    In: Journal of Neurochemistry, August 2002, Vol.82(3), pp.458-467
    Description: To investigate the effects of dopamine (DA) on the release of glutathione (GSH) from astrocytes, we used astroglia‐rich primary cultures from the brains of newborn rats. In the absence of DA, GSH accumulated in the medium of these cultures with a constant rate. In contrast, during incubation of the cells with 50 µ DA extracellular GSH was not detectable anymore. This disappearance of extracellular GSH was prevented by superoxide dismutase, indicating that DA does not affect GSH release but rather reacts with the released GSH in a superoxide‐dependent reaction. Incubation of astroglial cultures with 0.5 and 1 m DA established almost constant extracellular concentrations of HO of 5 µ and 15 µ, respectively. Under these conditions astroglial cultures release glutathione disulphide (GSSG). This GSSG export was blocked by catalase and by MK571, an inhibitor of the multidrug resistance protein 1. The effects of DA on the extracellular accumulations of GSH and GSSG were not modulated by inhibitors of DA receptors, DA transport, and monoamine oxidases. The other catecholamines adrenalineandnoradrenaline showed similar effects on the accumulation of GSH and GSSG in the medium compared with those obtained for DA. In conclusion, the data presented demonstrate that DA affects astroglial GSH metabolism by two mechanisms: (i) directly by chemical reaction with extracellular GSH, and (ii) indirectly by generation of hydrogen peroxide that leads to the efflux of GSSG from astroglial cells. These observations are discussed in the context of the brain's GSH metabolism in Parkinson's disease.
    Keywords: Astrocytes ; Dopamine ; Glutathione Efflux ; Oxidative Stress ; Parkinson'S Disease
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 7
    In: Journal of Neurochemistry, January 2001, Vol.76(2), pp.627-636
    Description: The release of glutathione disulfide has been considered an important process for the maintenance of a reduced thiol redox potential in cells during oxidative stress. In cultured rat astrocytes, permanent hydrogen peroxide‐induced oxidative stress caused a rapid increase in intracellular glutathione disulfide, which was followed by the appearance of glutathione disulfide in the medium. Under these conditions, the viability of the cells was not compromised. In the presence of cyclosporin A and the quinoline‐derivative MK571, inhibitors of multidrug resistance proteins (MRP1 and MRP2), glutathione disulfide accumulated in cells and the release of glutathione disulfide from astrocytes during HO stress was potently inhibited, suggesting a contribution of MRP1 or MRP2 in the release of glutathione disulfide from astrocytes. Using RT‐PCR we amplified a cDNA from astroglial RNA with a high degree of homology to MRP1 from humans and mouse. In contrast, no fragment was amplified by using primers specific for rat MRP2. In addition, the presence of MRP1 protein in astrocytes was demonstrated by its immunolocalization in cells expressing the astroglial marker protein glial fibrillary acidic protein. Our data identify rat astrocytes as a MRP1‐expressing brain cell type and demonstrate that this transporter participates in the release of glutathione disulfide from astrocytes during oxidative stress.
    Keywords: Astrocytes ; Glutathione ; Mrp ; Oxidative Stress ; Transport
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 8
    Language: English
    In: Chemosphere, 1992, Vol.25(7), pp.1207-1214
    Description: With routine methods of clinical chemistry and haematology we studied the possible effects of a single dose of 3,000 ng TCDD/kg body wt or of a continuous exposure to TCDD over 11 weeks in rats (3,000 ng TCDD/kg body wt initially and weekly maintenance-doses of 600 ng TCDD/kg body wt). Statistically significant differences between the vehicle- and the TCDD-treated rats one week after a single injection were found for serum cholesterol (TCDD 〈 vehicle) and glucose (TCDD 〉 vehicle). However, both differences were due to chance, and all values are within the range of historical control values. No corresponding effects were observed when exposure was kept at the same level for 11 weeks with weekly maintenance-doses. At the end of this 11-week treatment period tissue concentrations of TCDD were: 11,400 ± 1,900 ppt (pg/g wet wt) in liver and 3,100 ± 500 ppt in adipose tissue. These levels had been maintained over the entire period. After the continuous exposure to TCDD for 11 weeks the mean serum cholesterol level was slightly higher than in the current controls. However, this finding is without biological significance since the mean value is well within the normal range of the pooled controls of this study and of historical controls, and no single treated animal exhibited clearly increased values. The number of platelets was also significantly lower in the treated group when compared with the concurrent controls, but again the values of all the treated rats were well within the normal rage of the pooled control values. Although there was no statistically significant increase in the serum triglyceride levels, the values for four animals out of 12 were outside the range of the pooled controls of this study. Additionally, the total number of leucocytes was outside the control range (by −15%) in a single animal. The data suggest that in a short-term study (1 week) a dose of 3,000 ng TCDD/kg body wt did not induce any abnormal values in the variables of clinical chemistry or haematology tested - with the exception of two rats with clearly abnormal τ-GT values. When the corresponding exposure level of TCDD is kept constant over an extended period (11 weeks), an increase in serum triglyceride levels in 4 12 of the animals was observed. Since this dose level additionally also clearly reduces thymus weight, it must be considered generally toxic for this species. Beside an induction of hepatic monooxygenases, a dose of 1,000 ng TCDD/kg body wt was not found to induce signs of general toxicity in the rat.
    Keywords: 2,3,7,8-Tetrachlorodibenzo- P-Dioxin ; Tcdd ; Wistar Rats ; Clinical Chemistry ; Haematology ; Chemistry ; Ecology
    ISSN: 0045-6535
    E-ISSN: 1879-1298
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  • 9
    In: Traffic, January 2009, Vol.10(1), pp.2-15
    Description: The heptahelical G protein‐coupled receptors (GPCRs) are internalized following agonist treatment and either recycle rapidly to the plasma membrane or enter the lysosomal degradation pathway. Many conventional GPCR recycling assays suffer from the fact that receptors arriving from the secretory pathway may interfere with recycling receptors. In this study, we introduce a new methodology to study post‐endocytotic GPCR trafficking using fusions with the recently cloned Kaede protein. In contrast to the widely used green fluorescent protein, the fluorescence of Kaede can be converted from green to red using ultraviolet irradiation. Our methodology allows to study recycling of GPCRs microscopically in real‐time bypassing problems with secretory pathway receptors. Initially, receptors are internalized using an agonist. Fluorescence signals in endosomes are switched, and trafficking of the receptors to the plasma membrane can be easily visualized by monitoring their new fluorescence. Using this methodology, we show that the corticotropin‐releasing factor receptor type 1 belongs to the family of recycling GPCRs. Moreover, we demonstrate by fluorescence correlation spectroscopy that Kaede does not oligomerize when fused to membrane proteins, representing an additional advantage of this technique. The Kaede technology may be a powerful tool to study membrane protein trafficking in general.
    Keywords: Confocal Laser Scanning Microscopy ; Corticotropin‐Releasing Factor Receptor Type 1 ; Endosomes ; G Protein‐Coupled Receptors ; Internalization ; Kaede ; Lysosomes ; Recycling
    ISSN: 1398-9219
    E-ISSN: 1600-0854
    Source: John Wiley & Sons, Inc.
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  • 10
    Language: English
    In: Biochemical Pharmacology, 1995, Vol.50(9), pp.1517-1520
    Description: The induction of cytochrome P450 by enoxacin, ciprofloxacin, and ofloxacin was investigated in female Wistar rats. Animals were treated orally with daily doses ranging from 10 to 400 mg enoxacin per kg body wt, 400 mg ciprofloxacin, or 400 mg ofloxacin per kg body wt for up to 7 days. Activities of methoxyresorufin O-demethylase (MROD) and ethoxyresorufin O-deethylase (EROD) were determined fluorimetrically in hepatic microsomes. MROD activity was increased 2.6-fold after treatment with 100 mg enoxacin per kg body wt for 7 days. Lower doses of enoxacin did not induce MROD activity significantly. Antipeptide antibodies directed specifically against different rat cytochrome P450 enzymes demonstrated that CYP1A2, but not CYP1 A1, was induced in rats treated with enoxacin. After ciprofloxacin or ofloxacin treatment, no induction of MROD or EROD activity was observed. Neither ciprofloxacin nor ofloxacin caused any change in CYP1A1 or CYP1A2 apoprotein levels. Further investigations with antipeptide antibodies showed that there was no induction of CYP2B1, CYP2B2, CYP2E1, CYP3A1, CYP3A2, CYP4A1, or CYP4A2 following treatment with enoxacin, ciprofloxacin, or ofloxacin. It is concluded that enoxacin, but not ciprofloxacin or ofloxacin, is an inducer of CYP1A2 in rat liver.
    Keywords: Quinolones ; Induction ; Cyp1a2 ; Ethoxyresorufin ; Methoxyresorufin ; Pharmacy, Therapeutics, & Pharmacology ; Chemistry
    ISSN: 0006-2952
    E-ISSN: 1873-2968
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