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Selected AbstractsCadmium tolerance in the Nile tilapia (Oreochromis niloticus) following acute exposure: Assessment of some ionoregulatory parametersENVIRONMENTAL TOXICOLOGY, Issue 1 2006Sofia Garcia-Santos Abstract The Nile tilapia (Oreochromis niloticus) can tolerate very high levels of waterborne cadmium. It has one of the highest 96 h LC50 recorded for a freshwater teleost fish (14.8 mg/L Cd; hardness 50 mg/L CaCO3). Cadmium is known to perturb ion balance in teleost fishes. However, in an acute time course experiment, plasma Na+ concentrations were unaffected, and plasma Ca2+ values only decreased after 96 h exposure in a dose-independent manner. Branchial Na+/K+ -ATPase activity and ,-subunit protein level expression in crude gill homogenates were not affected by Cd exposure during this period. Branchial chloride cell numbers, identified as Na+/K+ -ATPase immunoreactive cells using immunohistochemistry, decreased 24 h after exposure but recovered thereafter. Histopathological changes did not follow a consistent pattern of variation with exposure time, and the alterations noted in gill epithelium were basically nonspecific to cadmium. Because of its tolerance, it can be concluded that the tilapia O. niloticus would not be a suitable test organism to evaluate sublethal toxicity of cadmium and the realistic impact of this pollutant in the environment. However, it certainly could contribute significantly to our understanding of the toxic mechanism of cadmium exposure in aquatic organisms. This is the first work to investigate the effect of waterborne pollutants on Na+/K+ -ATPase ,-subunit protein expression in fish gills. © 2006 Wiley Periodicals, Inc. Environ Toxicol 21: 33,46, 2006. [source] Routes of zinc entry in mouse cortical neurons: role in zinc-induced neurotoxicityEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2000Philippe Marin Abstract Exposure of central neurons to Zn2+ triggers neuronal death. The routes of Zn2+ entry were investigated in living cortical neurons from the mouse using the specific Zn2+ fluorescent dye N-(6-methoxy-8-quinolyl)-p-toluene sulphonamide (TSQ), which preferentially detects membrane-bound Zn2+. Exposure of cortical neurons to increasing concentrations of Zn2+ (1,100 ,m) induced a progressive increase in the fluorescence of TSQ. This fluorescence signal was not attenuated by the permeation of plasma membrane with digitonin. Accordingly, the major part of TSQ fluorescence (two-thirds) was associated to the particulate fraction of cortical neurons exposed to Zn2+. These results suggest that Zn2+ detected with TSQ in neurons is mainly bound to membranes. TSQ fluorescence measured in neurons exposed to 3 ,m Zn2+ was enhanced by Na+ -pyrithione, a Zn2+ ionophore, ,-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), N-methyl- d -aspartate (NMDA) or KCl-induced depolarization. However, in the absence of any treatment, TSQ labelling of neurons exposed to 3 ,m Zn2+ was only decreased by NMDA receptor antagonists, whereas it remained unaltered in the presence of antagonists of AMPA receptors or L-type voltage-gated Ca2+ channels. Zn2+ entry through NMDA receptors did not contribute to Zn2+ -induced neuronal death, as it was prevented by antagonists of NMDA receptors only when they were added after the Zn2+ exposure. Finally, Zn2+ induced a delayed accumulation of extracellular glutamate which might be responsible for the delayed NMDA receptor activation that leads to neuronal death. [source] Comparative single-strand conformation polymorphism (SSCP) and microscopy-based analysis of nitrogen cultivation interactive effects on the fungal community of a semiarid steppe soilFEMS MICROBIOLOGY ECOLOGY, Issue 2-3 2001Jennifer L. Lowell Abstract The effects of nitrogen accretion on fungal diversity and community structure in early-seral (cultivated) and native (uncultivated) shortgrass steppe soils were evaluated using single-strand conformation polymorphism (SSCP) and microscopy in a comparative experiment. Selected haplotypes generated from fungal 18S gene fragments were also sequenced for species identification. Microscopy-based analyses showed significantly shorter fungal hyphal lengths in the early-seral control plots in comparison with the native control plots (P<0.0003), independent of nitrogen addition. Although diversity indices did not show significant differences between the plots, SSCP analyses indicated that fungal community structure differed in the native and early-seral control sites. In nitrogen-amended sites, gene sequences from dominant haplotypes indicated a shift to a more common nitrogen-impacted fungal community. While nitrogen amendments appear to be more important than cultivation in influencing these soil fungal communities, hyphal lengths were only decreased due to cultivation. The use of microscopic and molecular techniques, as carried out in this study, provided integrative information concerning fungal community responses to wide spread stresses being imposed globally on terrestrial ecosystems, that is not provided by the individual techniques. [source] Protein kinase C, mediates ethanol withdrawal hyper-responsiveness of NMDA receptor currents in spinal cord motor neuronsBRITISH JOURNAL OF PHARMACOLOGY, Issue 3 2005Hui-Fang Li 1The present studies were designed to test the hypothesis that neuronal-specific protein kinase C, (PKC,) plays a critical role in acute ethanol withdrawal hyper-responsiveness in spinal cord. 2Patch-clamp studies were carried out in motor neurons in neonatal rat spinal cord slices. Postsynaptic currents were evoked by brief pulses of 2 mMN -methyl- D -aspartic acid (NMDA) in the presence of bicuculline methiodide 10 ,M; strychnine 5 ,M and tetrodotoxin 0.5 ,M. 3Both ethanol depression and withdrawal hyper-responsiveness of NMDA-evoked currents are dependent on increases in intracellular Ca2+. Blocking intracellular increase in Ca2+ by 30 mM 1,2-bis(2-aminophenoxy)-ethane- N,N,N,,N,-tetraacetic acid (BAPTA) not only decreased the ethanol-induced depression of NMDA-evoked currents (33±5% in control vs 20±3% in BAPTA, P<0.05) but also eliminated acute ethanol withdrawal hyper-responsiveness. 4Immunohistochemistry studies revealed that neonatal spinal cord motor neurons contain an abundance of nuclear PKC,. 5Exposure to ethanol (100 mM) induced PKC, translocation from the nucleus to cytoplasm in motor neurons. Pretreatment with the , -isozyme-specific peptide PKC inhibitor, ,V5-3, blocked ethanol-induced translocation and also blocked withdrawal hyper-responsiveness. 6The results show that PKC, mediates ethanol withdrawal hyper-responsiveness in spinal motor neurons; the results may be relevant to some symptoms of ethanol withdrawal in vivo. British Journal of Pharmacology (2005) 144, 301,307. doi:10.1038/sj.bjp.0706033 [source] | ||||||||||