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Showing papers by "Christer Hogstrand published in 2006"


Journal ArticleDOI
TL;DR: The results indicate that SNP induced cell death is caspase-3 related apoptosis and the treatment with CA inhibited the apoptotic pathway, suggesting that CA could be a beneficial additive to fish feeds in aquaculture.

68 citations


Journal ArticleDOI
TL;DR: Results suggest that NO plays an important role in regulation of cellular zinc homeostasis and that NO-mediated release of protein-bound Zn2+ may be an important signal in antioxidant defense.
Abstract: Metallothioneins (MTs) are small, cysteine-rich zinc binding proteins that are powerful antioxidants. In this study, we investigated the interaction between zinc, MTs, and other components of the antioxidant defense system in HepG2 cells. Cells were preincubated with zinc and then exposed to sodium nitroprusside (SNP), a nitric oxide (NO) donor. Both zinc pretreatment and SNP exposure separately induced transcription of MT genes (MT1A, MT2A, MT1E, MT1X), as measured using real time-polymerase chain reaction (PCR) after reverse transcription (RT). Pretreatment of HepG2 cells with zinc sulfate (ZnSO4) followed by SNP exposure caused MT and glucose-6-phosphate dehydrogenase (G6PD) mRNA levels to increase more than in cells only exposed to SNP. However, when cells were incubated with N,N,N',N'-tetrakis(2-pyridylmethyl)ethyl-enediamine (TPEN), a membrane-permeant Zn2+ chelator, the stimulation of MT transcription by SNP was blocked, suggesting that SNP-induced upregulation of these genes is zinc-dependent. Human glutathione-S-transferase (hGSTA1) and G6PD mRNA levels in the cells treated with 5 microM TPEN decreased. Additionally, the induction of MT by SNP after zinc pretreatment appears to be mediated by metal-activated transcription factor-1 (MTF-1), which is induced by labile zinc in the cytosol. SNP cytotoxicity was inhibited by preincubation with zinc. Taken together, these results suggest that NO plays an important role in regulation of cellular zinc homeostasis and that NO-mediated release of protein-bound Zn2+ may be an important signal in antioxidant defense.

55 citations


Journal ArticleDOI
TL;DR: An orthologue of the mammalian ZnT-1 (zinc transporter-1) gene was cloned from the intestine of the torafugu pufferfish (Takifugu rubripes), demonstrating that this gene predates the evolution of land-living vertebrates.
Abstract: An orthologue of the mammalian ZnT-1 (zinc transporter-1) gene was cloned from the intestine of the torafugu pufferfish (Takifugu rubripes), demonstrating that this gene predates the evolution of land-living vertebrates. TrZnT-1 (T. rubripes ZnT-1) shares overall topology with other members of the ZnT-1 family of zinc transporters, with six TMs (transmembrane domains) including a large histidine-rich intracellular loop between TM IV and V and intracellular C- and N-termini. Expression of TrZnT-1 in a metallothionein acquiescent cell line suggested that this protein reduces intracellular Zn2+ levels. Manipulation of the transporting media showed that several externally applied hydrominerals had no effect on TrZnT-1 activity. However, addition of N-ethylmaleimide increased TrZnT-1-mediated transport, possibly by increasing intracellular free Zn2+ levels by Zn2+ release from carrier proteins. Generation of a specific antibody and subsequent immunocytochemistry on fixed cells overexpressing TrZnT-1 indicated that the protein is localized to the plasma membrane in these cells. The genomic organization of TrZnT-1 is the same as that in mammals with two exons. The upstream regulatory region of the TrZnT-1 gene contains several putative cis-acting elements, including metal-response elements and an Sp1 site. Analysis of the DNA contigs surrounding the TrZnT-1 gene reveal limited synteny between corresponding regions in the rat, mouse and human; however, this was very low, with only two syntenic genes, ZnT-1 and NEK2 (never in mitosis gene A-related kinase).

26 citations


Journal ArticleDOI
TL;DR: Although fecundity was unaffected at all five tested concentrations during the test with silver in water only, it was significantly reduced at the two highest waterborne silver concentrations (12 and 24 microg/L) during thetest with silver dosed into food and water.
Abstract: Tests were conducted with mysids (Americamysis bahia) and silversides (Menidia beryllina) to evaluate the influence of salinity and organic carbon on the chronic toxicity of silver. During 7- and 28-d tests conducted at 10, 20, and 30‰ salinity, higher concentrations of dissolved silver generally were required to cause a chronic effect as the salinity of the seawater was increased. The 28-d mysid and silverside 20%-effective concentration values (expressed as dissolved silver) ranged from 3.9 to 60 and from 38 to 170 μg/L, respectively, over the salinity range. This pattern was not observed when the same test results were evaluated against the concentrations of free ionic silver (measured directly during toxicity tests), as predicted by the free-ion activity model. Increasing the concentration of dissolved organic carbon from 1 mg/L to the apparent maximum achievable concentration of 6 mg/L in seawater caused a slight decrease in chronic toxicity to silversides but had no effect on the chronic toxicity to mysids. The possible additive toxicity of silver in both food and water also was investigated. Even at the maximum achievable foodborne concentration, the chronic toxicity of silver added to the water was not affected when silver was also added to the food, based on the most sensitive endpoint (growth). However, although fecundity was unaffected at all five tested concentrations during the test with silver in water only, it was significantly reduced at the two highest waterborne silver concentrations (12 and 24 μg/L) during the test with silver dosed into food and water.

11 citations


Journal ArticleDOI
TL;DR: Preliminary experiments to deplete B cells indicate that neither the source of the soluble factors or the proliferating responder cells are B cells, which begins to define the cellular basis of CpG-mediated immunostimulation in trout.
Abstract: Bacterial DNA and synthetic oligodeoxynucleotides (ODN) that contain unmethylated cytosine-guanine dinucleotides (CpGs) have been shown to have immunostimulatory effects on B cells, natural killer cells and dendritic cells in mammals. However, little is known of the cellular basis of CpG immunostimulation in fish. We have addressed this question in the rainbow trout, Oncorhynchus mykiss. Prokaryotic DNA (from Escherichia coli), but not eukaryotic DNA (from calf), caused proliferation of spleen and head kidney cells, whereas CpG ODNs stimulated only head kidney cells. While spleen cells remained unresponsive to direct stimulation with CpG ODN, conditioned medium collected from spleen and head kidney cells both stimulated proliferation, suggesting CpG ODNs induce the secretion of immunomodulatory factors. Preliminary experiments to deplete B cells indicate that neither the source of the soluble factors or the proliferating responder cells are B cells. These data begin to define the cellular basis of CpG-mediated immunostimulation in trout.

9 citations