An enhanced photochemical vapor generation (PVG) sample introduction procedure is developed for the determination of trace Bi with inductively coupled plasma mass spectrometry (ICP MS) by the addition of iron. Gas chromatography mass spectrometry (GC−MS) reveals that (CH 3 ) 3 Bi is the major component of the volatile Bi species formed in the presence of 20% (v/v) acetic acid, 5% (v/v) formic acid, and 60 μg mL −1 Fe 3+ under UV irradiation. The addition of Fe 3+ not only largely increases the PVG efficiency of Bi 3+ but also accelerates the reaction kinetics of photochemical reduction of Bi 3+ . The analytical sensitivity was enhanced 30fold using PVG for sample introduction compared to that for direct solution nebulization detection by ICP MS detection. Furthermore, the proposed method shows much better tolerance of interference from Cu 2+ and Ni 2+ than that from conventional hydride generation (HG). Under the optimized conditions, a detection limit of 0.3 ng L −1 was obtained for Bi by ICP MS determination. The relative standard deviation (RSD) was 2.5% for seven replicate measurements of 0.5 ng mL −1 Bi 3+ standard solution. The proposed method has been successfully applied for the determination of Bi in environmental samples, including water samples, and certified reference material of soil (GSS-1) and sediments (GSD-5a and GSD-10) with satisfying results.
1 Previous studies have shown antifibrotic effects of somatostatin. Since hepatic stellate cells (HSC) express somatostatin receptors and play a key role in hepatic fibrogenesis, we investigated the in vitro antifibrotic effect of somatostatin on rat HSC. 2 At day 12 after isolation, cells were exposed to different concentrations of somatostatin (10 À6 -10 À9 mol l À1 ). 3 mRNA expression of collagen types I and III, and of smooth muscle a-actin (a-SMA) was analysed by Northern blotting. At 10 À9 mol l À1 , somatostatin significantly reduced mRNA expression of collagen I (72.3710.7%; 95% confidence interval (95% CI): 45.5-99.0), collagen III (79.074.5%; 95% CI: 67.6-90.4) and a-SMA (65.775.9%; 95% CI: 51.1-80.2), as compared to control normalized at 100%. These results were confirmed by quantitative RT-PCR. 4 Cycloheximide experiments indicated that somatostatin has no direct transcriptional effect.5 Using immunoprecipitation, we demonstrated that somatostatin also decreased de novo synthesis of collagen I (73710%; 95% CI: 48-98%), collagen III (65713%; 95% CI: 33-97%) and a-SMA (4779%; 95% CI: 25-69%). Remarkably, at higher concentrations, somatostatin did not suppress collagen mRNA expression nor de novo protein synthesis. We ascribe this observation to desensitization of the cells for somatostatin. 6 Cell proliferation, as measured by 5-bromo-2 0 -deoxyuridine labelling, was not altered by somatostatin. 7 No significant effect on the intermediate and actin cytoskeleton were detected by immunohistochemistry and Western blotting. 8 Our findings imply that in vivo antifibrotic effects of somatostatin could result partially from a direct action of somatostatin on HSC, but other, in vivo effects are probably also involved.
Exogenous hydrogen sulfide (H 2 S) protects kidneys from diabetic injuries in animal models. In order to explore the role of endogenous H 2 S in diabetic nephropathy, we determined the renal H2S producing enzymes in vivo and in vitro. In diabetic mice, H 2 S levels in blood and kidney were decreased while cystathionine β-synthase (CBS), mainly located in mouse renal proximal convoluted tubules (PCT), was reduced selectively. In cultured mouse PCT cells treated with high glucose, CBS protein and activity was reduced while ubiquitinated CBS was increased, which was abolished by a proteasome inhibitor MG132 at 1 hour; high glucose drove CBS colocalized with proteasome 26S subunit ATPase6, indicating an involvement of ubiquitination proteasome degradation. At 48 hours, high glucose also selectively decreased CBS protein, concentration-dependently, but increased the ubiquitination of CBS; silence of CBS by siRNA increased nitrotyrosine, a marker for protein oxidative injury. Nitrotyrosine was also increased by high glucose treatments. The increases of nitrotyrosine either by cbs-siRNA or by glucose were restored by GYY4137, indicating that the H 2 S donor may protect kidney from oxidative injury induced by CBS deficiency. In diabetic kidneys, ubiquitinated CBS and nitrotyrosine were increased but restored by GYY4137. The treatment also ameliorated albuminuria and renal morphologic changes in diabetic mice. Our findings suggest that high glucose induces reduction of renal CBS protein and activity in vivo and in vitro that is critical to the pathogenesis of diabetic kidney disease.
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