[Study on the solid sorbent tube for capturing mercury in the workplace air and determination by cold vapor atomic absorption spectrometry].

A new KMnO4-MnO2 solid multisorbent tube for capturing mercury in workplace air was developed. Experimental conditions for solid multisorbent tube, efficiency of sampling, desorption efficiency and stability were studied. Mercury and its compounds in air were captured by solid KMnO4-MnO2 sorbent filled tube and desorbed with 0. 90 mol L-1 sulfuric acid solution. Mercury and its compounds were quantitatively analyzed according to the method of GBZ/T 160. 14-2004 cold vapor atomic absorption spectrometry. The linear range of the proposed method was 0. 000 2-0. 015 0 mg L-1 with r=0. 999 1, the average efficiency of sampling was 99. 9%-100. 0% in the concentration range of 0. 001-2. 820 mg m-3 , and the breakthrough capacity was more than 505.4 microg for 300 mg KMnO4-MnO2 solid multisorbent, the average recovery rate was 96. 4% approximately103. 8%, the intra-day and inter-day precision was 3. 0% approximately 3. 3% and 3. 5% approximately 5. 2% respectively, the limit of detection was 0. 0013 mg m-3 (7. 5 L of air ) and 0. 000 6 mg m-3 (96 L of air), after sampling, and the solid multisorbent tube could be kept at least 30 d at room temperature without significant loss. The present method was simple and suitable for capturing mercury and its compounds in the workplace air and ambient air. The solid multisorbent tube was useful for personal sampling and time weighted average sampling.

C-Reactive protein-induced endothelial microparticle generation in HUVECs is related to BH4-dependent NO formation.

BACKGROUND: C-reactive protein (CRP) has been proven to facilitate endothelial injury via reduced NO production. Endothelial microparticles (EMPs) have emerged as a novel marker of endothelial injury. METHODS: In vitro cultured human umbilical vein endothelial cells (HUVECs) were incubated with CRP (20 mg/l) for 24 h. The numbers of EMPs with CD31- and CD51-positive staining were assessed flow-cytometrically, and NO production was measured using the Griess reaction in the presence or absence of tetrahydrobiopterin (BH(4)), respectively. RESULTS: The number of EMPs was significantly increased in HUVECs stimulated by CRP compared with the control group and, in parallel, NO production was decreased (p < 0.05). In the presence of CRP, pretreatment with BH(4) decreased EMP counts and restored NO production to baseline levels (p < 0.05) while pretreatment with 2,4-diamino-6-hydroxypyrimidine (DAHP), a BH(4) synthesis inhibitor, further prompted EMP formation and decreased NO production (p < 0.05). However, adding exogenous BH(4) after pretreatment with DAHP suppressed EMP formation and restored NO production (p < 0.05). CONCLUSIONS: This study demonstrates that CRP induces EMP generation in HUVECs and this effect is, at least in part, related to impaired BH(4)-dependent NO production. Augmented EMP generation in HUVECs is suggested as a novel potential mechanism contributing to the pathogenesis of vascular injury related to CRP.