In vitro bioavailability of heavy metals in pressure-treated wood dust.

Pressure treatment with chromium, copper, and arsenic (CCA) is the most prevalent method for protecting wood used in outdoor construction projects. Although these metals are tightly bound to the wood fibers and are not released under most conditions of use, we examined the bioavailability of metals in CCA pressure-treated wood dust in vitro. Cytotoxicity and metallothionein (MT) mRNA expression were examined in V79 Chinese hamster lung fibroblast cells incubated with respirable-size wood dust generated by sanding CCA-treated and untreated (control) Southern yellow pine. In colony survival studies, increased cytotoxicity (p < 0.05) occurred in V79 cells treated with CCA wood dust (351 +/- 77 microg/ml, mean +/- SE) compared with control wood dust (883 +/- 91 microg/ml). Increased cytotoxicity with CCA wood dust also occurred in an arsenic resistant subline of V79 cells, thus suggesting that arsenic was not responsible for the increased cytotoxicity. Metallothionein mRNA was significantly increased after 48 h of treatment with CCA wood dust compared with control wood dust. Incubation of CCA wood dust in cell culture media resulted in the transfer of copper, but not chromium or arsenic, into the media. Moreover, the treatment of cells with this filtered extract resulted in significantly increased metallothionein mRNA, suggesting that bioavailable copper is responsible for inducing metallothionein mRNA in V79 cells. Thus, these bioassays suggest that metals become bioavailable during in vitro culture of phagocytic V79 cells with CCA wood dust.     

三种牙科钴铬生物烤瓷合金抗拉强度的对比测试研究

目的 对比测试新型国产钴铬生物烤瓷合金（CW-CC）、德国产BEGO Wirron bord C合金和德国Reminum 2000合金的抗拉强度,为进一步的研制开发适合临床要求的生物合金提供实验依据.方法 将3种合金各制备5个试样,打磨修整后用万能测试机测量其合金的抗拉强度,并采用SEM分析其抗拉强度的差异.结果 CW-CC钴铬生物烤瓷合金抗拉强度（785±21）MPa与德国Reminum 2000合金抗拉强度（764±15）MPa比较差异无统计学意义（P＞0.05）,与德国产BEGO Wirron bord C合金抗拉强度（680±12）MPa比较,差异有统计学意义（P＜0.05）.结论 新型国产钴铬生物烤瓷合金的抗拉强度达到烤瓷合金的性能要求.     

五种常用口腔修复材料对细菌滞留影响的临床研究

目的:评价不同修复材料对牙周组织的潜在危害.方法:采用临床实验的方法观察了5种常用口腔修复材料在体内戴用2个月后的细菌粘附量及其种类.结果:(1)树脂粘附的微生物最多,其次为钴铬合金和镍铬合金,纯钛和Ⅲ型金合金最少;(2)G-杆菌在树脂组明显多于钴铬合金和镍铬合金组,在纯钛和Ⅲ型金合金上粘附最少.对于G-球菌,树脂组明显多于钴铬合金、镍铬合金和纯钛组,Ⅲ型金合金组最少.白色念珠菌在树脂组有少量粘附,但在4种牙科金属上粘附量极少.结论:从对牙周组织的危害程度看,纯钛和Ⅲ型金合金应为临床医生的首选材料,其次为钴铬合金和镍铬合金.     

Assessment of immunotoxicity in female Fischer 344/N and Sprague Dawley rats and female B6C3F1 mice exposed to hexavalent chromium via the drinking water

Sodium dichromate dihydrate (SDD), an inorganic compound containing hexavalent chromium (Cr(VI)), is a common environmental contaminant of groundwater sources due to widespread industrial use. There are indications in the literature that Cr(VI) may induce immunotoxic effects following dermal exposure, including acting as both an irritant and a sensitizer; however, the potential immunomodulatory effects of Cr(VI) following oral exposure are relatively unknown. Following the detection of Cr(VI) in drinking water sources, the National Toxicology Program (NTP) conducted extensive evaluations of the toxicity and carcinogenicity of SDD following drinking water exposure, including studies to assess the potential for Cr(VI) to modulate immune function. For the immunotoxicity assessments, female Fischer 344/N (F344/N) and Sprague Dawley (SD) rats and female B₆C₃F₁ mice were exposed to SDD in drinking water for 28 consecutive days and evaluated for alterations in cellular and humoral immune function as well as innate immunity. Rats were exposed to concentrations of 0, 14.3, 57.3, 172, or 516?ppm SDD while mice were exposed to concentrations of 0, 15.6, 31.3, 62.5, 125, or 250?ppm SDD. Final mean body weight and body weight gain were decreased relative to controls in 250?ppm B₆C₃F₁ mice and 516?ppm SD rats. Water consumption was significantly decreased in F344/N and SD rats exposed to 172 and 516?ppm SDD; this was attributed to poor palatability of the SDD drinking water solutions. Several red blood cell-specific parameters were significantly (5–7%) decreased in 250?ppm mice; however, these parameters were unaffected in rats. Sporadic increases in the spleen IgM antibody response to sheep red blood cells (SRBC) were observed, however, these increases were not dose-dependent and were not reproducible. No significant effects were observed in the other immunological parameters evaluated. Overall, exposure to Cr(VI) in drinking water had limited effects on the immune system in both rats and mice.     

In vivo chromium-enhanced MRI of the retina

Chromium (Cr) has been used histologically to stabilize lipid fractions in the retina and is suggested to enhance oxidizable lipids in brain MRI. This study explored the feasibility, sensitivity, and specificity of in vivo chromium‐enhanced MRI of retinal lipids by determining its spatiotemporal profiles and toxic effect after intravitreal Cr(VI) injection to normal adult rats. One day after 3 μL Cr(VI) administration at 1–100 mM, the retina exhibited a dose‐dependent increase in T₁‐weighted hyperintensity until 50 mM. Time‐dependently, significant T₁‐weighted hyperintensity persisted up to 2 weeks after 10 mM Cr(VI) administration. Three‐dimensional chromium‐enhanced MRI of ex vivo normal eyes at isotropic 50‐μm resolution showed at least five alternating bands across retinal layers, with the outermost layer being the brightest. This agreed with histology indicating alternating lipid contents with the highest level in the photoreceptor layer of the outer retina. Although Cr(VI) reduction may induce oxidative stress and depolymerize microtubules, manganese‐enhanced MRI after chromium‐enhanced MRI showed a dose‐dependent effect of Cr toxicity on manganese uptake and axonal transport along the visual pathway. These results potentiated future longitudinal chromium‐enhanced MRI studies on retinal lipid metabolism upon further optimization of Cr doses with visual cell viability. Magn Reson Med, 2012. © 2011 Wiley Periodicals, Inc.     

Quantifying subtle but persistent peri-spine inflammation in vivo to submicron cobalt–chromium alloy particles

Purpose

We evaluated the consequences of cobalt–chromium alloy (CoCr) wear debris challenge in the peri-spine region to determine the inflammation and toxicity associated with submicron particulates of CoCr-alloy and nickel on the peri-spine.

Methods

The lumbar epidural spaces of (n = 50) New Zealand white rabbits were challenged with: 2.5 mg CoCr, 5.0 mg CoCr, 10.0 mg CoCr, a positive control (20.0 mg of nickel) and a negative control (ISOVUE-M-300). The CoCr-alloy and Ni particles had a mean diameter of 0.2 and 0.6 μm, respectively. Five rabbits per dose group were studied at 12 and 24 weeks. Local and distant tissues were analyzed histologically and quantitatively analyzed immunohistochemically (TNF-α and IL-6).

Results

Histologically, wear particles were observed in all animals. There was no evidence of toxicity or local irritation noted during macroscopic observations in any CoCr-dosed animals. However, Ni-treated control animals experienced bilateral hind leg paralysis and were euthanized at Day 2. Histopathology of the Ni particle-treated group revealed severe neuropathy. Quantitative immunohistochemistry demonstrated a CoCr-alloy dose-dependent increase in cytokines (IL-6, TNF-α, p < 0.05) at 12 and 24 weeks.

Conclusions

Subtle peri-spine inflammation associated with CoCr-alloy implant particles was dose dependent and persistent. Neuropathy can be induced by highly reactive Ni particles. This suggests peri-spine challenge with CoCr-alloy implant debris (e.g., TDA) is consistent with past reports using titanium alloy particles, i.e., mild persistent inflammation.     

hOGG1基因在Cr(Ⅵ)诱导线粒体DNA氧化损伤中的作用

目的探讨hOGG1基因在Cr(Ⅵ)诱导线粒体DNA氧化损伤中的修复作用。方法取不同浓度的Cr(Ⅵ)(0、2、8和32μmol/L)处理L-02肝细胞24h,分别测定细胞内活性氧簇(ROS)与hOGG1 mRNA表达水平和线粒体内8-羟基脱氧鸟苷(8-OHdG)与hOGG1基因表达的人类8-羟基鸟嘌呤DNA糖苷酶蛋白(hOGG1蛋白)水平。结果 8μmol/L和32μmol/L剂量组与对照组比较,细胞内ROS平均水平及线粒体内8-OhdG平均水平均明显增加(P<0.05),而hOGG1基因mRNA水平和线粒体内hOGG1蛋白水平,与对照组比较,2μmol/L剂量组两者水平均上升(P<0.05),32μmol/L剂量组两者水平均降低(P<0.05)。结论 Cr(Ⅵ)可诱导细胞内ROS水平增加,引起线粒体DNA氧化损伤,而hOGG1基因表达水平的改变,影响了线粒体DNA的修复能力。hOGG1基因在Cr(Ⅵ)诱导线粒体DNA氧化损伤中起到了重要的作用。     

25家电镀企业中铬污染现状和作业者接触情况

目的 了解电镀企业铬污染现状和工人铬接触情况,寻找有效的铬接触生物标记物,为铬污染的防治提供科学依据.方法 采用整群抽样的方式抽取杭州市25家使用6价铬的电镀企业,进行职业卫生现场调查和空气中铬浓度检测,并对157名铬接触工人和93名非接触工人进行健康调查和体内红细胞中铬含量检测.结果 车间空气中6价铬短时间接触浓度中位数为0.06 mg/m3,范围0.01(检出限)～0.53 mg/m3,合格率89.4％;其中超标岗位均为电镀岗位,中位数0.10 mg/m3,范围0.01(检出限)～0.53 mg/m3,合格率76.3％.铬接触工人红细胞内铬含量的中位数为4.41( 2.50～5.29) μg/L,显著高于对照人群[1.54 (0.61～2.98) μg/L,P＜0.01).按性别、年龄、吸烟、饮酒分层后,除了小于30岁的人群(P=0.11),其余各层内两组间的差异都有统计学意义(P＜0.05).在接触工人中,吸烟者红细胞内铬含量[4.98(2.90～6.37) μg/L]明显高于不吸烟的人群[3.58( 2.25～4.40) μg/L],差异有统计学意义(P＜0.05).结论 杭州市电镀作业环境中存在6价铬污染,电镀作业工人体内铬负荷显著高于对照人群.应降低作业环境中铬浓度,加强工人个体防护,降低6价铬对工人的危害.     

Chromium-containing traditional Chinese medicine,Tianmai Xiaoke Tablet improves blood glucose through activating insulin-signaling pathway and inhibiting PTPIB and PCK2 in diabetic rats

OBJECTIVE： Chromium is an essential mineral that is thought to be necessary for normal glucose homeostasis. Numerous studies give evidence that chromium picolinate can modulate blood glucose and insulin resistance. The main ingredient of-13anmai Xiaoke （TMXK） Tablet is chromium picolinate. In China, TMXK Tablet is used to treat type 2 diabetes. This study investigated the effect of TMXK on glucose metabolism in diabetic rats to explore possible underlying molecular mechanisms for its action. METHODS： Diabetes was induced in rats by feeding a high-fat diet and subcutaneously injection with a single dose of streptozotocin （50 mg/kg, tail vein）. One week after streptozotocin-injection, model rats were divided into diabetic group, low dose of TMXK group and high dose of TMXK group. Eight normal rats were used as normal control. After 8 weeks of treatment, skeletal muscle was obtained and was analyzed using Roche NimbleGen mRNA array and quantitative polymerase chain reaction （qPCR）. Fasting blood glucose, oral glucose tolerance test and homeostasis model assessment of insulin resistance （HOMA-IR） index were also measured. RESULTS： The authors found that the administration of TMXK Tablet can reduce the fasting blood glucose and fasting insulin level and HOMA-IR index. The authors also found that 2 223 genes from skeletal muscle of the high-dose TMXK group had significant changes in expression （1 752 increased, 471 decreased）. Based on Kyoto encyclopedia of genes and genomes pathway analysis, the most three significant pathways were ＂insulin signaling pathway＂, ＂glycolysis/ gluconeogenesis＂ and ＂citrate cycle （-ICA）＂. qPCR showed that relative levels of forkhead box 03 （Fox03）, phosphoenolpyruvate carboxykinase 2 （Pck2）, and protein tyrosine phosphatase 1B （Ptplb） were significantly decreased in the high-dose TMXK group, while v-akt murine thymoma viral oncogene homolog 1 （Aktl） and insulin receptor substrate 2 （Its2） were increased. CONCLUSION： Our data show that TMXK Tablet reduces fasting glucose level and improves insulin resistance in diabetic rats. The mechanism may be linked to the inactivation of PTP1B and PCK enzymes, or through intracellular pathways, such as the insulin signaling pathway.