Increased nitric oxide levels and nitric oxide synthase isoform expression in the cerebellum of the taiep rat during its severe demyelination stage

We have previously reported progressive reactive astrocytes in the cerebellum of taiep rats, one of the most regions affected by demyelination, and activation of cerebellar glial cells in vitro. Based on the hypothesis that activated glial cells produce high levels of reactive nitrogen intermediates, we assessed the production of nitric oxide (NO) and the expression of the three NO synthases (NOS) in the cerebellum of 6-month-old taiep rats. A significant 40% increase of NO levels was measured in taiep rats when compared with controls. The protein and mRNA levels of the three NOS isoforms were also significantly increased. In contrast to controls, immunostaining assays against nNOS or iNOS showed an increased number of immunoreactive glial cells in the granular layer (nNOS) and Purkinje layer (iNOS) of cerebellum of taiep rats. Microglia-macrophages and both CD4- and CD8-immunoreactive cells were observed in cerebellar white matter of taiep rats only, thus suggesting other possible cell sources of those NOSs. Differences in the cellular location for eNOS immunoreactivity were not observed. The enhanced levels of NO, NOS proteins, mRNAs, and NOS immunoreactivities in glial cells and microglia strongly suggest glial activation together with the professional immune cells can aggravate the demyelination of aged taiep rats.     

Enhancement of nitric oxide release from nitrosyl hemoglobin and nitrosyl myoglobin by red/near infrared radiation: Potential role in cardioprotection

Nitric oxide is an important messenger in numerous biological processes, such as angiogenesis, hypoxic vasodilation, and cardioprotection. Although nitric oxide synthases (NOS) produce the bulk of NO, there is increasing interest in NOS independent generation of NO in vivo, particularly during hypoxia or anoxia, where low oxygen tensions limit NOS activity. Interventions that can increase NO bioavailability have significant therapeutic potential. The use of far red and near infrared light (R/NIR) can reduce infarct size, protect neurons from methanol toxicity, and stimulate angiogenesis. How R/NIR modulates these processes in vivo and in vitro is unknown, but it has been suggested that increases in NO levels are involved. In this study we examined if R/NIR light could facilitate the release of NO from nitrosyl heme proteins. In addition, we examined if R/NIR light could enhance the protective effects of nitrite on ischemia and reperfusion injury in the rabbit heart. We show both in purified systems and in myocardium that R/NIR light can decay nitrosyl hemes and release NO, and that this released NO may enhance the cardioprotective effects of nitrite. Thus, the photodissociation to NO and its synergistic effect with sodium nitrite may represent a noninvasive and site-specific means for increasing NO bioavailability.     

Assaying all of the nitrogen oxides in breath modifies the interpretation of exhaled nitric oxide

Exhaled nitric oxide (NO) assays measure the quantity of NO that emanates from the airway, not the amount of NO that is formed. Consumptive processes-including oxidation reactions-decrease the amount of gas phase NO available for exhalation. Higher oxides of nitrogen (HiNO(x)) are resulting reaction products, and are easily measured in exhaled breath condensate (EBC). We performed concurrent sampling of exhaled breath for gas phase NO and EBC HiNO(x) in controls and stable asthmatics. We identified that, mole for mole, asthma patients hourly exhale more HiNO(x) than they do NO, with a HiNO(x)/NO ratio of 1.21 (0.54-3.4). This is the reverse of the ratio found in controls, in whom the HiNO(x)/NO ratio was 0.75 (0.44-0.93), p=0.04. The sum of the hourly molar exhalation of NO and HiNO(x) was significantly higher in asthmatics (333 nmol/h (221-543) than controls (179 (138-231), p<0.001). We conclude that exhaled oxides of nitrogen are more informative when measured together as opposed to in isolation. We suggest that inflammation can be better evaluated with HiNO(x) and NO measured concurrently, and that the level of oxidation in the lung can be evaluated by comparing the easily measured ratios of HiNO(x) to NO in the exhaled breath.     

Nitrite toxicity to crayfish, Astacus leptodactylus, the effects of sublethal nitrite exposure on hemolymph nitrite, total hemocyte counts, and hemolymph glucose

The 48-h acute toxicity range of nitrite to narrow-clawed crayfish, Astacus leptodactylus was within 22 and 70 mg L(-1) (mean 29.43 mg L(-1)). Environmental chloride (100 mg L(-1) chloride) increased the 48-h toxicity of nitrite to a range of 31 and 80 mg L(-1) (mean 49.20 mg L(-1)). Hemolymph nitrite, total hemocyte counts (THCs), and hemolymph glucose were examined in A. leptodactylus exposed to different sublethal nitrite concentrations. The same parameters were also determined for A. leptodactylus exposed to different sublethal nitrite concentrations with additional environmental chloride. Additionally, hemolymph nitrite and THCs were analyzed for crayfish exposed to nitrite-free water after 24 h following a 48-h exposure to nitrite. In the nitrite-exposed tests, hemolymph nitrite increased directly with water nitrite; however, after recovery, nitrite in hemolymph decreased. In the nitrite plus chloride-exposed tests, the accumulation of nitrite in hemolymph was relatively low compared to the nitrite-exposed tests. Thus, hemolymph to environment ratios of nitrite in the nitrite-exposed tests were higher than those of nitrite plus chloride-exposed tests. THCs decreased following nitrite exposure and, in general, increased after recovery. In the nitrite with chloride exposed and recovery from nitrite tests, THCs increased. Hemolymph glucose levels elevated following nitrite exposure, independent of water nitrite concentrations. However, with environmental chloride nitrite exposure did not cause elevation of hemolymph glucose. Hemolymph nitrite accumulation was found to be closely related to the decrease in THCs and increase in hemolymph glucose.     

江苏省56起误用亚硝酸盐食物中毒分析

对1991～1998年56起亚硝酸盐食物中毒的分析, 发现89.3% 的亚硝酸盐中毒是由于将亚硝酸盐误用为食盐、味精、白糖等调料, 这与亚硝酸盐的外观与这些调料相似有关, 也与亚硝酸盐的销售、使用混乱有关。中毒主要发生在农村,家庭中毒占55.4% 。建议加强对亚硝酸盐的销售、使用的管理     

加工方法及加工后的存放对蔬菜中亚硝酸盐含量的影响

目的：研究不同加工方法及加工后的存放对蔬菜中亚硝酸盐含量的影响。方法：我们选择淮南市舜耕菜市场蔬菜作为调查点，将青菜、芹菜在生、熟、腌三种不同烹调加工方法和熟菜在室温（14℃）和冰箱（4℃）中存放条件下的样品用碘酸萘乙胺比色法测定亚硝酸盐含量。结果：青菜在三种不同加工方法下，亚硝酸盐含量随着存放时间均出现先下降后上升的现象，达48h明显高于开始的亚硝酸盐含量。芹菜中亚硝酸盐含量则随时间继续下降，直到48h仍有下降趋势。室温（14℃）与冰箱（4℃）保存，熟菜中亚硝酸盐含量差异均无显著意义。结论：蔬菜中亚硝酸盐的变化可能与蔬菜中维生素C的含量及微生物的生长繁殖有关。     

吖啶红荧光猝灭法测定痕量亚硝酸根

〔目的〕建立测定痕量亚硝酸根的新方法。〔方法〕在盐酸介质中 ,吖啶红与亚硝酸根发生亚硝化反应 ,其荧光强度降低 ,用吖啶红荧光猝灭值标准曲线法测定痕量亚硝酸根。〔结果〕在实验最适条件下 ,吖啶红的荧光猝灭强度与亚硝酸根的含量在 0 0 5～ 0 5 μg ml之间存在线性关系 (r =0 998)。方法的检出限为 7 5ng ml ;RSD =1 43 %～ 3 77% ;样品加标回收率为 90 40 %～ 10 0 3 0 %。〔结论〕方法操作简便 ,灵敏度高。用于环境水样中痕量亚硝酸根的测定 ,结果满意     

离子色谱法测定水中氟、氯、硝酸盐氮和硫酸根的不确定度分析

通过对离子色谱法测定水样中氟、氯、硝酸盐氮和硫酸根不确定度的来源分析 ,找出影响测量的各种因素 ,计算不确定度分量及合成不确定度 ,以确定测量结果的可信程度和准确性 ,建立测量不确定度的评估方法。     

药用辅料乳糖中痕量亚硝酸盐和硝酸盐的离子色谱-电导/紫外检测研究

目的：建立药用辅料乳糖中痕量亚硝酸盐、硝酸盐的离子色谱-抑制电导（IC-CD）检测法和高效液相色谱-紫外（HPLC-UV）检测法。搭建在线膜抑制系统,结合LC-MS/MS技术进行结构确证,为药用辅料乳糖的前置风险控制提供新的策略。方法：IC-CD检测法和HPLC-UV检测法均采用高容量阴离子交换柱Dionex IonPacTM AS11-HC RFICTM（4.0 mm × 250 mm）和保护柱Dionex IonPacTM AS11-HC RFICTM（4.0 mm × 50 mm）。IC-CD检测法流动相为氢氧化钾溶液,梯度洗脱,抑制型电导检测器的电导池温度为30℃;HPLC-UV检测法流动相为5 mmol·L-1氢氧化钠溶液,检测波长为210 nm;两种方法的流速均为1.0 mL·min-1,柱温均为30℃,进样量均为25 μL。结果：两种方法测定亚硝酸根在0.03 ~ 10 μg·mL-1范围内、硝酸根在0.02 ~ 200 μg·mL-1范围内线性关系均为良好（r > 0.999）;亚硝酸根检测限和定量限分别为0.25 ng和0.75 ng,硝酸根检测限和定量限分别为0.25 ng和0.50 ng;回收率在84.00% ~ 100.70%之间;进样精密度RSD（n = 6）在0.27% ~ 1.33%之间;均满足检验需求。结论：两种方法均具有灵敏度高、专属性强、分离度好、前处理简单的优势,可表征药用辅料乳糖中痕量亚硝酸盐、硝酸盐的含量,也为其他药用辅料前置风险研究提供新的思路和参考。     

一种新的水中亚硝酸盐点滴检验法

目的介绍一种水中亚硝酸盐快速点滴检验法,以适应污染事故应急监测亚硝酸盐的需要.方法根据欧洲饮水法规亚硝酸盐限值(0.10 mg/L),使用一种优化的试剂混合物和二元的阳性-阴性反应,建立一种水中亚硝酸盐快速点滴检验法.结果将1片含磺胺、N-(1-萘)乙二胺二盐酸盐和氯化钠的固体试剂混合物放在聚四氟乙烯模的点滴检验板上.加1滴30%(体积分数)盐酸和1滴水样于试剂片上.在此情况下,所有含NO-2≥0.10 mg/L的检验水样均产生紫红色阳性反应,而给出阴性反应(无色)的水样表明NO2-含量低于此限值.实际水样均显示明确的阴性或阳性反应,且均由光度法根据相同的试剂测定得到确认.结论该方法简易、快速和准确,适合现场水中亚硝酸盐的监测.