低聚氨基葡萄糖的吸湿、保湿和抑菌性质

采用双氧水在中性条件下对壳聚糖进行氧化降解,制备了低聚氨基葡萄糖,研究了它的吸湿性、保湿性及抗菌性能,结果表明,低聚氨基葡萄糖具有优良的水溶性、吸湿性、保湿性,并对大肠杆菌和绿脓杆菌有较强的抑菌作用。     

双氧水加顺铂腹腔灌洗对肿瘤细胞的影响

目的: 探讨双氧水加顺铂腹腔灌洗对肿瘤细胞的影响,为临床腹腔灌洗防治胃癌腹腔种植奠定实验基础.方法: 利用胃癌细胞的形态学改变和腹水癌小鼠的平均存活期来观察不同处理因素(双氧水组、DMEM对照组、顺铂组和双氧水加顺铂组)腹腔灌洗对肿瘤细胞的影响.结果: 经双氧水加顺铂组处理的细胞核改变的比率明显高于对照组、双氧水组和顺铂组.双氧水加顺铂腹腔灌洗组的小鼠平均存活期14.1d,明显长于对照组的4.5d、双氧水组的8.4d和顺铂组9.3d.结论: 双氧水加顺铂腹腔灌洗对胃癌细胞具有杀伤作用,能明显延长腹水癌小鼠的平均存活期.     

子宫输卵管双氧水造影34例B超观察分析

子宫输卵管双氧水造影３４例Ｂ超观察分析杜玲莉双氧水用于子宫输卵管超声学造影是较为理想的造影剂。本文报告３４例不孕症患者双氧水子宫输卵管超声学造影的方法和结果。临床资料我科从１９９３年至１９９６年５月，对３４例患者用３％双氧水为造影剂，在Ｂ超监测下行...     

稀释双氧水置管冲洗闭式引流治疗25例慢性骨髓炎的临床体会

目的探讨稀释双氧水置管冲洗、闭式引流治疗慢性骨髓炎的临床疗效。方法对25例确诊患者行彻底病灶清理后,以稀释双氧水持续置管冲洗,闭式引流,连续冲洗4～8周。结果稀释双氧水置管冲洗后,25例患者均得到治愈。随访6～24个月,未出现感染复发。结论稀释双氧水置管冲洗、闭式引流是治疗慢性骨髓炎一种可靠方法。     

双氧水在抢救急性一氧化碳中毒中的应用

我科在1974年12月至1975年2月,抢救了七例急性一氧化碳中毒患者。在抢救过程中,除沿用过去常规治疗方法外,还学习了北京友谊医院应用双氧水治疗缺氧疾患的经验,采用了双氧水静脉注射。     

2—氯—3—氨基吡啶的制备

2-氯 - 3-氨基吡啶 ( 1 )为一重要的医药中间体 ,用来合成抗消化性溃疡药哌仑西平[1] 、二氮杂类抗艾滋病药 [2～ 4 ] ,并可用作杀虫剂的中间体 [5]。文献报道 1可用 2 -氯烟酰胺为原料进行霍夫曼降解[6] ,或氯化亚锡还原 2 -氯 - 3-硝基吡啶[7] 等方法来制备 ,但所用原料来源有困难 ,不宜工业化生产。另有文献 [8]以双氧水和盐酸反应生成的氯对 3-氨基吡啶 ( 2 )进行氯代 ,反应结束后 ,调节反应液到碱性 ,即得到粗品。而 2可从烟酰胺制得 [9] ,故该法较为实用。　　文献中双氧水用量为 2的 1 .2当量 ,两者于 70～ 90°C反应 ,粗品中含 2…     

B 超观察下双氧水子宫输卵管造影

Ｂ超观察下双氧水子宫输卵管造影玉溪市人民医院妇产科（６５３１００）邹美，陈兰君关键词双氧水，子宫输卵管造影我院自１９９０年４月至１９９３年１０月，对９０例不孕症患者使用３％双氧水作为声学造影剂进行９９次子宫输卵管造影￣〔１〕，取得较为满意的效果，报告...     

鼻内镜手术联合双氧水冲洗治疗真菌性鼻-鼻窦炎

目的评价鼻内镜手术联合双氧水冲洗在真菌性鼻-鼻窦炎治疗中的应用价值。方法对36例真菌性鼻-鼻窦炎患者采用鼻内镜手术,术中、术后使用双氧水冲洗治疗。结果全部病例均治愈,随访6个月～4年,未见复发。结论娴熟的鼻内镜手术联合双氧水冲洗能彻底清除病变,消除真菌赖以生存的低氧微环境,是微创治疗真菌性鼻-鼻窦炎的理想方式。     

应用双氧水治疗婴幼儿肺炎严重缺氧的一点体会

用双氧水静脉推注或滴注,纠正机体组织的缺氧状态,在最近几年来,国内外屡见报道。我们从1974年11月以来,应用双氧水抢救婴幼儿肺炎严重缺氧46例,取得了良好效果。现报道如下:     

双氧水冲洗上颌窦治疗慢性化脓性上颌窦炎的疗效观察及护理

慢性化脓性上颌窦炎为耳鼻喉科的常见病，其细菌学表现为多细菌、厌氧菌和需氧菌的混合感染。双氧水对厌氧菌的生长具有抑制、杀灭作用，我们观察上颌窦穿刺3％双氧水冲洗对慢性化脓性上颌窦炎的治疗效果，现报告如下。     

Factors Influencing Polysorbate's Sensitivity Against Enzymatic Hydrolysis and Oxidative Degradation

The aim was to compare the sensitivity of different grades of polysorbate 20 (PS20) and polysorbate 80 (PS80) against enzymatic hydrolysis and oxidative degradation in pharmaceutically relevant buffer systems. For this purpose, a fast liquid chromatography charged aerosol detection method was developed which allows to (1) differentiate between hydrolytic and oxidative PS degradation and (2) to monitor the PS decay over time. Systematic enzymatic and oxidative forced degradation studies were conducted with multicompendial PS20 and PS80, as well as all-laurate PS20 and all-oleate PS80 (with >98% oleic acid, as required by the Chinese Pharmacopoiea since 2015). No differences in the sensitivity toward enzymatic degradation were observed between multicompendial PS and high purity grade PS. However, all-laurate PS20 and all-oleate PS80 have a higher predisposition for oxidative degradation as compared to multicompendial PS20 and PS80. The buffer system used within the study played thereby a key role: histidine showed a protective effect against hydrogen peroxide–induced oxidation, whereas hydrogen peroxide oxidation of PS in acetate buffer was severe under the experimental conditions. Furthermore, ethylenediaminetetraacetic acid protected PS20 and PS80 against oxidative degradation in histidine buffer.     

A novel accelerated oxidative stability screening method for pharmaceutical solids

Despite the fact that oxidation is the second most frequent degradation pathway for pharmaceuticals, means of evaluating the oxidative stability of pharmaceutical solids, especially effective stress testing, are still lacking. This paper describes a novel experimental method for peroxide-mediated oxidative stress testing on pharmaceutical solids. The method utilizes urea-hydrogen peroxide, a molecular complex that undergoes solid-state decomposition and releases hydrogen peroxide vapor at elevated temperatures (e.g., 30°C), as a source of peroxide. The experimental setting for this method is simple, convenient, and can be operated routinely in most laboratories. The fundamental parameter of the system, that is, hydrogen peroxide vapor pressure, was determined using a modified spectrophotometric method. The feasibility and utility of the proposed method in solid form selection have been demonstrated using various solid forms of ephedrine. No degradation was detected for ephedrine hydrochloride after exposure to the hydrogen peroxide vapor for 2 weeks, whereas both anhydrate and hemihydrate free base forms degraded rapidly under the test conditions. In addition, both the anhydrate and the hemihydrate free base degraded faster when exposed to hydrogen peroxide vapor at 30°C under dry condition than at 30°C/75% relative humidity (RH). A new degradation product was also observed under the drier condition. The proposed method provides more relevant screening conditions for solid dosage forms, and is useful in selecting optimal solid form(s), determining potential degradation products, and formulation screening during development.     

Degradation pathways of a peptide boronic acid derivative, 2-Pyz-(CO)-Phe-Leu-B(OH)(2)

The peptide boronic acid derivative 2-Pyz-(CO)-Phe-Leu-B(OH)(2) is a potent inhibitor of 20S proteasome and a proposed anticancer agent. During preformulation studies, the compound presented erratic stability behavior. Efforts were made to isolate and identify the degradation products, thereby helping to identify possible mechanisms for the degradation. The reaction of 2-Pyz-(CO)-Phe-Leu-B(OH)(2) with hydrogen peroxide not only provided a convenient way to isolate the initial degradation products seen from hydrolysis in aqueous buffers but also showed that the major, initial degradation pathway was probably oxidative in nature. The isolated degradation products were characterized by nuclear magnetic resonance spectroscopy, mass spectrometry, and optical rotation dispersion. In the presence of hydrogen peroxide, the boronic acid group was cleaved from 2-Pyz-(CO)-Phe-Leu-B(OH)(2) to give an alcohol with an apparent retention of the original stereochemistry. Subsequent isomerization and further hydrolysis were then seen. Surprisingly, added ascorbate and EDTA accelerated rather than inhibited degradation. Degradation of 2-Pyz-(CO)-Phe-Leu-B(OH)(2) under acidic and basic conditions seemed to be mediated by an initial oxidative degradation pathway similar to that seen with the peroxide.     

Protection against hydrogen peroxide induced oxidative damage in rat erythrocytes by Mangifera indica L. peel extract

Phytochemicals such as polyphenols and carotenoids are gaining importance because of their contribution to human health and their multiple biological effects such as antioxidant, antimutagenic, anticarcinogenic and cytoprotective activities and other therapeutic properties. Mango peel is a major by-product in pulp industry and it contains various bioactive compounds like polyphenols, carotenoids and others. In the present study, the protective effect of peel extracts of unripe and ripe mango fruits of two varieties namely, Raspuri and Badami on hydrogen peroxide induced hemolysis, lipid peroxidation, degradation of membrane proteins and its morphological changes are reported. The oxidative hemolysis of rat erythrocytes by hydrogen peroxide was inhibited by mango peel extract in a dose dependent manner. The IC₅₀ value for lipid peroxidation inhibition on erythrocyte ghost membrane was found to be in the range of 4.5–19.3 μg gallic acid equivalents. The mango peel extract showed protection against membrane protein degradation caused by hydrogen peroxide. Morphological changes to erythrocyte membrane caused by hydrogen peroxide were protected by mango peel extract. The results demonstrated that mango peel extracts protected erythrocytes against oxidative stress and may impart health benefits and it could be used as a valuable food ingredient or a nutraceutical product.     

Identification of the degradation product of ezlopitant,a non-peptidic substance P antagonist receptor,by hydrogen deuterium exchange,electrospray ionization tandem mass spectrometry (ESI/MS/MS) and nuclear magnetic resonance (NMR) spectroscopy

The degradation product of ezlopitant was isolated from low specific activity material and identified by solution phase hydrogen/deuterium (H/D) exchange and electrospray ionization tandem mass spectrometry (ESI/MS/MS) to be an isopropyl peroxide analog of ezlopitant. The structure of the degradant was further confirmed by nuclear magnetic resonance (NMR) spectroscopy utilizing complete ¹H and ¹³C assignments. Studies were also performed to identify the factors responsible for the oxidative degradation of ezlopitant, which included salt form, storage conditions and salt formation solvent. Of all the variable studies over a 3 weeks period, only a change in the salt form prevented this oxidative degradation.     

Is malonaldehyde a valuable indicator of lipid peroxidation?

Malonaldehyde (MDA), a decomposition product of lipid hydroperoxides which is used as an indicator of oxidative damage to cells and tissues, reacts, in vitro, with hydrogen peroxide to form undetermined degradation products. Since human polymorphonuclear leukocytes (PMNs) release reactive oxygen species including hydrogen peroxide when stimulated with phorbol myristate acetate (PMA), we incubated specific amounts of MDA with resting PMNs and PMA-stimulated PMNs. The amount of MDA recovered after 30 min incubation with stimulated cells, as determined by MDA-thiobarbituric acid assay, was 25% lower than that recovered with resting cells. In the presence of catalase 18% of MDA disappeared and in the presence of superoxide dismutase 15% disappeared. This indicates that measurements of MDA production in living systems, in the presence of reactive oxygen species, could be underestimated.     

Hydrogen peroxide induced stress in human keratinocytes and its effect on bithionol toxicity.

Exposure to hydrogen peroxide causes oxidative stress in keratinocytes. Previous work has shown that the antiparasitic drug bithionol has an EC(50) of 0.7 microg/ml (2 microM) with primary human keratinocytes, but that these cells do not respond to photoactivated bithionol. Bithionol is known to be photoactivated by UV-A visible light, therefore this study aims to investigate the effects of inducing oxidative stress in the cells prior to bithionol treatment alone and in the presence of UV-A visible light. Oxidative stress, by hydrogen peroxide treatment, caused the cells to become sensitive to photoactivated bithionol. Bithionol alone reduced the amount of oxidative stress, while following photoactivation, an augmentation in the amount of oxidative stress and cell cytotoxicity was observed. The hydrogen peroxide treatment did not alter the sensitivity of the keratinocytes to 5 J/cm(2) UV-A visible light.     

Accumulation of alpha-oxoaldehydes during oxidative stress: a role in cytotoxicity.

Glyoxal, methylglyoxal (MG), and 3-deoxyglucosone (3-DG) are physiological alpha-oxoaldehydes formed by lipid peroxidation, glycation, and degradation of glycolytic intermediates. They are enzymatically detoxified in cells by the cytosolic glutathione-dependent glyoxalase system (glyoxal and MG only) and by NADPH-dependent reductase and NAD(P)+-dependent dehydrogenase. In this study, the changes in the cellular and extracellular concentrations of these alpha-oxoaldehydes were investigated in murine P388D1 macrophages during necrotic cell death induced by median toxic concentrations of hydrogen peroxide and 1-chloro-2,4-dinitrobenzene (CDNB). Alpha-oxoaldehyde concentrations were determined by derivatization with 1,2-diamino-4,5-dimethoxybenzene. There were relatively small increases in cellular and extracellular glyoxal concentration, except that extracellular glyoxal was decreased with hydrogen peroxide. The cytosolic concentration of 3-DG and the cytosolic and extracellular concentrations of MG, however, increased markedly. Aminoguanidine inhibited alpha-oxoaldehyde accumulation and prevented cytotoxicity induced by hydrogen peroxide and CDNB. The accumulation of glyoxal and MG in toxicant-treated cells was a likely consequence of decreased in situ activity of glyoxalase 1. The effect was marked for MG but not for glyoxal, suggestive of a greater metabolic flux of MG formation than of glyoxal. The accumulation of 3-DG in toxicant-treated cells was probably due to the decreased availability of pyridine nucleotide cofactors for the detoxification of 3-DG. Impairment of alpha-oxoaldehyde detoxification is cytotoxic, and this may contribute to toxicity associated with GSH oxidation and S conjugation in oxidative stress and chemical toxicity, and to chronic pathogenesis associated with diabetes mellitus where there is oxidative stress and the formation of glyoxal, MG, and 3-DG is increased.     

Stability studies of ionised and non-ionised 3,4-diaminopyridine: hypothesis of degradation pathways and chemical structure of degradation products

3,4-Diaminopyridine is used to treat some symptoms met in Lambert-Eaton myasthenia syndrome. It was shown efficient to reduce a form of variable muscle weakness and fatigability typical of the disease and correlated to a block of acetylcholine release. In France, 3,4-diaminopyridine is nowadays given to patients under capsules form and the status of hospital preparation. Whatever the diluant used in the formulation, the stability period could not exceed 12 months. Preliminary studies were made on a salt form in order to test the influence of various stress factors and determine if there is interaction between them. From this study, the most influent stress condition, presence of hydrogen peroxide, was selected and a comparative study was performed to compare the stability of molecular and salt species. Solutions of each species were exposed to 5 or 15% of hydrogen peroxide and analyzed at 8, 24, 72 and 216 h of degradation by HPLC-UV. Fractions of detected impurities were purified and collected by semi-preparative HPLC-UV and analyzed by HPLC-UV-ESI-MS and IR spectroscopy in order to determine their structure hypotheses. Theses experiments demonstrate that the salt species were more stable under oxidative stress condition than molecular species. The two main degradation products were collected and identified as 4-amino, 3-nitropyridine and 3,4-diaminopyridine-N-oxide when the molecular form was degraded whereas only 4-amino, 3-nitropyridine was found in less quantity in the salt solutions. Nitrogen pyridine and pyridine amine could not easily be oxidized by hydrogen peroxide in salt comparatively to molecular species due to the lone pair of electron engaged in a bound with hydrogen in the first case and by resonance change of the pyridine in the second case. This modification of structure promoted different pathways of degradation for the salt form which are more dependent of energy. Owing to the better stability of the salt species, a new pharmaceutical form containing it was developed to assess its stability under ICH standard conditions allowing an industrial manufacture of this drug.     

过氧化氢氧化降解法制备低分子玻璃酸

目的制备低分子玻璃酸 (HA)。方法过氧化氢氧化降解法。结果随着过氧化氢浓度增加 ,反应温度的升高 ,降解速率加快。中性条件下HA的氧化降解速率较快 ,而酸性或碱性时却较慢。为了方便降解过程的可控性 ,过氧化氢浓度选 0 .0 5 % ,反应温度定为 5 0℃ ,反应pH为中性。随着HA相对分子质量的降低 ,运动黏度迅速下降 ,而糖醛酸含量基本不变。不同过氧化氢浓度降解时 ,低分子HA收率基本相同。结论过氧化氢氧化降解法可用于制备低分子HA。