双波长薄层扫描法测定氢醌酯霜中氢醌酯的含量

本文建立了氢醌酯的薄层扫描测定方法。以甲苯:乙醚(4:1)为展开剂,氢氧化钠的醇溶液浸渍显色,λ_R=620nm,λ_?=375nm,对氢醌酯的含量进行了双波长薄层扫描法测定,结果回收率99.5%,CV=1.2%,表明该法简单,可行。     

氢醌脂肪酸单酯的简便合成

氢醌脂肪酸单酯是一类皮肤祛色素剂 ,其作用机理与氢醌相同 ,即抑制皮肤组织中酪氨酸酶的活性 ,从而阻断黑色素形成。与氢醌相比 ,氢醌脂肪酸单酯具有对皮肤刺激性小 ,性质更加稳定 ,且祛色素性能更好等优点[1] 。氢醌脂肪酸单酯的合成方法 ,文献 [2 ,3] 报道较多的是以氢醌与酰氯在 DMAP催化下反应制备。此方法反应复杂 ,所用试剂比较昂贵 ,反应副产物多 ,后处理较困难 ,且产率不高 ,文献[2 ] 收率 58%～ 65% ,文献[3 ] 收率 >70 % ,因此不宜于大规模制备。本文参考文献 [4 ]以氢醌单丙酸酯 (1 )为例 ,采用氢醌二丙酸酯 (2 )为原料 ,在甲…     

高效液相色谱法测定复方氢醌霜中氢醌的含量

目的 :建立测定复方氢醌霜中氢醌含量的高效液相色谱方法。方法 :采用KromasilC18 柱 ,以甲醇 -水 (30∶70)为流动相 ,检测波长293nm。结果 :在2 5～60μg/ml范围内 ,氢醌的峰面积与浓度呈现良好线性关系 ;方法平均回收率为99 9 % ,RSD=0 73 %。结论 :本方法可用于测定复方氢醌霜中氢醌的含量。     

双波长紫外分光光度法测定复方氢醌乳膏中氢醌的含量

目的:建立复方氢醌乳膏中氢醌的含量测定方法。方法:采用双波长紫外分光光度法测定氢醌的含量。结果:氢醌在4.06~24.36μg/mL范围内线性关系良好(r=0.9998,n=6),平均回收率95.87%,相对标准偏差为0.51%。结论:该含量测定方法简便快速,结果准确。     

氢醌酯的合成及其霜剂的制备

目的　增强氢醌消除皮肤色素的能力和抗氧化性能。方法　以氢醌和醋酐合成氢醌二乙酸酯并制成霜剂。结果　氢醌酯霜比氢醌霜具有更强的抗氧化性能。结论　酯化能提高氢醌制剂的稳定性。     

维甲酸对体外培养的正常人黑素细胞的影响

目的　观察不同浓度的维甲酸及其与氢醌协同对体外培养正常人黑素细胞的影响。方法　采用体外细胞培养技术培养正常人黑素细胞 ,观察了不同浓度的维甲酸及其与氢醌协同对正常人黑素细胞酪氨酸酶活性、黑素含量和黑素细胞增殖率的影响。结果　维甲酸在较高浓度 ( >5 0 0 μmol L)可以下调酪氨酸酶活性和黑素含量 ,对细胞无明显毒性作用 ,同时还有促进黑素细胞增殖的作用。较高浓度的维甲酸 ( >5 0 0 μmol L)与氢醌可以互相协同 ,增强彼此下调酪氨酸酶活性和黑素含量的作用 ,而且维甲酸还可以减轻氢醌对细胞增殖的抑制作用。结论　维甲酸在一定浓度时可以下调酪氨酸酶活性和黑素含量 ,并与氢醌有协同作用 ,促进黑素细胞增殖 ,减轻氢醌对细胞增殖的抑制作用     

甲萘氢醌二磷酸酯钠注射液处方和工艺研究

目的研究甲萘氢醌二磷酸酯钠注射液的制备工艺。方法对抗氧剂用量、pH值,灭菌条件进行筛选。用紫外分光光度法测定甲萘氢醌二磷酸酯钠的含量及有关物质。结果加入0．4％抗氧剂,药液pH值调为7．0～8．0,105℃热压灭菌30分钟,制剂质量符合药典有关注射剂的质量标准。结论本品处方工艺合理,质量稳定。     

基质及附加剂对氢醌乳膏稳定性的影响

氢醌乳膏（又名褪色霜）为皮肤脱色剂，临床主要用于色素性皮肤病，如黄褐斑雀斑、黑变病等。氢醌（对苯二酚）为光感性物质，性质不稳定，在碱性或金属离子存在的条件下易氧化变质。在实际工作中发现，依照《中国医院制剂规范》（简称《规范》）处方制得的氢醌乳膏，膏剂容易破相，贮藏过程中颜色容易加深变成黄褐色，从而影响本品的外观和临床疗效。本文通过比较两种不同基质及附加剂制成的氢醌乳膏稳定性差异，寻找出一种更适合于配制氢醌乳膏的基质及附加剂。     

氢醌乳膏含量测定方法的实验研究

氢醌乳膏由于对皮肤病有较好的疗效,临床应用比较广泛,其含量测定多用紫外分光光度法,但受干扰的因素很多,由于氢醌具有较强的还原性,我们利用氢醌的这一件质,     

紫外分光光度法测定祛斑霜中氢醌的含量

目的　建立紫外分光光法测定氢醌乳膏中氢醌的含量。方法　在 2 95nm测其紫外吸收 ,从而求得其浓度。结果　在 5 3 5ug .mL-1之间线性良好 ,方法回收率为 10 1.6% ,RSD为 0 .9%。结论　本方法操作简便 ,准确性好 ,适合于氢醌乳膏中氢醌的含量测定     

The Use of Cellulose Nanocrystals for Potential Application in Topical Delivery of Hydroquinone

Nanotechnology‐based drug delivery systems can enhance drug permeation through the skin and improve the drug stability. The biodegradability and biocompatibility of cellulose nanocrystals have made these nanoparticles good candidates to use in biomedical applications. The hyperpigmentation is a common skin disorder that could be caused by number of reasons such as sun exposure and pregnancy. Hydroquinone could inhibit the production of melanin and eliminate the discolorations of skin. This study is aimed at introducing cellulose nanocrystals as suitable carriers for drug delivery to skin. Prepared cellulose nanocrystals were characterized by dynamic light scattering and atomic force microscopy. The size of cellulose nanocrystals determined using dynamic light scattering was 301 ± 10 nm. Hydroquinone–cellulose nanocrystal complex was prepared by incubating of hydroquinone solution in cellulose nanocrystals suspension. The size of hydroquinone–cellulose nanocrystal complex determined using dynamic light scattering was 310 ± 10 nm. The hydroquinone content of the hydroquinone–cellulose complex was determined using UV/vis spectroscopy. Hydroquinone was bound to cellulose nanocrystals representing 79.3 ± 2% maximum binding efficiency when 1.1 mg hydroquinone was added to 1 mL of cellulose nanocrystals suspension (2 mg cellulose nanocrystal). The hydroquinone–cellulose nanocrystal complex showed an approximately sustained release profile of hydroquinone. Approximately, 80% of bound hydroquinone released in 4 h.     

微生物法测定家兔体内鹿蹄草素药动学参数

采用微生物法测定家兔血清中鹿蹄草素血药浓度，经（MCPKP）程序处理数据。表明鹿蹄草素在家兔体内动力学过程符合双室模型，求得一系列动力学参数。     

X线修复交叉互补基因1对氢醌致人支气管上皮细胞DNA损伤的保护作用(英文)

目的探索氢醌对人支气管上皮细胞遗传毒性的分子机制,并研究X线修复交叉互补基因1(XRCC1)对氢醌致人支气管上皮细胞DNA损伤是否有保护作用。方法通过RNA干扰敲除XRCC1基因,通过转染重组质粒pEGFP-C1-pU6-dsRNA建立XRCC1缺陷细胞;正常人支气管上皮细胞和转染空载体pEGFP-C1的细胞分别作为正常对照组和载体对照组;3种细胞用不同浓度(10 ～100 μmol.L-1)的氢醌作用4 h,分别进行MTT实验和彗星实验来检测氢醌的毒性。结果 MTT结果显示,不同浓度(10 ～100μmol.L-1)氢醌作用的XRCC1缺陷细胞,490 nm波长处吸光度值低于对照组细胞,提示缺陷细胞的细胞存活率比正常细胞低;彗星实验结果显示,不同浓度的氢醌对XRCC1缺陷细胞DNA损伤比对照组细胞更严重,而2个对照组细胞之间没有明显差异。结论 XRCC1基因在氢醌导致的细胞损伤的修复方面起着重要的作用。     

New High-performance Liquid Chromatography-DAD Method for Analytical Determination of Arbutin and Hydroquinone in Rat Plasma

Natural substances present in herbal preparations should be carefully used because they can give toxic or therapeutic effects despite of their amount or the way of administration. The safety of products of vegetable origin must be assessed before commercialisation by monitoring the active ingredients and their metabolites. This study was therefore designed to identify and quantify arbutin and its metabolite hydroquinone, naturally present in Arctostaphylos uva-ursi (L.) Spreng plant in rat plasma, after an acute and subacute administration of aqueous arbutin solution in Wistar rats. For this purpose a reversed-phase high-performance liquid chromatography coupled with photodiode array detection was developed to assess the pharmacokinetic of arbutin and hydroquinone in plasma of female rats treated with aqueous arbutin solutions. The detection (arbutin: 0.0617 µg/ml and hydroquinone 0.0120 µg/ml) and quantification (arbutin: 0.2060 µg/ml and hydroquinone: 0.0400 µg/ml) limits were determined. At the arbutin concentration level of 10.7 µg/ml repeatability was 13.33% and its recovery 93.4±6.93%, while at the hydroquinone concentration level of 10.6 µg/ml repeatability was 11.66% and its recovery 92.9±7.75%. Furthermore the method was fully validated and the obtained data indicate that the new method provides good performances.     

Anticancer activity of botanical alkyl hydroquinones attributed to topoisomerase II poisoning

Cytotoxic alkyl hydroquinone compounds have been isolated from many plants. We previously isolated 3 structurally similar cytotoxic alkyl hydroquinone compounds from the sap of the lacquer tree Rhus succedanea L. belonging to the sumac family, which have a long history of medicinal use in Asia. Each has an unsaturated alkyl chain attached to the 2-position of a hydroquinone ring. One of these isolates, 10'(Z),13'(E),15'(E)-heptadecatrienylhydroquinone [HQ17(3)], being the most cytotoxic, was chosen for studying the anticancer mechanism of these compounds. We found that HQ17(3) was a topoisomerase (Topo) II poison. It irreversibly inhibited Topo IIalpha activity through the accumulation of Topo II-DNA cleavable complexes. A cell-based assay showed that HQ17(3) inhibited the growth of leukemia HL-60 cells with an EC50 of 0.9 microM, inhibited the topoisomerase-II-deficient cells HL-60/MX2 with an EC50 of 9.6 microM, and exerted no effect on peripheral blood mononuclear cells at concentrations up to 50 microM. These results suggest that Topo II is the cellular drug target. In HL-60 cells, HQ17(3) promptly inhibited DNA synthesis, induced chromosomal breakage, and led to cell death with an EC50 about one-tenth that of hydroquinone. Pretreatment of the cells with N-acetylcysteine could not attenuate the cytotoxicity and DNA damage induced by HQ17(3). However, N-acetylcysteine did significantly reduce the cytotoxicity of hydroquinone. In F344 rats, intraperitoneal injection of HQ17(3) for 28 days induced no clinical signs of toxicity. These results indicated that HQ17(3) is a potential anticancer agent, and its structural features could be a model for anticancer drug design.     

Cytotoxic effects of polychlorinated biphenyl hydroquinone metabolites in rat hepatocytes

Polychlorinated biphenyls (PCBs) are persistent organic pollutants that exhibit various toxic effects in animals and exposed human populations. The molecular mechanisms of PCB toxicity have been attributed to the toxicological properties of its metabolites, such as hydroquinones, formed by cytochrome‐P‐450 oxidation. The effects of PCB hydroquinone metabolites towards freshly isolated rat hepatocytes were investigated. Hydroquinones can be oxidized to semiquinones and/or quinone metabolites. These metabolites can conjugate glutathione or can oxidize glutathione as a result of redox cycling. This depletes hepatocyte glutathione, which can inhibit cellular defence mechanisms, causing cell death and an increased susceptibility to oxidative stress. However in the following, glutathione‐depleted hepatocytes became more resistant to the hydroquinone metabolites of PCBs. This suggested that their glutathione conjugates were toxic and that there was a third type of quinone toxicity mechanism which involved a hydrogen peroxide‐accelerated autoxidation of the hydroquinones to form toxic electrophilic quinone and semiquinone–glutathione conjugates. Copyright © 2009 John Wiley & Sons, Ltd.     

Inhibition of topoisomerase II in 32D.3(G) cells by hydroquinone is associated with cell death

Studies showing the inhibition of isolated human topoisomerase II (topo II) by benzene metabolites such as hydroquinone, coupled with the recognition that benzene-induced acute myelogenous leukemia bears a resemblance to second cancers caused by topo II inhibitors such as etoposide, suggested that topo II inhibition by hydroquinone might induce leukemogenic mutations. In these studies the inhibition of topo II by hydroquinone or etoposide was studied in parallel with the effects of these agents on differentiation, maturation and viability in murine bone marrow 32D.3(G) cells. Topoisomerase II of 32D.3(G) cells was inhibited by hydroquinone at concentrations of 5 micro M or higher and by etoposide at concentrations of 50 micro M or higher. At concentrations of either agent below those that inhibited topo II the cells responded normally to interleukin-3, which promoted proliferation, and to granulocyte colony-stimulating factor, which promoted differentiation and maturation. In dose ranges in which topo II was inhibited by either hydroquinone or etoposide, the cells became progressively less viable and cell counts decreased during the incubation period. Progressive inability to detect topo II protein by Western blot analysis as hydroquinone concentrations were increased suggested that either association of the probe with the enzyme was inhibited by hydroquinone or there was degradation of the protein as a function of hydroquinone-induced apoptosis.     

Pseudoverticin B,a novel geldanamycin analog obtained as new cell cycle inhibitor from Streptomyces pseudoverticillus YN17707

Pseudoverticin B (1), a novel naturally occurring geldanamycin analog with cell cycle inhibitory activity, was isolated from the fermentation broth of Streptomyces pseudoverticillus YN17707, together with the known ansamycin antibiotic, hydroquinone geldanamycin (2), through bioassay-guided fractionation procedures. The structure of compound 1 was elucidated by spectroscopic methods, being characterized by an ansa bridge, same as that in geldanamycin and a novel hydroquinone-derived moiety. Compounds 1 and 2 arrested the cell cycle of tsFT210 cells at the G0/G1 phase with the minimum inhibitory concentration values of 10.1 and 20.2 μmolL^?1, respectively.     

Rationale of using hypopigmenting drugs and their clinical application in melasma

Among the pigmentary disorders, melasma is the prototype disorder characterized by hyperpigmentation. Although, conventionally, triple combination creams are used, there is a need for alternatives to hydroquinone as the drug has restrictions on its widespread use. This needs an understanding of the steps involved in the melanogenesis and the drugs that inhibit the key steps. The data on in vitro inhibition need to be then translated into clinical in vivo results, before a rationale compounded fixed drug preparation is marketed that inhibits the major steps in the pigmentation pathway. There is also a need to look for drugs that are superior to hydroquinone, as only then will they have a meaningful clinical utility. For now, a few drugs like deoxyarbutin, ellagic acid, dioic acid, n-butylresorcinol and azelaic acid have such properties in clinical trials, while metformin is a recent addition.