半胱氨酸测定试剂性能评价

目的对利德曼同型半胱氨酸测定试剂盒进行性能评价。方法用日立7600全自动生化分析仪检测血清中同型半胱氨酸含量,对试剂的准确度,精密度;线性,灵敏度,特异性,稳定性,系统比对等对试剂性能验证和系统评估…。结果测试数据经过计算,在浓度0—70μmol／L范围内,理论浓度Y与实测数值x之间的线性方程为Y=0．984X-0．2096相关系数r=1．000,分析灵敏度的计算值为0．1μmol／L,当胆红素〈20mg／dl,血红蛋白〈500mg／dl,甘油三脂〈500mg／dl,抗坏血酸〈50mg／dl,红细胞〈0．4％时,测定结果偏差小于10％,试剂准确度、批内精密度,批间精密度,线性范围,灵敏度,特异性,稳定性,系统比对均达到要求标准。结论利德曼同型半胱氨酸试剂符合临床诊断试剂标准要求,可以用于临床诊断。     

中老年人高同型半胱氨酸血症与颈总动脉狭窄的关系

目的 探讨高同型半胱氨酸血症对中老年人颈总动脉狭窄的影响.方法 选取北京市某社区年龄在45 ～ 75岁的190例中老年人为研究对象,根据其血浆同型半胱氨酸水平分为高同型半胱氨酸组（同型半胱氨酸＞ 15 μmol/L,79例）和同型半胱氨酸正常组（同型半胱氨酸6～ 15μmol/L,111例）,通过颈部血管超声检查,观察并比较2组颈总动脉狭窄程度.结果 190例患者中同型半胱氨酸升高的比例为41.6％（79/190）,高同型半胱氨酸组平均年龄及男性受试者比例高于同型半胱氨酸正常组,差异均有统计学意义[（56±10）岁比（52±8）岁,t=-0.31,P＜0.01;74.7％ （59/79）比33.3％（37/111）,Х^2 =31.57,P＜0.01].同型半胱氨酸正常组轻度狭窄29例（26.1％）、中度狭窄5例（4.5％）、重度狭窄或闭塞4例（3.6％）;高同型半胱氨酸组分别为31例（39.2％）、17例（21.5％）、7例（8.9％）,高同型半胱氨酸组颈总动脉中重度狭窄或闭塞的比例明显多于同型半胱氨酸正常组,差异有统计学意义[24例（30.4％）比9例（8.1％）,Х^2 =27.98,P＜0.01].结论 同型半胱氨酸水平与中老年人颈总动脉狭窄的严重程度相关.     

血清脂蛋白(a)、同型半胱氨酸联合测定对冠心病预防及早期诊断的意义

目的探索血清脂蛋白(a)、同型半胱氨酸联合检测对冠心病的预防及早期诊断有无意义。方法选取冠心病患者50例,健康体检者50例,分别检测两组人群血清脂蛋白(a)、同型半胱氨酸水平,比较两指标在两组人群中有无差异。结果冠心病试验组血清脂蛋白(a)水平为(27.93±8.07)mg/d L,高于健康对照组(14.19±6.44)mg/d L,同型半胱氨酸水平为(17.48±5.28)μmol/L,高于健康对照组(11.02±4.32)μmol/L,有统计学差异(P<0.05);结论冠心病患者血清脂蛋白(a)、同型半胱氨酸水平均显著高于健康人群,定期检测这两项指标对冠心病的预防及早期诊断具有重要意义。     

原发性高血压与同型半胱氨酸关系的研究

目的:探讨高血压与同型半胱氨酸的关系。方法:选取高血压患者190例,分为高血压中危组(117例)和高血压高危组(73例);选取健康体检人群中血压正常待检者30例作为对照组。所有患者于早晨空腹抽取静脉血测定同型半胱氨酸浓度。结果:正常对照组、高血压中危组及高血压高危组血同型半胱氨酸的浓度分别为(9.2±1.4)μmol/L,(21.3±3.5)μmol/L,(33.4±8.3)μmol/L,不同组间比较,差异有统计学意义(P<0.05);高血压组男性血同型半胱氨酸浓度高于女性,两者比较差异有统计学意义(P<0.05)。结论:高血压与高同型半胱氨酸血症关系密切,且两者均为脑卒中的危险因子。测定血同型半胱氨酸对于心脑血管疾病的诊断和预防具有重要意义。     

高同型半胱氨酸与冠心病的关系

目前所进行的研究已证实高同型半胱氨酸血症为冠心病的独立危险因素眼1演。本文就高同型半胱氨酸血症对冠心病的影响综述如下:1.高同型半胱氨酸血症的定义及产生原因高同型半胱氨酸(HCY)指的是血浆中游离的及与蛋白结合的同型半胱氨酸和混合性二硫化物,包括同型半胱氨酸和同型半胱氨酸巯基内脂。其中与蛋白结合的同型半胱氨酸占总量70～90%。空腹血浆同型半胱氨酸浓度为5～15μmol/l,15～30μmol/l为轻度HCY,30～100μmol/l为中度HCY,大于100μmol/l为重度HCY。目前认为维生素B6、维生素B12和叶酸缺乏为其重要原因之一,因为它们是同型…     

青年脑梗死患者血清同型半胱氨酸和尿酸水平与颈动脉粥样硬化斑块稳定性的关系探讨

目的：探讨青年脑梗死患者血清同型半胱氨酸（ Hcy）和尿酸（ UA）水平与颈动脉粥样硬化斑块稳定性的关系。方法150例青年脑梗死患者行颈动脉超声检查,依据结果分为无斑块组37例、稳定斑块组52例和不稳定斑块组61例,测定三组血清Hcy和UA水平,并进行分析比较。结果稳定斑块组Hcy和UA水平分别为（15．92±2．52）μmol/L 和（294．85±25．52）μmol/L,均高于无斑块组（ t ＝7．33、6．89,均P＜0.05）;不稳定斑块组Hcy和UA水平分别为（23．17±3．82）μmol/L和（388．57±26．61）μmol/L,均显著高于无斑块组和稳定斑块组（t＝9．82、10．02、6．90、7．12,均P＜0．05）。结论颈动脉斑块的形成及其稳定性与Hcy和UA水平具有密切相关性。     

同型半胱氨酸及血清铁蛋白与绝经后女性冠心病的相关性研究

目的探讨同型半胱氨酸及血清铁蛋白与绝经后女性冠心病（CHD）的相关性及其相对危险度。方法搜集绝经后女性CHD患者32例（CHD组）,绝经后女性无CHD对照22例（对照组）,测定两组血浆同型半胱氨酸、血清铁蛋白、血脂各组分、血糖及动脉血压。结果 CUD组血浆同型半胱氨酸及血清铁蛋白分别为（19.12±5.99）μmol/L和（358.16±170.171）μg/L,均显著高于对照组[（5.58±1.65）μmol/L,（111.97±73.70）μg/L],（P〈0.01）。同型半胱氨酸及铁蛋白的相对危险度（OR值）大于高血压、血脂异常和糖尿病等传统危险因素。结论高同型半胱氨酸及高血清铁蛋白均可能是绝经后女性CHD的独立危险因素,且同型半胱氨酸及血清铁蛋白对冠心病的相对危险度大于高血压、血脂异常和糖尿病。     

微粉硅胶对抗坏血酸片稳定性的影响

本文作者列出6个抗坏血酸片处方,试验观察了微粉硅胶对抗坏血酸稳定性的影响。结果表明:应用1‰以下微粉硅胶时,抗坏血酸的稳定性较对照(不含微粉硅肢者)为佳,含1～3％微粉硅胶时与对照相近,含微粉硅胶在5％时,抗坏血酸稳定性较对照差。作者认为:微粉硅胶对抗坏血酸有一定稳定作用,但其用量应严格控制。     

氧化低密度脂蛋白和同型半胱氨酸与循环内皮细胞和内皮素在冠心病患者血浆中的相关性

目的:探讨循环内皮细胞、内皮素、氧化低密度脂蛋白和同型半胱氨酸与动脉粥样硬化发生过程中的关系,以及氧化低密度脂蛋白和同型半胱氨酸与循环内皮细胞和内皮素之间的相关性。方法:分别用酶联免疫吸附法和高效液相色谱分析法测定血浆中氧化低密度脂蛋白和同型半胱氨酸水平,同时测定血浆中循环内皮细胞和内皮素水平,进行对比和直线相关性分析。结果:冠心病组循环内皮细胞7.78±3.31cells/0.9μL,内皮素98.14±35.08 ng/L,氧化低密度脂蛋白809.25±311.89μg/L,同型半胱氨酸19.40±7.03μmol/L。对照组上述指标分别为:4.10±1.60cells/0.9μl,52.61±15.71ng/L,438.24±200.54μg/L和11.19±2.94μmol/L。两组比较差异有显著性P<0.001。冠心病组血氧化低密度脂蛋白与血浆循环内皮细胞、内皮素均呈正相关,相关系数分别为0.926(P<0.001)、0.979(P<0.001),同型半胱氨酸同样与循环内皮细胞、内皮素呈正相关,相关系数分别为0.947(P<0.001)、0.900(P<0.001),且冠心病组血浆循环内皮细胞和内皮素呈正相关,相关系数为0.939(P<0.001)。结论:氧化低密度脂蛋白和高同型半胱氨酸可能造成VEC损伤及功能改变,对动脉粥样硬化的发生发展有促进作用。     

二甲胺在体内形成二甲基亚硝胺的危险性——催化和抑制作用的研究

本文报道了给予大鼠二甲胺(DMA)125μmol和NaNO_225μmol时,化学物质对DMA亚硝化的促进和抑制作用。硫氰酸钾(80和320μmol)和NaCl(250和1000μmol)对DMA亚硝化未见有促进作用。抗坏血酸(25μmol),L-脯氨酸(125μmol)和L-半胱氨酸(150umol)有效地阻断了二甲基亚硝胺(NDMA)合成,阻断率分别为88、89和87％。NDMA在饱食基础饲料的大鼠体内的合成显著低于空腹大鼠,降低80%。     

Thermal Stability and Degradation Kinetics of Patulin in Highly Acidic Conditions: Impact of Cysteine

The thermal stability and degradation kinetics of patulin (PAT, 10 μmol/L) in pH 3.5 of phosphoric-citric acid buffer solutions in the absence and presence of cysteine (CYS, 30 μmol/L) were investigated at temperatures ranging from 90 to 150 °C. The zero-, first-, and second-order models and the Weibull model were used to fit the degradation process of patulin. Both the first-order kinetic model and Weibull model better described the degradation of patulin in the presence of cysteine while it was complexed to simulate them in the absence of cysteine with various models at different temperatures based on the correlation coefficients (R² > 0.90). At the same reaction time, cysteine and temperature significantly affected the degradation efficiency of patulin in highly acidic conditions (p < 0.01). The rate constants (k_T) for patulin degradation with cysteine (0.0036–0.3200 μg/L·min) were far more than those of treatments without cysteine (0.0012–0.1614 μg/L·min), and the activation energy (E_a = 43.89 kJ/mol) was far less than that of treatment without cysteine (61.74 kJ/mol). Increasing temperature could obviously improve the degradation efficiency of patulin, regardless of the presence of cysteine. Thus, both cysteine and high temperature decreased the stability of patulin in highly acidic conditions and improved its degradation efficiency, which could be applied to guide the detoxification of patulin by cysteine in the juice processing industry.     

Effect of amino acids,peptides and related compounds on the autooxidation of ascorbic acid

The autooxidation rate of ascorbic acid (AA) at 10^-5 m under aerobic conditions at pH 7.4 was found to be 1.16 μmol/min/1. A number of compounds at low concentrations were found to inhibit this oxidation rate. These were in order of effectiveness: EDTA (10^-6 m ) > Mercaptoethanol > aminoethyl cysteine, oxidized glutathione > glycylglycylhistidine > glycylhistidyllysine > 3-methyl histidine ? histidine > histamine > hypertensin > cysteic acid > imidazole > glutamine > hydroxyproline, and lysine. All other amino acids and peptides examined had little or no effect on the autooxidation rate of ascorbic acid. Ascorbate solutions, treated with Chelex-100 (divalent chelating resin) or containing low concentrations of EDTA (10^-7 m ) did not show a significant reduction of the rate of autooxidation. Of particular interest was the finding that 3-methyl histidine had a significant inhibitory effect on ascorbic acid oxidation whereas 1-methyl histidine had no effect. These data suggest that ascorbic acid forms complexes with certain compounds and that this interaction stabilizes ascorbic acid against auto-oxidation.     

Kinetics of talampicillin decomposition in solutions

Talampicillin stability in aqueous solutions was studied in a broad range of pH values using as medium solutions of hydrochloric acid (pH 0.4-1.8), phosphate buffers (pH 2.05-3.13 and 6.03-8.04), acetate buffer (pH 3.87-5.28) and borate buffer (pH 8.90-9.10) as well as sodium hydroxide solution (pH 11.48). For the determination of talampicillin concentration changes in kinetic studies, two methods were used: iodometric and spectrophotometric in UV (lambda(max) = 254.5 nm). The catalytic velocity constants (k(H+), k(x), k(o)) were established, the log k-pH profile (35 degrees C) was found, thermodynamic parameters were calculated of the hydrolysis reaction of the beta-lactam bond (k(H+): E(A)= 67.9 kJ mol(-1), delta S = -92.4 J K(-1) mol(-1), delta G = 92.6 kJ mol(-1); k(x): E(A) = 31.8 kJ mol(-1), delta S = -347.1 J K(-1) mol(-1), delta G = 131.1 kJ mol(-1); k(o), pH = 5.28: E(A) = 98.0 kJ mol(-1), delta S = -50.3 J K(-1) mol(-1), delta G = 110.3 kJ mol(-1) at 20 degrees C), and the stability of the lactone bond was studied in the medium with the highest stability of beta-lactam bond of talampicillin (pH 5.28: k(o): E(A)= 32.5 kJ mol(-1), delta S = -220.5 J K(-1) mol(-1), delta G = 94.7 kJ mol(-1) in 20 degrees C), at controlled ionic strength (mu = 0.5 mol l(-1)).     

Kinetics and mechanistic studies of the hydrolysis of diisocyanate-derived bis-thiocarbamates of cysteine methyl ester

Diisocyanates (dNCOs) are the most commonly reported cause of chemically induced occupational asthma, but the ultimate antigenic form is unknown. Reactions of the three most common monomeric dNCOs, hexamethylene dNCO (HDI), methylene diphenylisocyanate (MDI), and toluene dNCO (TDI), with cysteine methyl ester (CME) gave the corresponding bis-dithiocarbamates (HDI-CME, TDI-CME, and MDI-CME). The dissociation kinetics of these bis-thiocarbamates, in aqueous conditions, was followed spectrophotometrically under varying pH and temperature conditions. Reaction of the adducts with methylamine or human serum albumin (HSA) produced diurea, monourea, and diamine products, and this was consistent with the base-catalyzed elimination reaction (E1cB) pathway being the dominant, but not exclusive, dissociation mechanism. The hydrolysis of the adducts was first-order with respect to OH(-) concentration and overall second-order (HDI-CME, k = 3.36 x 10(2) M(-)(1) min(-)(1); TDI-CME, k = 2.49 x 10(4) M(-)(1) min(-)(1); and MDI-CME, k = 5.78 x 10(4) M(-)(1) min(-)(1) at pH 7.4) with deviation from second-order when the dNCO had an aromatic functional group. Arrhenius plots gave activation energies (HDI-CME, E(a) = 70.6 kJ/mol; TDI-CME, E(a) = 46.1 kJ/mol; and MDI-CME, E(a) = 44.5 kJ/mol) that were consistent with the following order of stability: HDI-CME > TDI-CME > MDI-CME. Therefore, the stability of different dNCO-derived thiocarbamates in aqueous environments can vary greatly. Thiocarbamate dissociation rates and type of products formed may potentially influence antigenicity and subsequent hypersensitivity/toxic reactions following dNCO exposures.     

Thermodynamic characterization of three polymorphic forms of piracetam

Combustion calorimetry, solution calorimetry, and differential scanning calorimetry (DSC) were used to determine the standard (p° = 0.1 MPa) molar enthalpies of formation of Forms I, II, and III piracetam at 298.15 K, namely, Δ(f) H(m)° (C(6)H(10)O(2)N(2), cr I) = -520.6 ± 1.6 kJ·mol(-1), Δ(f) H(m)° (C(6)H(10)O(2)N(2), cr II) = -523.8 ± 1.6 kJ·mol(-1), and Δ(f) H(m)° (C(6)H(10)O(2)N(2), cr III) = -524.1 ± 1.6 kJ·mol(-1). The enthalpy of formation of gaseous piracetam at 298.15 K was also derived as Δ(f) H(m)° (C(6)H(10)O(2)N(2), g) = -401.3 ± 2.1 kJ·mol(-1), by combining the standard molar enthalpy of formation of Form II piracetam with the corresponding enthalpy of sublimation, Δ(sub) H(m)° (C(6) H(10) O(2) N(2), cr II) = 122.5 ± 1.4 kJ·mol(-1), obtained by drop-sublimation Calvet microcalorimetry and the Knudsen effusion method. The Δ(f) H(m)° (C(6)H(10)O(2)N(2), g) value was used to assess the corresponding predictions by the B3LYP/cc-pVTZ (-335.3 kJ·mol(-1)), G3MP2 (-388.7 kJ·mol(-1)), and CBS-QB3 (-402.8 kJ·mol(-1)) methods, based on the calculation of the atomization enthalpy of piracetam. Finally, the results of the solution and DSC experiments indicate that the stability hierarchy of Forms I, II, and III piracetam at 298.15 K, for which there was conflicting evidence in the literature, is III > II > I.     

Towards an understanding of the molecular mechanism of solvation of drug molecules: a thermodynamic approach by crystal lattice energy, sublimation, and solubility exemplified by hydroxybenzoic acids

Temperature dependencies of saturated vapor pressure and heat capacities for the 2-, 3-, and 4-hydroxybenzoic acids were measured and thermodynamic functions of sublimation calculated (2-hydroxybenzoic acid: DeltaG(sub) (298) = 38.5 kJ/mol; DeltaH(sub) (298) = 96.6 +/- 0.8 kJ/mol; DeltaS(sub) (298) = 191 +/- 3 J/mol . K; 3-hydroxybenzoic acid: DeltaG(sub) (298) = 50.6 kJ/mol; DeltaH(sub) (298) = 105.2 +/- 0.8 kJ/mol; DeltaS(sub) (298) = 180 +/- 2 J/mol . K; 4-hydroxybenzoic acid: DeltaG(sub) (298) = 55.0 kJ/mol; DeltaH(sub) (298) = 113.3 +/- 0.7 kJ/mol; DeltaS(sub) (298) = 193 +/- 2 J/mol . K). Analysis of crystal lattice packing energies based on geometry optimization of the molecules in the crystal using diffraction data and the program Dmol(3) was carried out. The energetic contributions of van der Waals, Coulombic, and hydrogen bond terms to the total packing energy were analyzed. The fraction of hydrogen bond energy in the packing energy increases as: 3-hydroxybenzoic (29.7%) < 2-hydroxybenzoic (34.7%) < 4-hydroxybenzoic acid (42.0%). Enthalpies of evaporation were estimated from enthalpies of sublimation and fusion. Temperature dependencies of the solubility in n-octanol and n-hexane were measured. The thermodynamic functions of solubility and solvation processes were deduced. Specific and nonspecific solvation terms were distinguished using the transfer from the "inert" n-hexane to the other solvents. The transfer of the molecules from water to n-octanol is enthalpy driven process.     

Efficacy of 2,3-dimercapto-1-propanesulfonic acid (DMPS) and diphenyl diselenide on cadmium induced testicular damage in mice

The deleterious effect of acute cadmium-intoxication in mice testes was evaluated. Animals received a single dose of CdCl₂ (2.5 or 5 mg/kg, intraperitoneally) and a number of toxicological parameters in mice testes were examined, such as δ-aminolevulinic acid dehydratase (δ-ALA-D) activity, lipid peroxidation, hemoglobin and ascorbic acid contents. Furthermore, the parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were also determined. Thus, a possible protective effect of 2,3-dimercapto-1-propane-sulfonic acid (DMPS) and diphenyl diselenide (PhSe)₂ were studied. The results demonstrated an inhibition of δ-ALA-D activity, a reduction of ascorbic acid and an increase of lipid peroxidation induced by cadmium, indicating testes damage. Furthermore, we observed an increase of plasma LDH, AST and ALT activities. DMPS (400 mol/kg) and (PhSe)₂ (100 μmol/kg) partially protected from the inhibitory effect of 2.5 mg/kg CdCl₂ on δ-ALA-D and from the increase of TBARS (thiobarbituric acid reactive species) levels. (PhSe)₂ therapy was effective in ameliorate ascorbic acid content when the cadmium dose was 2.5 mg/kg. Treatment with DMPS and (PhSe)₂, individually or combined, was inefficient in reducing cadmium-induced plasma LDH and ALT activity increase. The use of combined therapy (DMPS plus (PhSe)₂) proved to be efficient in decreasing cadmium levels in testes and in ameliorating plasma AST activity from animals that received the highest dose of cadmium.     

Reaction of 5-Aminosalicylic Acid with Peroxyl Radicals: Protection and Recovery by Ascorbic Acid and Amino Acids

Purpose The aims of the study are to analyze the interaction between 5-aminosalicylic acid (5-ASA) and peroxyl radicals and to evaluate the effect of some endogenous compounds such as ascorbic acid and amino acids on the oxidation of 5-ASA induced by 2,2′-azo-bis(2-amidinopropane) dihydrochloride. Methods The consumption and/or the recovery of 5-ASA (7.6 μM) exposed to a peroxyl radical source [2,2′-azo-bis(2-amidinopropane)] was followed by techniques such as spectrofluorescence, high-performance liquid chromatography, and differential pulse voltammetry. Results 5-Aminosalicylic acid was found to readily react with peroxyl radicals at micromolar concentrations and to protect c-Phycocyanin in a very similar fashion to that shown by Trolox. Exposure of 5-ASA to peroxyl radicals led to its oxidation into the corresponding quinone-imine. Disappearance of 5-ASA was prevented by tryptophan, cysteine, glutathione, and ascorbic acid. Furthermore, some of these compounds induced the partial (cysteine and glutathione) or total (ascorbic acid) recovery of 5-ASA when added after its almost total consumption. Conclusions 5-Aminosalicylic acid is a very efficient peroxyl radical scavenger. The 5-ASA oxidation by peroxyl radicals was prevented by ascorbic acid, cysteine, and glutathione. In addition, 5-ASA can be regenerated by these endogenous compounds, which would be a valuable mechanism to preserve 5-ASA in tissues undergoing oxidative stress conditions.     

The fate of 2-chlorobenzylidene malononitrile (CS) in rats

1. The fate of ³H-ring labelled, ¹⁴C-cyanide labelled and (¹⁴C=C) side chain labelled 2-chlorobenzylidene malononitrile (CS), 2-chlorobenzyl alcohol and 2-chlorobenzyl malononitrile (dihydro CS) in rats and isolated rat liver cells has been examined.

2. CS was administered both i.v. and i.g. to rats at doses from 0.08 to 159 ümol/kgand in most cases the greatest proportion of the dose was eliminated in the urine (44–100%). The principal urinary metabolites were 2-chlorohippuric acid, 1-O-(2-chlorobenzyl) glucuronic acid, 2-chlorobenzyl cysteine and 2-chlorobenzoic acid. Lesser amounts of 2-chlorophenyl acetyl glycine, 2-chlorobenzyl alcohol and 2-chlorophenyl 2-cyano propionate were identified.

3. The major urinary metabolite from 2-chlorobenzyl alcohol was 2-chlorohippuric acid (43%), 2-chlorobenzyl cysteine, 2-chlorobenzoic acid and 2-chlorobenzyl glucuronic acid were identified.

4. The products of dihydro-CS metabolism were 2-chlorophenyl acetyl glycine, 2-chlorophenyl 2-cyanopropionate and 2-chlorophenyl proprionamide.

5. Urinary thiocyanate levels increased with the dose of CS up to 159 ümol/kg. At 212ümol/kg there was a large increase in the amount of thiocyanate produced (molar conversion: 21.5–29.9%). Similarly malononitrile, the hydrolysis product of CS, gave a dose related increase in urinary thiocyanate levels. However at a higher dose (212 ümol/kg) the molar conversion was greater than 60%.

6. The metabolism of CS by isolated rat liver cells confirmed the results in vivo but demonstrated a marked limitation of this preparation to form conjugates.

7. It is concluded that CS in vivo is hydrolysed mainly to 2-chlorobenzaldehyde which is then either oxidized to 2-chlorobenzoic acid for subsequent glycine conjugation, or reduced to 2-chlorobenzyl alcohol for ultimate excretion as 2-chlorobenzyi acetyl cysteine or 1-O-(2-chlorobenzyl) glucuronic acid. Malononitrik is converted to thiocyanate via the formation of cyanide.     

Glutathione and ascorbic acid concentrations in the duodenum of rats with cysteamine-induced ulcers: influence of cysteine and ascorbic acid pretreatments

Duodenal ulceration in rats was induced by a single subcutaneous injection of cysteamine at doses of 7, 28, 42 and 65 mg/100 g body weight 24 h before killing. Duodenal ulceration induced by cysteamine was dose-dependent. However, at 65 mg/100 g body weight, 5 of 6 animals died within 24 h. The concentrations of reduced glutathione (GSH) and ascorbic acid were measured in the duodenal homogenates of cysteamine-treated rats. The ulcerogen, at doses of 28 and 42 mg/100 g body weight, significantly reduced the GSH concentration. At a dose of 28 mg/100 g body weight, however, it did not significantly affect the duodenal ascorbic acid concentration. Pretreatment of rats with daily intramuscular injections of cysteine at 25, 50 and 100 mg/kg or ascorbic acid at 50, 100 and 200 mg/kg for 7 days had no significant effect on the duodenal ulceration produced by cysteamine (28 mg/100 g body weight), although each pretreatment significantly raised the duodenal concentrations of GSH and ascorbic acid respectively, in control rats, and to a lesser extent in cysteamine-treated animals.