乌司他丁对犬肺缺血再灌注损伤的保护作用

目的 探索乌司他丁(UTI)在肺缺血再灌注损伤中对肺的保护作用.方法 18只实验用犬随机分成对照组、抑肽酶组(抑肽酶30000U/kg)和UTI组(UTI 20000U/kg),每组6只.建立在体肺缺血再灌注模型,并检测血清丙二醛(MDA)、过氧化物歧化酶(SOD)及肺组织中的MDA、髓过氧化物酶(MPO).进行再灌注肺肺泡灌洗液(BALF)白细胞计数和肺组织病理切片并计算肺湿干重比(W/DR).结果 再灌注后UTI组动脉血和肺组织中MDA水平、MPO活性较抑肽酶组及对照组低(P＜0.05),血清SOD活性较抑肽酶组及对照组高(P＜0.05和P＜0.01).再灌注肺BALF白细胞计数UTI组低于对照组(P＜0.05);肺W/DR UTI组低于抑肽酶组和对照组(P＜0.01).病理切片显示,UTI组肺损伤比抑肽酶组和对照组轻.结论 UTI 20000U/kg可减轻犬肺缺血再灌注损伤,对犬肺的保护作用优于抑肽酶30000U/kg.     

高密度脂蛋白预处理对缺血再灌注大鼠肺组织的影响

目的 探讨高密度脂蛋白(high-density lipoprotein,HDL)预处理对缺血再灌注损伤(ischemia-reperfusion injury,IRI)大鼠肺组织的影响.方法 将24只SD大鼠随机分成3组:假手术组(SO)、缺血再灌注损伤组(I/R组)和缺血再灌注高密度脂蛋白预处理组(H/IPC组).建立大鼠肺脏缺血再灌注模型,并检测各组PH、PaO2、PaCO2、肺湿/干重比值(wet-to-dry weight ratio,W/D)、支气管肺泡灌洗液(bronchial alveolar lavage fluid,BALF)中白细胞(White blood cell,WBC)计数、测定髓过氧化酶(myeloperoxidase,MPO)水平,并观察肺组织病理变化.结果 ①HDL改善大鼠换气功能,升高PaO2和降低PaCO2;②HDL降低肺组织湿/干重比值(W/D)和髓过氧化酶(MPO)的活性(P<0.05),降低肺泡灌洗液中WBC数量;③病理形态学显示,HDL预处理组大鼠在肺水肿及肺组织内中性粒细胞浸润的程度均低于I/R所致损伤组.结论 经90 min缺血,180 min再灌后,HDL预处理能减轻I/R所致PaO2的降低、血管通透性增高,中性粒细胞浸润,减轻I/R大鼠肺组织损伤.     

雌激素对骨骼肌缺血再灌注损伤的保护作用

目的:探讨17β-雌二醇对大鼠骨骼肌缺血再灌注损伤的作用.方法:制作右后肢缺血再灌注模型,30只大鼠随机分为3组,假手术组;缺血再灌注对照组:骨骼肌缺血冉灌注+生理盐水;雌激素干预组:骨骼肌缺血再灌注+雌激素干预.用全自动牛化分析仪测定血浆肌酸磷酸激酶(CPK)、乳酸脱氢酶(LDH),用硫代巴比妥酸比色法测定丙二醛(MDA),用比色法测定小腿三头肌组织中髓过氧化酶(MPO)活性;高倍显微镜观察小腿三头肌组织结构变化.结果:缺血再灌注对照组、雌激素十预组与假手术组比较,血浆CPK、LDH、MDA及MPO含量明显升高(P<0.01),雌激素干预组与缺血再灌注对照组相比血浆CPK、LDH、MDA及MPO含量明硅降低(P<0.01);缺血冉灌注对照组、雌激素干预组均可见骨骼肌损伤,缺血再灌注对照组明显重于雌激素干预组.结论:雌激素对肢体骨骼肌缺血再灌注损伤具有保护作用,其作用与抑制中性粒细胞的效应有关.     

灵芝多糖对失血性休克复苏时肺损伤的保护作用

目的 探讨灵芝多糖(GLP)对失血性休克复苏时肺损伤的保护作用.方法 复制家兔失血性休克再灌注(SH-R)复苏模型,随机分成假手术组(S组)、生理盐水再灌注复苏组(NS组)和质量分数为1%的GLP再灌注复苏组(LS组).于再灌注复苏90 min时快速处死动物,观察肺组织一氧化氮(NO)含量和一氧化氮合酶(NOS)活性与肺组织损伤性变化的关系.结果 NS和LS组肺组织NOS活性、NO含量均明显低于S组,但LS组明显高于NS组(P<0.05);NS和LS组肺组织湿/于比(W/D)、损伤肺泡百分率(IAR)和凋亡细胞百分数、支气管肺泡灌洗液(BALF)中自细胞计数和肺通透指数(PPI)明显高于S组,而LS组明显低于NS组(P<0.05);病理显示:NS组肺损伤明显,LS组肺损伤不明显.结论 GLP可通过激活NOS、增加NO含量、减少多形核白细胞(PMN)在肺部的集聚而对SH-R肺损伤起保护作用.     

缺血后处理对再灌注损伤鼠肺IL-17和IL-8的影响

目的研究缺血后处理对再灌注损伤鼠肺IL17和IL-8的影响,并分析其可能的肺保护作用机制。方法构建大鼠在体肺脏缺血再灌注损伤模型,30只SD大鼠随机分为假手术对照组(Sham组)、缺血再灌注组(IR组)和缺血后处理组(IPostC组),每组10只。在体大鼠IR损伤模型制备完成后,阻断左肺门,终止血供及通气,造成左肺缺血,达预定时间后松开阻断带恢复血供及通气形成再灌注损伤。Sham组开胸游离左肺门穿阻断带而不结扎持续180 min;IR组缺血60 min后再灌注120 min;IPostC组缺血60 min后给予重复三次的5 min灌注和5 min缺血的后处理,继以恢复血供行再灌注90 min。三组实验结束后均留取左肺组织、左支气管肺泡灌洗液标本,分别用于测定IL-17、IL-8的含量,留取小块肺组织测定肺湿/干重比(W/D)。结果Sham组支气管肺泡灌洗上清液中IL-17含量明显低于IR组和IPostC组(P0.05);IPostC组支气管肺泡灌洗上清液中IL-17含量明显低于IR组(P0.05)。Sham组支气管肺泡灌洗上清液中IL-8含量明显低于IR组和IPostC组(P0.05);IPostC组支气管肺泡灌洗上清液中IL-8含量明显低于IR组(P0.05)。Sham组肺组织中IL-17明显低于IR组和IPostC组(P0.05);IPostC组肺组织中IL-17明显低于IR组(P0.05)。Sham组肺组织中IL-8明显低于IR组和IPostC组(P0.05);IPostC组肺组织中IL-8明显低于IR组(P0.05)。Sham组肺组织W/D明显低于IR组(P0.05)和IPostC组;IPostC组肺组织W/D明显低于IR组(P0.05)。结论缺血后处理能明显减轻大鼠肺缺血再灌注损伤。其机制可能与抑制IL-17、IL-8活性从而减轻肺组织炎症损害有关。     

脂氧素A_4对大鼠肺缺血再灌注损伤氧化损伤的影响

目的探讨脂氧素A_4对大鼠肺缺血再灌注损伤氧化应激的影响。方法取36只大鼠(体重220~280g)随机分为假手术组、缺血再灌注组和脂氧素A_4干预组。阻断左肺门45min后再灌注2h建立肺缺血再灌注损伤模型,脂氧素A_4干预组在大鼠恢复血供前5min股静脉注射脂氧素A4 0.1mg/kg。收集标本,检测肺组织的湿/干重量(W/D)比值、支气管肺泡灌洗液的蛋白总量(TP)、检测肺组织匀浆中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性。结果缺血再灌注组肺组织W/D比值、MDA水平和支气管肺泡灌洗液中总蛋白均较假手术组明显升高,而SOD活性较假手术组明显降低(P0.05)。脂氧素A_4干预组的上述指标高于明显低于缺血再灌注组,而SOD活性较缺血再灌注组明显升高(P0.05)。结论脂氧素A_4对大鼠肺缺血再灌注损伤有一定的保护作用,其机制可能是脂氧素A_4清除自由基抗氧化作用。     

支气管肺泡灌洗对兔肺泡内TNF-α的影响

目的 观察生理盐水、亚胺培南、氟康唑支气管肺泡灌洗后对兔肺泡内炎症因子的影响.方法 新西兰白兔34只气管插管后分为四组:A组(3只)作为空白对照;B组(11只)用生理盐水支气管肺泡灌洗;C组(8只)用亚胺培南灌洗;D组(12只)用氟康唑灌洗.2 h后处死动物,ELISA法比较肺泡灌洗液及肺组织匀浆中肿瘤坏死因子α(TNF-α)含量.结果 四组肺泡灌洗液的TNF-α水平各组间差异无统计学意义(P>0.05).C组肺组织匀浆TNF-α水平低于A、B、D组(P<0.05).结论 生理盐水、亚胺培南、氟康唑支气管肺泡灌洗并未增加局部TNF-α的释放.     

厄多司坦祛痰作用的疗效观察

目的 观察国产厄多司坦祛痰作用的疗效.方法 78例患者随机分为治疗组(n:40)和对照组锄=38),治疗组口服国产厄多司坦胶囊300 mg,一日2次:对照组口服溴已新片16 mg,一日3次.疗程均为7天.结果 治疗组和对照组的临床总有效率分别为67.5%和57.9%,两组对比差异无统计学意义(P>0.05);祛痰有效率分别为85.0%和63.1%,两组比较有显著性差异(P<0.05);不良反应发生率分别为5%和7.9%,两组对比无显著性差异(P>0.05).结论 国产厄多司坦胶囊用于祛痰治疗疗效和安全性与溴已新相当.     

大鼠高血糖－局灶性脑缺血再灌注损伤模型建立的初步研究

目的:建立快速、稳定的大鼠高血糖-局灶性脑缺血再灌注损伤(I/R)模型,探讨将其用于脑缺血再灌注损伤相关研究的可行性.方法:24只大鼠随机等分为4组,分别为正常血糖和高血糖下假手术组(NG-sham,HG-sham),正常血糖和高血糖下脑缺血再灌注损伤组(NG-FCIR, HG-FCIR).术前1 h腹腔注射10%右旋葡萄糖制备高血糖大鼠;采用线栓法阻断大脑中动脉(MCAO)建立I/R模型,脑缺血1 h再灌注3 h.测定各组注射葡萄糖前、缺血开始和再灌注3 h后的血糖;TTC染色比较各组脑组织水肿程度和脑梗死面积;比较各组脑组织乳酸脱氢酶活性、总NOS和iNOS、SOD酶活性,以及NO、MDA含量.结果:与对照组相比,缺血前注射葡萄糖的各组血糖明显升高(P<0.01),并且持续至再灌注3h(P<0.01).与NG-FCIR组相比,HG-FCIR组的脑组织水肿程度增加、脑梗死面积明显增大(P<0.05),脑组织乳酸脱氢酶、总NOS、iNOS活性增加(P<0.05),SOD酶活性明显降低(P<0.05),NO、MDA含量明显增多(P<0.05).结论:术前1 h腹腔注射右旋葡萄糖(2g·kg-1)可诱导大鼠高血糖状态,加速、加重MCAO引起的局灶性脑缺血再灌注损伤.采用高血糖模型,缺血1 h、再灌注3 h时即可用于ROS、NO等相关的药物疗效或机制研究,可显著缩短观察时间.     

维司力农对缺血再灌注大鼠心肌NO含量及PKC活性的影响

目的　探讨维司力农对缺血再灌注心肌的保护作用机制。方法　采用NO和PKC测定试剂盒分别测定了两个对照组、心肌缺血预适应组、不同剂量维司力农组的大鼠心肌细胞内一氧化氮 (NO)含量和蛋白激酶C(PKC)活性。结果　高、低剂量维司力农组PKC活性高于两个对照组 ;低剂量组PKC活性与缺血预适应组相当 ,高剂量组PKC活性明显高于缺血预适应组。同时 ,NO含量也高于两个对照组和缺血预适应组。结论　维司力农可使大鼠心肌细胞内NO含量和PKC活性提高 ,由此推断 :维司力农对缺血再灌注心肌的保护作用很可能是通过NO激活PKC而实现的。     

The activities of tissue xanthine oxidase and adenosine deaminase and the levels of hydroxyproline and nitric oxide in rat hearts subjected to doxorubicin: protective effect of erdosteine

The aim of this experimental study was to investigate the effects of erdosteine, an antioxidant agent, on doxorubicin (DXR)-induced cardio-toxicity through nitric oxide (NO) levels, collagen synthesis, xanthine oxidase (XO) and adenosine deaminase (ADA) activities in rats. Rats were treated with erdosteine (10 mg/kg b.wt. per day, orally) or saline starting 2 days before administrating a single dose of DXR (20 mg/kg i.p.) or saline. At the 10th day of the DXR administration, hearts were removed under anesthesia for biochemical measurements. Enzyme activities as well as OH-proline and NO levels were found to be significantly increased in DXR group compared with the control group. All of the parameters studied except ADA activity were decreased significantly approximating to the control levels upon erdosteine administration. In conclusion, erdosteine seems to be an alternative agent for protection of cardiac tissue against DXR-induced cardio-toxicity through its regulatory effect on XO activity and NO level.     

Examination of lung toxicity, oxidant/antioxidant status and effect of erdosteine in rats kept in coal mine ambience

Occupational exposure to coal dust causes pneumoconiosis and other diseases. Reactive oxygen species (ROS) have been implicated in the pathogenesis of coal dust-induced lung toxicity. In this experimental study, we investigated the oxidant/antioxidant status, nitric oxide (NO) and hydroxyproline (HP) levels in lungs and blood of rats exposed to coal dust in mine ambience. In addition, we also investigated the attenuating effects of erdosteine. At the end of the experiment processes, tissue levels of HP, malondialdehyde (MDA) and NO, as well as the activities of superoxide dismutase, glutathione peroxidase, catalase, xanthine oxidase (XO), myeloperoxidase (MPO) and proinflammatory cytokines (IL-6 and TNF-α) were evaluated in the lung tissues, plasma samples or erythrocytes of rats. Exposure to coal dust resulted in a significant increase in the oxidant parameters (MDA, NO levels, and XO activity) and HP levels, as compared to the controls. A decrease in activities of antioxidant enzymes, and an increase in MPO activity were found in the study group, compared to the controls. Increased NO levels of lung were found in the study groups, that were significantly reduced by erdosteine. Our studies provide evidence that supports the hypothesis for ROS mediated coal workers' pneumoconiosis. Erdosteine may be beneficial in the coal dust-induced lung toxicity via antioxidant and free radical scavenger properties.     

Nitric oxide inhalation inhibits inducible nitric oxide synthase but not nitrotyrosine formation and cell apoptosis in rat lungs with meconium-induced injury

AIM: To investigate the effects of inhaled nitric oxide (NO) on pulmonary inflammation, apoptosis, peroxidation and protein nitration in a rat model of acute lung injury (ALI) induced by meconium. METHODS: Twenty-four healthy male Sprague-Dawley rats were randomly devided into 3 groups (n=8): meconium-induced ALI with intratracheal instillation of 1 mL/kg saline (Mec/saline group), continuous inhalation of NO at 20 muL/L. (Mec/iNO), and the control group (control). Electromicroscopic examination was used to determine the extent of epithelial apoptosis. TUNEL was used to detect DNA fragmentation in pulmonary apoptotic cells, expressed as the apoptosis index (AI). Western blotting was used to detect pulmonary inducible NO synthase (iNOS) expression. RT-PCR was used to detect interleukin (IL)-1beta mRNA expression. Cell count in bronchoalveolar lavage (BAL), myeloperoxidase (MPO) activity, as well as malondialdehyde (MDA) and nitrotyrosine formation, the markers of toxic NO-superoxide pathway in rat lung parenchyma specimens, were also examined. RESULTS: Expression of iNOS protein and IL-1beta mRNA were increased significantly in the Mec/saline group (both P<0.01) compared with the control group. BAL cell count, MPO activity, lung injury score, pulmonary AI, MDA level and nitrotyrosine formation were also increased significantly (all P<0.01). The meconium-induced iNOS protein and IL-1beta mRNA expression were inhibited significantly by NO inhalation when compared with the Mec/saline group (both P<0.01). BAL cell count, MPO activity and lung injury score were also decreased significantly (P<0.01 or P<0.05). However, there were no statistical differences in MDA level, nitrotyrosine formation or pulmonary AI between the Mec/saline and Mec/iNO groups. Electromicroscopic examination revealed a significant degree of epithelial apoptosis in both the Mec/saline and Mec/iNO groups. CONCLUSIONS: Early continuous inhalation of NO 20 muL/L may protect the lungs from inflammatory injury, but does not decrease epithelial apoptosis or lung nitrotyrosine formation. Inhalation of NO alone is not associated with a detectable increase in oxidant stress.     

The effects of erdosteine, N-acetylcysteine, and vitamin E on nicotine-induced apoptosis of pulmonary cells

This study was conducted to investigate the frequency of apoptosis in the pulmonary epithelial cells of rats after intratraperitoneal nicotine injection, in order to examine the role of inflammatory markers [myeloperoxidase (MPO) and tumor necrosis factor-alpha (TNF-alpha)] in nicotine-induced lung damage, and to determine the protective effects of three known antioxidant agents [N-acetylcysteine (NAC), erdosteine, and vitamin E] on the lung toxicity of nicotine in the lungs. Female Wistar rats were divided into seven groups, each composed of nine rats: two negative control groups, two positive control groups, one erdosteine-treated group (500 mg/kg), one NAC-treated group (500 mg/kg), and one vitamin E-treated group (500 mg/kg). Nicotine was injected intraperitoneally at a dosage of 0.6 mg/kg for 21 days. Following nicotine injection, the antioxidants were administered orally, treatment was continued until the rats were killed. Lung tissue samples were stained with hematoxylin-eosin (H&E) for histopathological assessments. The apoptosis level in the lung bronchiolar and alveolar epithelium was determined by using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) method. Cytoplasmic TNF-alpha in the bronchiolar and alveolar epithelial cells and the lung MPO activity were evaluated immunohistochemically. The protective effect of vitamin E on lung histology was stronger than that of erdosteine or NAC. Treatment with erdosteine, NAC, and vitamin E significantly reduced the rate of nicotine-induced pulmonary epithelial cell apoptosis, and there were no significant differences in apoptosis among the three antioxidants groups. Erdosteine, NAC, and vitamin E significantly reduced the increases in TNF-alpha staining and lung MPO activity. The effects of erdosteine on the increases in the local TNF-alpha level and lung MPO activity were weaker than that of NAC or vitamin E. This findings suggest that erdosteine and NAC can be as effective as vitamin E in protecting against nicotine-induced pulmonary cell apoptosis.     

Inhaled nitric oxide improves the survival of the paraquat-injured rats

The purpose of this study was to evaluate the effects of inhaled nitric oxide (NO) on the paraquat-induced lung injury in rats. The rats were assigned to four groups: control; inhaled NO (5 ppm); paraquat (PQ, 30 mg/kg); and PQ+NO group. For first 18 h the inhalation of NO mixed with room air was performed. Total white blood cell (WBC), neutrophil, total protein, lactate dehydrogenase (LDH), transforming growth factor-beta1 (TGF-beta1) in serum and/or bronchoalveolar lavage (BAL) fluid, serum malonaldehyde (MDA), and myeloperoxidase (MPO) of lung were measured and lung histopathology were also reviewed. The 72-h survival rate of PQ group was 58%, but the survival rate of PQ+NO group, NO group and control group were 100%, respectively. The serum MDA and TGF-beta1 in BAL fluid and blood of PQ+NO group were significantly lower than those of PQ group. However, inhaled NO did not decrease the elevated total WBC and neutrophil counts, and total protein, LDH and MPO activity in the lung injured by PQ. The alveolar septal thickening and inflammatory cell infiltration were not different between PQ and PQ+NO groups. NO inhalation may be beneficial for the survival of paraquat-induced injured rats by attenuating lipid peroxidation and production of TGF-beta1.     

The effects of caffeic acid phenethyl ester on tissue damage in lung after hindlimb ischemia-reperfusion.

AIM: The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE) on the lungs as a remote organ after performing hindlimb ischemia-reperfusion (I/R) and by assessing biochemical and histopathological analysis. METHODS: The animals were divided into three groups: control, I/R, and I/R with CAPE. I/R period for 8 h was performed on the right hindlimb of all the anesthesied rats in I/R and CAPE with I/R group. In the CAPE with I/R group, the animals received CAPE 10 microM by intraperitoneal injection 1h before the reperfusion. The animals in the control and I/R groups received a similar volume of saline solution by means of intraperitoneal injection. At the end of the reperfusion period, a midsternotomy was performed. Blood, bronchoalveolar lavage (BAL) and lung tissue were obtained, and were used for biochemical and histopathological examination. RESULTS: The tissue and serum malondyaldehyde levels were significantly lower in the control (P=0.0001 and 0.001, respectively) and in the CAPE with I/R groups (P=0.0001 and 0.003, respectively) compared to the I/R group. Tissue Na(+)-K(+) ATPase activity in the CAPE with I/R group was significantly higher than in the I/R group (P=0.0001). Reduced activity was found in the I/R group compared to the control group (P=0.0001). Myeloperoxidase activity (P=0.001) and protein concentration (P=0.034) in BAL were significantly reduced in CAPE-treated animals when compared with the I/R group. A decreased activity and protein concentration were found in the control group compared to the I/R group (P=0.0001 and 0.024, respectively). The lungs of the I/R group displayed intense peribronchial and perivascular leukocytic infiltration in histopathological examination compared to the CAPE with I/R group (P<0.05). CONCLUSION: CAPE seems to be effective in protecting remote organ injury caused by increased oxidative stress and neutrophil accumulation that results from an I/R injury.     

Protective effects of L-arginine on pulmonary oxidative stress and antioxidant defenses during exhaustive exercise in rats

AIM: To assess the effects of L-arginine (L-Arg) supplementation on pulmonary oxidative stress and antioxidant defenses in rats after exhaustive exercise. METHODS: Rats were randomly divided into four groups: sedentary control (SC), sedentary control with L-Arg treatment (SC+Arg), exhaustive exercise with control diet (E) and exhaustive exercise with L-Arg treatment (E+Arg). Rats in groups SC+Arg and E+Arg received a 2% L-Arg diet. Rats in groups E and E+Arg underwent an exhaustive running test on a motorized treadmill. Pulmonary oxidative stress indices [xanthine oxidase (XO), myeloperoxidase (MPO), and malondialdehyde (MDA)] and antioxidant defense systems [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and glutathione (GSH)] were investigated in this study. RESULTS: L-Arg supplementation significantly reduced exercise-induced elevations of XO and MPO activities in lung. L-Arg reversed the exercise-induced increase in SOD and GR activities, but increased CAT and GPX activities. L-Arg administration also significantly increased the GSH levels in plasma. CONCLUSION: L-Arg supplementation can prevent elevations of XO and MPO activities in the lung and favorably influence pulmonary antioxidant defense systems after exhaustive exercise.     

Effects of erdosteine treatment against doxorubicin-induced toxicity through erythrocyte and plasma oxidant/antioxidant status in rats.

The clinical use of doxorubicin (Dxr), an antineoplastic agent, is limited by its extensive toxicity which is mostly mediated by oxidant injury. We have studied the effect of erdosteine, a mucolytic drug showing antioxidant properties, in preventing Dxr-toxicity to improve future Dxr therapy. Male Sprague-Dawley rats were divided into four groups. The first group that underwent no medication was accepted as control group; the second group was treated with a single i.p. injection of Dxr (20 mg kg(-1) b.wt.); the third group was treated with oral erdosteine alone (10 mg kg(-1) b.wt. day(-1) for 12 days); and in the last group erdosteine was administered starting before Dxr injection for 12 days. The thiobarbituric acid reactive substances (TBARS) level of Dxr group was higher in both plasma and erythrocyte than the other groups. In plasma and erythrocyte, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were increased in Dxr plus erdosteine group in comparison with control group, and the activities of GSH-Px were increased in Dxr plus erdosteine group in comparison with Dxr group. The erythrocyte catalase (CAT) activity of Dxr plus erdosteine group was higher than control and Dxr groups. Plasma xanthine oxidase activities and nitric oxide (NO) levels were not significantly different between groups, however erythrocyte NO level of Dxr group was higher than control. In conclusion, Dxr administration resulted in increased lipid peroxidation in plasma as well as erythrocyte and erdosteine treatment helped to prevent oxidative injury by increasing antioxidant enzymes, especially SOD, GSH-Px and CAT, in rats.     

Nitric oxide, adenosine deaminase, xanthine oxidase and superoxide dismutase in patients with panic disorder: alterations by antidepressant treatment

OBJECTIVE: In the present study, we aimed to investigate whether nitric oxide (NO) levels and activities of xanthine oxidase (XO), superoxide dismutase (SOD), and adenosine deaminase (ADA) are associated with Panic disorder (PD) as well as impact of psychopharmacological treatments on NO, SOD, ADA, and XO levels in PD. METHOD: In this study, 32 patients and 20 healthy controls were included. The serum levels of NO, XO, SOD, and ADA were measured in the patients and controls. The patients were treated with antidepressant. RESULTS: ADA and XO levels of the patients were significantly higher than the controls. SOD levels of the patients were significantly lower than the controls but the difference was not statistically significant. Although NO levels of the patients were higher than the controls, the difference was not statistically significant. There was no correlation between PAS and the parameters studied (SOD, ADA, XO, and NO) of the patients. After 8 weeks of antidepressant treatment, ADA and SOD activities were increased whereas NO and XO levels decreased significantly. CONCLUSION: ADA, XO activity may have a pathophysiological role in PD, and prognosis of PD. Activity of these enzymes may be used to monitor effects of the antidepressant treatment.