职业性锰接触工人脂质过氧化改变观察

目的探讨锰接触对机体脂质过氧化的影响。方法选择84名锰焊作业人员及84名对照人员,测定其血清丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力。结果锰接触组MDA含量高于对照组,血清SOD、GSH-Px活力低于对照组,差异有显著性(P<0.05);MDA、SOD与作业场所空气锰呈现一定的剂量反应关系。结论锰能使机体脂质过氧化增加、抗氧化能力下降。MDA、SOD可作为锰中毒的早期观察指标。     

锰烟尘对男工红细胞某些金属元素的影响

目的探讨长期高浓度锰烟尘暴露对男工红细胞金属元素的影响。方法用电感耦合等离子发射光谱法测定59名接触锰男工和59名对照组男工红细胞Zn、Cu、Fe、Ca、Mn和Mg浓度。结果作业环境空气中MnO2平均浓度为0.75 mg/m3(0.19~1.60 mg/m3)时,接锰作业组红细胞Ca含量明显低于对照组,而Mn含量明显高于对照组。分层分析显示,接触锰工龄10a~组红细胞Cu含量明显低于其对照组和接触锰工龄<5a组;接触锰工龄5a~组红细胞Fe含量明显低于其对照组;接触锰工龄<5a组红细胞Ca含量明显低于其对照组及接触锰工龄10a~组;接触锰各工龄组红细胞Mn含量均高于相应的对照组;接触锰工龄<5a组红细胞Mg含量明显高于其对照组。结论长期接触高浓度锰可使男工红细胞Mn含量增高,Ca含量降低。分层分析表明接触锰作业的时间长短对红细胞Mn、Cu、Fe、Ca和Mg含量也有一定的影响,但变动无明显规律性。     

镍接触作业工人抗氧化能力的研究

目的探讨职业性镍接触对工人抗氧化能力的影响。方法根据生产工艺的不同,选取某钢铁企业镍接触工人男性炼钢工、轧钢工及钢渣处理工共181人作为镍接触组,同时选择该企业的男性水处理工55人为对照组。黄嘌呤氧化酶法、化学比色法和硫代巴比妥酸法分别测定两组人群血清中总超氧化物歧化酶(SOD)活力、谷胱甘肽过氧化物酶(GSH-Px)活力和丙二醛(MDA)含量。结果不同工种镍接触组总SOD活力、GSH-Px活力和MDA含量分别与对照组相比,差异均有统计学意义(P0.05);不同工龄组总SOD活力、GSH-Px活力和MDA含量分别与对照组相比,除0～5 a组总SOD活力、GSH-Px活力分别与对照组相比,差异无统计学意义(P0.05)外,其他各年龄组差异均有统计学意义(P0.05);不同工龄组MDA含量分别与对照组相比,差异均有统计学意义(P0.05)。结论镍接触对工人抗氧化能力有影响,抗氧化酶活力降低,脂质过氧化产物增加。     

接触沥青筑路工人脂质过氧化水平调查

目的探讨接触沥青对筑路工人体内脂质过氧化水平的影响。方法测定直接接触沥青、间接接触沥青、非接触沥青工人血清中丙二醛(MDA)、总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)的浓度或活性。结果两个接触组MDA含量均显著高于非接触组(P0.05),T-AOC较非接触组明显降低(P0.0001)。结论接触沥青的筑路工人存在脂质过氧化损伤,可能会影响到作业工人的健康。     

冶炼作业人群铅、砷负荷对脂质过氧化和抗氧化能力的影响

目的探讨冶炼工人体内铅(Pb)、砷(As)负荷对脂质过氧化产物和抗氧化酶的影响。方法选取212名冶炼作业人员为接触组,以106名无Pb、As接触史的健康人为对照组,分别测定两组人员血清中Pb、As的含量为体内负荷指标,测定两组人员血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和谷胱甘肽硫转移酶(GST)水平,接触组按工龄分组将上述各项指标进行相关分析。结果接触组血清Pb、As平均水平分别为(0.18±0.03)和(0.39±0.01)μmol/L,血清SOD、GSH-Px和GST活力分别为(161.22±29.26)、(116.42±20.16)和(38.36±10.06)U,MDA含量为(7.32±2.35)μmol/L;对照组血清Pb、As平均水平分别为(0.07±0.02)和(0.11±0.07)μmol/L,血清中SOD、GSH-Px和GST活力分别为(181.61±28.34)、(153.14±20.36)和(46.20±10.26)U,MDA含量为(4.35±2.26)μmol/L。接触组与对照组上述对应各项指标进行统计学分析,差异呈高度显著性(P<0.01)。对接触组以工龄分组比较,显示≥10年工龄组较短工龄组(≤5年)血清Pb、As平均水平与MDA均较高(P<0.01);SOD、GSH-Px和GST活力较低(P<0.01)。结论Pb、As接触有增加体内脂质过氧化产物含量,降低机体抗氧化能力的作用。     

金属镉作业人群的脂质过氧化与抗氧化能力的观察

目的 观察金属镉接触作业人群体内的脂质过氧化产物和抗氧化酶的变化。方法 选取91名接触金属镉（Cd）的作业人员为接触组，并以79名不接触任何毒物的健康人作为对照组，测定血清中丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）和谷胱甘肽硫转移酶（GST）。结果 接触组的SOD、GSH-Px和GST的活性明显下降，而MDA明显增高（P〈0．05）。以工龄分组比较，显示长工龄组较短工龄组MDA高，SOD、GSH-Px和GST活性低（P〈0．05）。结论 Cd能增加体内脂质过氧化产物含量，降低机体的抗氧化能力，增加职业接触人群对氧化应激的易感性。     

134名放射诊疗工作人员脂质过氧化水平调查

目的 了解长期低剂量职业性接触电离辐射的放射诊疗工作人员脂质过氧化及其抗氧化能力。方法 收集134名职业接触电离辐射的放射诊疗工作人员个人剂量,血清中丙二醛(MDA)、过氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)含量。结果 放射工龄<5年的放射诊疗工作人员血清中SOD、GSH-Px活力、MDA含量与5年及20年以上工龄组比较,差异有统计学意义,累积剂量当量<2 mSv的放射诊疗工作人员血清中GSH-Px活力与累积剂量2~5 mSv及>5 mSv组比较,差异有统计学意义。结论 本研究中放射诊疗工作人员虽然长期接触低剂量射线,但不会对身体健康造成明显损伤。     

长期接触有机磷农药农民体内氧化应激水平的调查

调查农民长期接触有机磷农药体内氧化应激水平,寻找长期接触有机磷农药与疾病发生的靶点。采用随机抽取新乡市农村地区长期接触有机磷农药史的农民382人,分别检测血浆中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧物酶(GSH-Px)、过氧化物酶(LPO)含量。结果显示,与对照组比较,接触有机磷农药10 a的农民体内SOD活力降低,差异有统计学意义(P0.05),MDA含量和GSH-Px、LPO活力比较,差异均无统计学意义(P0.05),接触有机磷农药10 a的农民体内MDA含量与LPO活力明显增加,SOD与GSH-Px活力明显降低,差异均有统计学意义(P0.05),性别与工作类别对农民体内氧化应激水平的影响差异无统计学意义。提示,农民长期接触有机磷农药会引起体内氧化应激水平增加。     

长期接触有机磷农药机体抗氧化能力调查

目的 调查农民长期接触有机磷(OP)农药后机体抗氧化能力的改变.方法 随机抽取新乡市4区8县农村地区有长期接触OP农药史的农民382人,分别检测体内丙二醛(MDA)和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化物酶(LPO)的水平和活力.结果 接触OP农药＞10年的农民机体抗氧化能力明显下降,但下降程度无年限差异.结论 农民长期接触OP农药会引起机体抗氧化能力下降.     

电焊作业对工人血清抗氧化系统的影响

目的了解电焊作业有害因素对血清抗氧化系统的影响。方法以65名电焊作业工人为接触组,55名不接触职业病危害因素的工人为对照组。对两组人员的血清总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力及丙二醛(MDA)含量进行测定分析。结果接触组工人血清T-AOC、SOD活力较对照组降低,差异有显著性(P<0.05)。结论电焊作业产生的锰尘、噪声等职业有害因素可影响工人体内抗氧化系统。     

炼油污水挥发物对作业工人脂质过氧化反应的影响

目的 探讨低浓度炼油污水作业对人体氧化和过氧化反应的影响。方法 检测73例污水处理作业工人和129例健康对照血清丙二醛（MDA）含量和血清超氧化物歧化酶（SOD）、全血谷胱甘肽过氧化物醇（GSH－Px)和过氧化氢酶（CAT）活力。结果 污水处理作业工人血清SOD和全血GSH－Px活力与对照组相比,差异具有显著性（P＜0．01）,CAT的差异不具有显著性。中工龄组（5－20年）GSH－Px活力明显高于对照组,而高工龄组（＞20年）差异不具有显著性。接触组SOD活力仅低工龄组（＜5年）较对照组高（P＜0．05）。结论 低浓度长期接触炼油污水挥发物,体内的脂质过氧化反应和抗氧化机制均处于亢奋状态,后者可能是机体的一种防御机制。     

石棉作业女工血脂质过氧化与抗氧化活性的研究

为探讨温石棉对人体的脂质过氧化作用机制，对４７名接触温石棉的女工和１５名女性石棉肺病人血清ＭＤＡ、ＳＯＤ、ＧＳＨ－Ｐｘ进行了研究，并分别与１５名无石棉接触女工和接尘女工对照，采用ｔ检验、相关分析。结果可见接尘组女工血清中ＭＤＡ、ＳＯＤ、ＧＳＨ－Ｐｐｘ等显著高于对照组（Ｐ＜０．００１），接尘组与石棉肺病人组血清ＭＤＡ、ＳＯＤ、ＧＳＨ－ｐｘ等各项指标均无显著差别（Ｐ＞０．０５）。提示温石棉可引起接触女工和石棉肺患者的脂质过氧化和抗氧化荫等的变化，表明脂质过氧化在温石棉致病中起着重要作用。ＭＤＡ及抗氧化酶如ＳＯＤ等有望成为早期诊断和动态观察的敏感指标。     

三氯乙烯对职业接触人群脂质过氧化作用

目的 探讨三氯乙烯（trichloroethylene，TCE）对职业接触人群外周血脂质过氧化作用的影响。方法采集207名直接接触TCE工人的班末尿和外周肘静脉血，分析尿中三氯乙烯（Trichloroactic acid，TCA）含量，测定外周血过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-PX）、丙二醛（MDA）的活性或含量。结果接触组工人红细胞CAT、血清总SOD和GSH-PX活性以及血清中脂质过氧化产物MDA含量均呈现升高趋势，CAT、总SOD与接触TCE的工龄，以及CAT、总SOD、GSH-PX与接触剂量间均呈显著的抛物线性关系，MDA与接触工龄及接触剂毋间均呈直线关系。结论TCE可引起职业接触人群脂质过氧化水平增高。脂质过氧化指标可作为早期职业接触损伤的生物效应指标之一。CAT可作为早期、敏感的生物效应监测指标。     

Mobile phone-induced myocardial oxidative stress: protection by a novel antioxidant agent caffeic acid phenethyl ester

Electromagnetic radiation (EMR) or radiofrequency fields of cellular mobile phones may affect biological systems by increasing free radicals, which appear mainly to enhance lipid peroxidation, and by changing the antioxidant defense systems of human tissues, thus leading to oxidative stress. Mobile phones are used in close proximity to the heart, therefore 900 MHz EMR emitting mobile phones may be absorbed by the heart. Caffeic acid phenethyl ester (CAPE), one of the major components of honeybee propolis, was recently found to be a potent free radical scavenger and antioxidant, and is used in folk medicine. The aim of this study was to examine 900 MHz mobile phone-induced oxidative stress that promotes production of reactive oxygen species (ROS) and the role of CAPE on myocardial tissue against possible oxidative damage in rats. Thirty rats were used in the study. Animals were randomly grouped as follows: sham-operated control group (N: 10) and experimental groups: (a) group II: 900 MHz EMR exposed group (N: 10); and (b) group III: 900 MHz EMR exposed+CAPE-treated group (N: 10). A 900 MHz EMR radiation was applied to groups II and III 30 min/day, for 10 days using an experimental exposure device. Malondialdehyde (MDA, an index of lipid peroxidation), and nitric oxide (NO, a marker of oxidative stress) were used as markers of oxidative stress-induced heart impairment. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status. In the EMR exposed group, while tissue MDA and NO levels increased, SOD, CAT and GSH-Px activities were reduced. CAPE treatment in group III reversed these effects. In this study, the increased levels of MDA and NO and the decreased levels of myocardial SOD, CAT and GSH-Px activities demonstrate the role of oxidative mechanisms in 900 MHz mobile phone-induced heart tissue damage, and CAPE, via its free radical scavenging and antioxidant properties, ameliorates oxidative heart injury. These results show that CAPE exhibits a protective effect on mobile phone-induced and free radical mediated oxidative heart impairment in rats.     

Preventive effect of vitamin E on iron-induced oxidative damage in rabbit

Although iron (Fe), plays an important role in different oxidative steps during the metabolism of the human body, it can cause free radical damage. Iron ions seem to play a major role in initiation and promotion reactions of intracellular lipid peroxidation. The aim of this study was to investigate if vitamin E has a protective effect on oxidative changes in erythrocytes induced by Fe treatment. Thirty male New Zealand white rabbits weighing 1400 +/- 50 g were used in the study. The animals were divided into three groups. The first group (n:10) was given 500 mg/kg iron-dextran through intraperitoneal (ip) injection. The second group was given 500 mg/kg iron-dextran+100 mg/kg vitamin E(ip). The third group constituted the control group and received a saline solution injection. The activities of erythrocyte antioxidant enzymes; Superoxide Dismutase (SOD), Glutatione peroxidase (GSH-Px), Catalase (CAT) and Malondialdehyde (MDA) level, an indicator of lipid peroxidation, were determined. Erythrocyte SOD, GSH-Px and CAT activities were decreased and MDA level was increased in iron-dextran treated animals compared to the control group (P < 0.05). The activities of the three antioxidant enzymes were increased and MDA level was decreased in iron-dextran and vitamin E treated group compared to the control group (P < 0.05). Our data indicate that lipid peroxidation occurs after iron overload in the blood. In the light of our findings, vitamin E administration can prevent the toxic oxidative effects induced by iron-dependent free radical damage in erythrocytes.     

PM_(2.5)对大鼠肝、脾、肾组织的氧化损伤效应

目的探讨PM2.5对大鼠肝、脾、肾组织抗氧化酶活力和脂质过氧化(LPO)水平的影响。方法选取32只雄性Wistar大鼠,随机分为4组,分别用0、1.5、7.5、37.5mg/kg的PM2.5经气管注入染毒后24h处死大鼠,测定肝、脾、肾组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活力,谷胱甘肽(GSH)和硫代巴比妥酸反应物(TBARS)含量。结果PM2.5染毒组大鼠肝、肾组织内SOD、CAT、GSH-Px活力和SOD/TBARS比值均较对照组降低(P<0.05,P<0.01),具有剂量-效应关系。各染毒组TBARS/GSH-Px比值较对照组显著升高(P<0.01,P<0.001)。染毒组脾、肾组织GSH含量较对照组显著下降(P<0.05,P<0.01),而染毒组肝组织GSH含量则出现先升高后降低的非线性变化特征(P<0.01,P<0.05)。染毒组肝组织LPO水平出现剂量-效应性升高(P<0.05),染毒组脾组织各种抗氧化酶活力、LPO水平和TBARS/GSH-Px比值均未见显著变化。结论PM2.5可引起大鼠肝、肾组织的氧化损伤。     

Erythrocyte antioxidant enzyme activities and lipid peroxidation in the erythrocyte membrane of stainless-steel welders exposed to welding fumes and gases

The erythrocyte antioxidant system (superoxide dismutase, SOD; catalase, CAT) and lipid peroxidation (malondialdehyde, MDA) in the erythrocyte membrane were studied in workers continously exposed to welding fumes and gases, which are thought to be oxidant pollutants. Thirty-five welders using the manual metal arc method on stainless steel and 30 controls were studied. Plasma chromium (Cr), manganese (Mn), and cupper (Cu) levels were determined by atomic absorption spectrophotometer (AAS). The erythrocyte antioxidant system activity and lipid peroxidation in the erythrocyte membrane were evaluated. Not only the possible effects of welding fumes but also the effects of smoking were considered. The plasma concentrations of Cr, Mn, and Cu for the exposed welders were significantly higher compared to the control subjects (p<0.001, p<0.01, p<0.001, respectively,). The erythrocyte CAT (p<0.05) and SOD (p<0.05) enzyme activities were significantly higher in the welders but there were not any significant changes in the MDA levels which reflect the lipid peroxidation in the erythrocyte membrane (p>0.05). Smoking has increased the SOD activity in both controls (p<0.05) and welders (p<0.01) and increased the CAT activity in control subjects (p<0.05). Moreover, regardless of smoking, there were some significant correlations between the duration of the exposure to welding fumes and antioxidant defence system (SOD: p<0.05; CAT: p<0.05). The synergistic effects of smoking and other risk factors (welding fumes and gasses), which had been shown previously by some clinical data should also be taken into account. As a consequence, the welders should be warned and informed of the synergistic effects of smoking on the adverse effect of welding fumes and gases.     

Effect of dietary n-3 and n-6 oils with and without food restriction on activity of antioxidant enzymes and lipid peroxidation in livers of cyclophosphamide treated autoimmune-prone NZB/W female mice

OBJECTIVE: Cyclophosphamide (CTX), an alkylating agent, is extensively used in the treatment of lupus nephritis, but its administration has been associated with free radical mediated oxidative stress. The present study was designed to investigate the effect of dietary corn oil (CO), fish oil (FO) and food restriction (FR) on the activities of hepatic antioxidant enzymes, fatty acid composition and lipid peroxidation following CTX administration in autoimmune-prone NZB/W female mice. METHODS: Autoimmune-prone NZB/W female mice were fed either ad libitum (AL) or food restricted (60% of AL intake), semipurified diets containing 5% CO or 5% FO supplemented with equal levels of antioxidants and injected with either phosphate buffered saline (PBS), or CTX (50 mg/kg body weight) every 10 days. Proteinuria was measured biweekly. The treatment was stopped at 10 months and diets were continued until the mice were killed at 12 months. Fatty acid composition, activity of antioxidant enzymes and lipid peroxidation were analyzed in liver homogenates, and anti-DNA antibodies were analyzed in the serum. RESULTS: Mice in the FO/AL dietary group exhibited significantly higher liver catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities compared to the CO/AL dietary group. CTX significantly decreased SOD and GSH-Px activity in the FO/AL group and CAT and GSH-Px in the CO/AL group. In AL fed mice given CTX, activities of CAT, GSH-Px and GST were significantly higher in mice fed FO diets than in mice fed CO diets. FR increased the activity of enzymes in both the CO and FO diet groups. In FR mice, CTX decreased CAT and GSH-Px activity in both the CO and FO dietary groups, but glutathione S-transferase (GST) only in the CO group. The decrease in SOD activity was not significant in either of the restricted groups. CTX significantly increased generation of thiobarbituric acid reactive substances (TBARS) in both AL groups. FR significantly decreased lipid peroxidation in both the CO and FO groups, with or without CTX. CTX decreased serum anti-DNA antibody levels in both the CO and FO dietary groups. FR also decreased antibody titer in both the CO and FO dietary groups, and it was decreased further with CTX treatment. FO fed animals had higher levels of n-3 fatty acids, whereas CO fed animals had high levels of n-6 fatty acids. CTX significantly increased 20:4 and decreased 18:1 in CO/AL fed animals, whereas it increased 18:1 and decreased 22:6 in FO/AL fed animals. CONCLUSIONS: Results obtained in the present study suggests that FO and, more significantly, FO combined with FR can have a beneficial effect in hepatic tissues subjected to CTX induced oxidative stress by regulating the activity of antioxidant enzymes. In addition, the study also indicates that n-3 and n-6 dietary lipids are susceptible to lipid peroxidation, particularly in the presence of a prooxidant like CTX, and that FR is beneficial in decreasing lipid peroxidation. The study also suggests that FO and CTX can have additive effects in preventing kidney disease in NZB/W mice.     

Methotrexate-induced renal oxidative stress in rats: the role of a novel antioxidant caffeic acid phenethyl ester

The exact mechanisms of methotrexate-induced renal toxicity have not yet been determined. However, several hypotheses have been put forward, including oxidative stress. The aim of this study was to investigate the role of caffeic acid phenethyl ester (Caffeic Ester), a novel antioxidant, on methotrexate-induced renal oxidative stress in rats. Nineteen adult male rats were equally divided into three experimental groups as follows: control group, methotrexate-treated group, and methotrexate+Caffeic Ester-treated group. A single dose of methotrexate (20 mg/kg) was administered intraperitoneally (ip). Caffeic Ester (10 micromol/kg) was administered ip, once daily for seven days. Malondialdehyde (MDA) levels (an index of lipid peroxidation) were used as a marker of oxidative stress-induced renal injury. Similarly, the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were determined to evaluate the changes of antioxidant status in renal tissue. Methotrexate administration to control rats increased MDA levels (P<0.0001), but decreased SOD, CAT and GSH-Px activities in renal tissue (P<0.0001). Caffeic Ester+ methotrexate treatment caused a significant decrease in MDA levels (P<0.001), and caused an increase in SOD, CAT and GSH-Px activities when compared with methotrexate treatment alone (P<0.001, <0.05, <0.0001, respectively). In conclusion, methotrexate leads to a reduction in antioxidant enzymatic defense capacity and causes lipid peroxidation in renal tissue. Similarly, Caffeic Ester exhibits protective effects on methotrexate-induced renal oxidative impairment in rats.