石棉作业对工人血浆中谷胱甘肽S转移酶活性的影响

目的　探讨接触石棉是否会影响工人体内的谷胱甘肽S转移酶 (GST)活性及GSTM1基因型对体内GST活性的影响。方法　选择 94名石棉作业工人及 5 1名对照工人作为研究对象 ,通过问卷调查收集每人的一般情况和职业史等。采集静脉血分离血浆和淋巴细胞 ,血浆用于GST活性测定 ,淋巴细胞用于提取DNA进行GSTM1基因型分析。结果　石棉作业工人血浆中的GST活性 (2 3 0± 6 9)U/L ,明显低于对照组工人的 (32 6± 11 8)U/L ,且随着石棉作业工龄的延长及累积石棉接触剂量的增加 ,工人血浆中的GST活性呈逐渐下降的趋势。用GSTM1基因型对两组工人进行分层后发现 ,携带GSTM1+/ +和GSTM1- / -基因型的石棉作业工人 ,其血浆中的GST活性分别为 (2 4 0±6 1)U/L和 (2 2 5± 7 3)U/L ,均低于同种基因型的对照组工人 ,对照组分别为 (38 1± 13 2 )U/L和(2 6 8± 6 6 )U/L。同时还发现 ,携带GSTM1- / -的对照组工人血浆中的GST活性明显低于携带GSTM1+/ +者 ,而石棉作业工人组虽也有类似趋势 ,但差异无统计学意义。结论　接触石棉可明显降低体内GST的活性。在对照人群中 ,GST活性受GSTM1基因型的影响 ,而在石棉作业工人中 ,这种影响不明显。     

铅对作业工人甲状腺功能的影响

目的　了解铅对作业工人甲状腺功能的影响。方法　选择暴露于铅作业环境下的人群 ,了解工人作业工龄 ,采用火焰原子吸收光谱法测定其作业环境中铅浓度 ,用原子吸收光谱法测定作业工人血铅 (PbB)浓度 ,用血液锌原卟啉测定仪测定血锌原卟啉 (ZPP)浓度 ,用放射免疫分析法检测血清中促甲状腺素 (TSH)、三碘甲状腺原氨酸 (T3)、甲状腺素 (T4 )、游离T3(FT3)、游离T4 (FT4 ) 5项甲状腺功能指标。结果　血铅 >2 .88μmol/L时 ,T3[(1 .54± 0 .39)nmol/L]、FT3[(5 .50± 1 .2 6)pmol/L]含量明显低于血铅 (1 .92～ 2 .88) μmol/L组 [T3(1 .71± 0 .45)nmol/L、FT3(6 .1 2± 1 .64)pmol/L] ,差异有显著性(P <0 .0 5)。铅作业工龄长短对甲状腺激素 (TH)含量未见明显影响。结论　高浓度血铅可能抑制了T4 的脱碘 ;铅作业工龄对甲状腺功能未见明显影响     

镍电解工人体内镍与脂质过氧化关系的研究

目的 研究从事镍电解工人体内镍负荷与自由基代谢变化的关系.方法 以100名镍电解作业人员为接触组,以80名无镍接触的健康者作为对照组,分别测定两组人员血清中镍含量作为体内负荷;同时测定两组人员中血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平,并将上述各项指标进行相关分析.结果 与对照组比较,镍作业组血清中MDA含量[(14.98±2.03)μmol/L]明显升高;SOD活力[(90.33±18.76)U/L]、GSH活力[(101.48±19.76)U/L]明显下降,差异有统计学意义(P＜0.01).结论 镍具有增加体内脂质过氧化产物、降低机体抗氧化能力的作用.     

镍电解工人体内镍与脂质过氧化关系的研究

目的 研究从事镍电解工人体内镍负荷与自由基代谢变化的关系.方法 以100名镍电解作业人员为接触组,以80名无镍接触的健康者作为对照组,分别测定两组人员血清中镍含量作为体内负荷;同时测定两组人员中血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平,并将上述各项指标进行相关分析.结果 与对照组比较,镍作业组血清中MDA含量[(14.98±2.03)μmol/L]明显升高;SOD活力[(90.33±18.76)U/L]、GSH活力[(101.48±19.76)U/L]明显下降,差异有统计学意义(P＜0.01).结论 镍具有增加体内脂质过氧化产物、降低机体抗氧化能力的作用.     

镍电解工人体内镍与脂质过氧化关系的研究

目的 研究从事镍电解工人体内镍负荷与自由基代谢变化的关系.方法 以100名镍电解作业人员为接触组,以80名无镍接触的健康者作为对照组,分别测定两组人员血清中镍含量作为体内负荷;同时测定两组人员中血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平,并将上述各项指标进行相关分析.结果 与对照组比较,镍作业组血清中MDA含量[(14.98±2.03)μmol/L]明显升高;SOD活力[(90.33±18.76)U/L]、GSH活力[(101.48±19.76)U/L]明显下降,差异有统计学意义(P＜0.01).结论 镍具有增加体内脂质过氧化产物、降低机体抗氧化能力的作用.     

镍电解工人体内镍与脂质过氧化关系的研究

目的 研究从事镍电解工人体内镍负荷与自由基代谢变化的关系.方法 以100名镍电解作业人员为接触组,以80名无镍接触的健康者作为对照组,分别测定两组人员血清中镍含量作为体内负荷;同时测定两组人员中血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平,并将上述各项指标进行相关分析.结果 与对照组比较,镍作业组血清中MDA含量[(14.98±2.03)μmol/L]明显升高;SOD活力[(90.33±18.76)U/L]、GSH活力[(101.48±19.76)U/L]明显下降,差异有统计学意义(P＜0.01).结论 镍具有增加体内脂质过氧化产物、降低机体抗氧化能力的作用.     

镍电解工人体内镍与脂质过氧化关系的研究

目的 研究从事镍电解工人体内镍负荷与自由基代谢变化的关系.方法 以100名镍电解作业人员为接触组,以80名无镍接触的健康者作为对照组,分别测定两组人员血清中镍含量作为体内负荷;同时测定两组人员中血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平,并将上述各项指标进行相关分析.结果 与对照组比较,镍作业组血清中MDA含量[(14.98±2.03)μmol/L]明显升高;SOD活力[(90.33±18.76)U/L]、GSH活力[(101.48±19.76)U/L]明显下降,差异有统计学意义(P＜0.01).结论 镍具有增加体内脂质过氧化产物、降低机体抗氧化能力的作用.     

镍电解工人体内镍与脂质过氧化关系的研究

目的 研究从事镍电解工人体内镍负荷与自由基代谢变化的关系.方法 以100名镍电解作业人员为接触组,以80名无镍接触的健康者作为对照组,分别测定两组人员血清中镍含量作为体内负荷;同时测定两组人员中血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平,并将上述各项指标进行相关分析.结果 与对照组比较,镍作业组血清中MDA含量[(14.98±2.03)μmol/L]明显升高;SOD活力[(90.33±18.76)U/L]、GSH活力[(101.48±19.76)U/L]明显下降,差异有统计学意义(P＜0.01).结论 镍具有增加体内脂质过氧化产物、降低机体抗氧化能力的作用.     

镍电解工人体内镍与脂质过氧化关系的研究

目的 研究从事镍电解工人体内镍负荷与自由基代谢变化的关系.方法 以100名镍电解作业人员为接触组,以80名无镍接触的健康者作为对照组,分别测定两组人员血清中镍含量作为体内负荷;同时测定两组人员中血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平,并将上述各项指标进行相关分析.结果 与对照组比较,镍作业组血清中MDA含量[(14.98±2.03)μmol/L]明显升高;SOD活力[(90.33±18.76)U/L]、GSH活力[(101.48±19.76)U/L]明显下降,差异有统计学意义(P＜0.01).结论 镍具有增加体内脂质过氧化产物、降低机体抗氧化能力的作用.     

镍电解工人体内镍与脂质过氧化关系的研究

目的 研究从事镍电解工人体内镍负荷与自由基代谢变化的关系.方法 以100名镍电解作业人员为接触组,以80名无镍接触的健康者作为对照组,分别测定两组人员血清中镍含量作为体内负荷;同时测定两组人员中血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)水平,并将上述各项指标进行相关分析.结果 与对照组比较,镍作业组血清中MDA含量[(14.98±2.03)μmol/L]明显升高;SOD活力[(90.33±18.76)U/L]、GSH活力[(101.48±19.76)U/L]明显下降,差异有统计学意义(P＜0.01).结论 镍具有增加体内脂质过氧化产物、降低机体抗氧化能力的作用.     

Plasma lipid peroxides among workers exposed to silica or asbestos dusts

Plasma malondialdehyde (MDA) (an indicator of lipid peroxidation) was determined in random samples of workers (age range 25-60 years) exposed to silica dust (n = 31, mean exposure duration 21.3 +/- 8.3 years) or asbestos dust (n = 59, mean exposure duration 15.6 +/- 4.5 years) and in 52 age-matched healthy male controls. MDA levels of both exposed groups were significantly higher than that of the controls and were significantly higher among workers exposed to asbestos than among those exposed to silica dusts. Neither age nor smoking was related to MDA levels among both controls and exposed workers; among the latter group MDA was not significantly correlated with duration of exposure. Mean MDA levels of exposed workers with radiographic signs of lung fibrosis or pleural thickening and of those without such signs were not significantly different, except in the case of asbestos-exposed workers where it was significantly less than that of those without such signs. Differences between mean durations of dust exposure of workers with radiographic signs of lung fibrosis and those without such signs were statistically insignificant. The results suggest the possible involvement of lipid peroxidation on exposure to silica or asbestos dusts in humans and possible development of antioxidant mechanism(s) on prolonged dust exposure and support the opinion that development of pneumoconiosis depends on susceptibility factor(s).     

硒与氟对人肝细胞凋亡和脂质过氧化的影响

目的　研究硒、氟对离体培养的人肝细胞凋亡和脂质过氧化的影响。方法　体外培养的人肝细胞分别接触一定剂量的氟和 /或硒 1 2h后 ,检测肝细胞凋亡小体百分率、细胞周期构成比、还原型谷胱甘肽 (GSH)含量和脂质过氧化物 (LPO)的水平以及培养液中LPO和乳酸脱氢酶 (LDH)、丙氨酸转氨酶 (ALT)和天冬氨酸转氨酶 (AST)的活性。结果　加氟组肝细胞凋亡小体百分率 (1 5 557±2 0 56) % ,S期细胞数 (4 82 3± 0 454) % ,肝组织和培养液中LPO水平 [分别为 (2 884± 0 589)和 (3 547± 0 561 )nmol/LMDA/mg prot) ,培养液中AST和LDH含量 (分别为 91 1± 36 4和 1 4 0 4± 7 6U/L) ,均明显高于对照组 [分别为 (1 0 31 3± 1 0 2 3) % ,(3 2 53± 0 743) % ,(1 473± 0 40 1 )nmol/LMDA/mg ,(1 694± 0 443)nmol/LMDA/mg,(54 5± 3 2 )U/L和 (1 2 6 4± 2 6)U/L] ,而氟组肝组织GSH含量则明显低于对照组 [分别为 (4 2 2 5± 0 781 ) μg/mg和 (7 595± 1 0 4 2 ) μg/mg) ;硒可通过升高GSH含量 ,降低LPO、AST、LDH水平和凋亡小体百分率而拮抗氟产生的毒性作用。结论　一定剂量的硒可拮抗氟所诱导的肝细胞凋亡和脂质过氧化     

对氧磷酶1 55 Met/Leu、对氧磷酶2 148 Ala/Gly和锰超氧化物歧化酶9 Ala/Val基因多态性与冠心病

目的 探讨对氧磷酶155 Met/Leu(PON1 55 Met/Leu)、对氧磷酶2148 Ala/Gly(PON2148 Ala/Gly)和锰超氧化物歧化酶9 Ala/Val(MnSOD 9 Ala/Val)基因多态性与冠心病(CHD)、血浆对氧磷酶(PON)、总超氧化物歧化酶(T-SOD)和锰超氧化物歧化酶(MnSOD)活性以及丙二醛(MDA)浓度的关系.方法 采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法检测262例CHD患者和100名对照组的PON1 55 Met/Leu、PON2 148 Ala/Gly和MnSOD 9 Ala/Val基因多态性的基因型,采用比色法测定血浆PON、T-SOD和MnSOD活性以及MDA浓度.结果 与对照组比较,CHD患者的血浆PON[(349.27±138.36 vs 454.75±166.00)nmol·min-1·ml-1,P＜0.001]、T-SOD[(23.61±16.51 vs.44.01±22.68)U/ml,P＜0.001]和MnSOD活性[(21.56±13.11 vs.28.79±8.65)U/ml,P＜0.001]明显降低,MDA浓度显著增高[(2.47±0.73 vs.2.15±0.55)nmol/ml,P＜0.01];CHD患者的PON1 55 LM杂合子基因型、M等位基因频率,PON2 148 GG纯合子基因型和AG杂合子基因型、G等位基因频率和MnSOD 9 AA基因型、A等位基因频率较对照组明显增多;PON1 55 LM杂合子基因型的PON和T-SOD活性较LL纯合子基因型明显降低;PON2 148GG基因型和AG基因型的PON活性较AA基因型明显降低;MnSOD AA基因型的PON和MnSOD活性较VV基因型明显降低;logistic回归分析显示PON1 55 LM杂合子基因型、M等位基因、PON2148 GG/AG基因型、G等位基因是CHD的危险因子.结论 CHD患者的抗氧化能力明显降低,脂质过氧化物显著增高;PON1 55 Met/Leu、PON2 148 Ala/Gly和MnSOD 9 Ala/Val基因多态性通过影响血浆PON和MnSOD活性而参与CHD的发病.     

焦炉逸散物对焦炉工氧化还原物及P53和P21表达的影响

目的 观察接触焦炉逸散物(coking oven emissions,COE)的焦炉工血清丙二醛(MDA)含量、超氧化物歧化酶(T-SOD)水平,以及外周血淋巴细胞P53、P21蛋白质表达.方法 选择焦炉作业工人56人为接触组,非焦炉作业工人40人为对照组.采用硫代巴比妥酸法和黄嘌呤氧化快速比色法,分别测定血清MDA含量和T-SOD水平,并用免疫组织化学法,检测外周血淋巴细胞P53及P21蛋白质表达.结果 接触组血清MDA含量[(5.35±2.29)mnol/ml]明显高于对照组,差异有统计学意义(P＜0.05),血清T-SOD水平[(100.04±10.75)NU/ml]明显低于对照组,差异有统计学意义(P＜0.05);接触组外周血P53及P21蛋白质表达阳性率分别为21.4%和23.2%,均高于对照组,差异有统计学意义(P＜0.05).结论 COE可导致职业性接触人群MDA含量增高及T-SOD水平降低,P53和P21蛋白质表达阳性率增高.     

甲萘威对雌性大鼠血清雌激素水平及抗氧化系统功能的影响

目的观察甲萘威对雌性大鼠的生殖毒性并初步探讨其机制。方法雌性SD大鼠经口染毒甲萘威,剂量为0、1.028、5.140、25.704mg·kg-1·d-1。阴道脱落细胞涂片法观察大鼠动情周期的变化;放射免疫法测定其血清雌二醇(E2)、孕酮(P4)水平;分光光度法测定其血清超氧化物歧化酶(SOD)、谷胱甘肽硫转移酶(GST)的活力以及丙二醛(MDA)、谷胱甘肽(GSH)的含量。结果各剂量甲萘威染毒组大鼠动情周期数明显低于对照组。染毒后15d大鼠动情各期出现变化,与对照组的差异有统计学意义(P<0.05,P<0.01)。25.704mg·kg-1·d-1组大鼠体重增长明显低于对照组。各剂量染毒组大鼠的多个脏器系数均明显降低。25.704mg·kg-1·d-1组大鼠血清中E2水平为(19.93±2.21)nmoll,1.028mg·kg-1·d-1组大鼠P4水平为(1.21±0.40)nmoll,与对照组[(28.76±6.12)、(0.63±0.39)nmolL]的差异均有统计学意义(P<0.05)。随染毒剂量增高,大鼠SOD活力在卵巢先降后升,在血清中略升后下降;MDA含量则呈在卵巢中渐升高、在血清中略升后降低趋势;GSH含量和GST活力在卵巢中呈先降后升趋势,但在血清中,GSH含量呈下降趋势,GST活力先上升后下降。结论甲萘威可致雌性大鼠动情周期紊乱及雌激素水平改变,对大鼠的抗氧化系统产生一定影响。     

口服亚硒酸钠和维生素E对高海拔地区心血管病患者甲状腺激素的影响

目的探讨使用亚硒酸钠和维生素E对高海拔地区心血管病患者甲状腺激素的影响.方法将心血管病患者随机分为3组A组42例患者口服亚硒酸钠,同时加服维生素E;B组28例患者口服亚硒酸钠;对照组20例,未服用亚硒酸钠及维生素E.观察对象分别于治疗前和治疗6个月后抽血检测血清硒(Se)、血浆谷胱甘肽过氧化物酶(GSH-Px)活力、丙二醛(MDA)含量及甲状腺激素(T3、T4)等指标,以观察远期疗效.结果治疗后A组和B组血清Se含量[(0.71±0.22)、(0.68±0.18)μmol/L]明显高于治疗前[(0.31±0.17)、(0.33±0.14)μmol/L],差异有显著性(P＜0.01);A组和B组血浆GSH-Px活力分别为(87.12±13.61)、(84.79±12.13)U/L,较治疗前[分别为(58.43±18.93)、(57.12±17.36)U/L]明显增加.A组和B组MDA含量[(4.86±1.18)、(4.18±1.23)nmol/ml]较治疗前[(8.66±0.96)、(8.71±0.87)nmol/ml]明显降低,差异均有显著性(P＜0.01);A组和B组患者T3和T4较对照组明显降低,趋于正常.血清Se与血浆GSH-Px呈正相关(r=0.781,P＜0.01),与MDA、T3、T4浓度呈负相关(r=-0.385;r=-0.687;r=-0.412,均P＜0.05).甲状腺激素恢复正常者A组31例(73.81%)、B组20例(71.42%);部分恢复者A组4例(9.52%)、B组2例(7.43%),其恢复率明显高于对照组,差异有显著性(P＜0.05),远期疗效较好.结论补充适量硒和维生素E可纠正高原环境下因低Se而引起的甲状腺激素代谢异常.     

Oxidative stress in painters exposed to low lead levels

Lead toxicity is a public health problem particularly to the children and to occupationally exposed adults. Evidence is mounting successively regarding the adverse health effects of lead at low levels. This study was undertaken to assess the antioxidant status of lead-exposed residential and commercial painters of Lucknow city in Uttar Pradesh, India.Thirty-five painters aged 20 to 50 years who had blood lead levels 相似文献   

Metallothionein in mice reduces intestinal zinc loss during acute endotoxin inflammation, but not during starvation or dietary zinc restriction

Normal metallothionein [(MT)+/+] and MT-null (MT-/-) mice were used to examine the influence of MT on Zn retention and the metabolic consequences of 2 d food deprivation, with and without inflammation induced by intraperitoneal injection of bacterial endotoxin lipopolysaccharide (LPS). LPS reduced fecal Zn concentration in MT+/+ mice from 5.9 +/- 0.2 micromol/g on d 1 to 2.2 +/- 0.2 micromol/g on d 2, but not in MT-/- mice, 5.9 +/- 0.2 and 5.7 +/- 0. 5 micromol/g, respectively. MT+/+ mice fed an 8 mg Zn/kg diet and injected with LPS excreted 40% less Zn over 2 d than their MT-/- counterparts. Starvation for 2 d did not lower fecal Zn concentration in either genotype, although in MT+/+ mice, urinary Zn excretion was reduced from 12.7 +/- 1.3 nmol on d 1 to 5.9 +/- 1.8 nmol on d 2 and plasma Zn concentration was lowered to 9.8 +/- 0.4 micromol/L. Zn was not reduced in urine or plasma of MT-/- mice, with respective values of 10.8 +/- 2.0 nmol on d 1, 9.3 +/- 2.9 nmol on d 2 and 13.0 +/- 1.0 micromol/L. LPS injection resulted in much higher total liver Zn (677 +/- 27 nmol) and MT (106 +/- 2 nmol Cd bound/g) than starvation (Zn = 405 +/- 21, MT = 9 +/- 3) in MT+/+ mice after 2 d, but did not further reduce urinary Zn. LPS-injected MT-/- mice had no rise in liver Zn or fall in plasma and urine Zn. MT-/- mice fed a Zn-deficient (0.8 mg Zn/kg) diet lost 10% of body weight over 25 d compared with no loss in MT+/+ mice. Despite this, MT-/- mice excreted no more Zn via the gut than did MT+/+ mice. In summary, MT inhibits intestinal Zn loss when highly expressed. When uninduced, typically during Zn deficiency, MT appears to conserve Zn and body mass by reducing only urinary and other nonintestinal Zn losses.     

Influence of GSTM1 genotypes on anti-BPDE–DNA adduct levels in mononuclear white blood cells of humans exposed to PAH

OBJECTIVE: Association between genetic deletion polymorphism of GSTM1 (*0/*0 or active) and levels of anti (+/-)-r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE)-DNA adducts in the peripheral blood lymphocyte plus monocyte fraction (LMF) of PAH-exposed subjects was investigated. METHODS: A total of 94 Caucasian subjects comprised the sample population: 13 coke-oven workers, 19 chimney sweeps, 36 aluminum-anode plant workers, and 26 non-occupationally PAH-exposed subjects (controls). PAH exposure was assessed in each group by means of the urinary excretion of 1-pyrenol (mean group levels 1.2, 0.7, 0.3, and 0.1 mumol/mol creatinine in coke-oven workers, chimney sweeps, aluminum-anode plant workers, and control subjects, respectively). Anti-BPDE-DNA adducts were detected by HPLC/fluorescence analysis of anti-BPDE tetrols (tetrol I-1) released after acid hydrolysis of DNA samples. RESULTS: In coke-oven workers the percentage of cases with adduct levels exceeding the 95th percentile control value (4.4 adducts/10(8) nucleotides) was significantly higher in the subgroup with the null GSTM1 genotype (*0/*0) (100%) than in that with active GSTM1 (43%; chi 2 test, P < 0.05). In the other groups with different and lower levels of PAH exposure the percentages of positive samples were always higher in the subgroup with GSTM1 *0/*0 than in the active one, although the differences were not statistically significant. Univariate (odds ratio) and multivariate (relative risk) analyses showed that the risk of having high anti-BPDE-DNA levels increased with occupational exposure to PAH. Such risks, moreover, were further significantly increased by the lack of GSTM1 activity (RR = 5.94; CI = 1.15-30.7; P < 0.05). In coke-oven workers, chimney sweeps, and aluminum workers, respectively, the multiplicative effect of the null genotype with occupational PAH exposure gives risks of 162 (= 27.2 x 5.94), 10 (= 1.70 x 5.94), and 3 (= 0.50 x 5.94) times higher probability (risk) of high BPDE-DNA adduct formation than that of non-exposed subjects with the active GSTM1 genotype. CONCLUSION: Our results indicate a greater risk of anti-BPDE-DNA adduct formation resulting from occupational high-level PAH-exposure in GSTM1 null (GSTM1 *0/*0) workers.