矽肺患者血清一氧化氮和一氧化氮合成酶的浓度变化的研究

目的：探讨一氧化氮（ＮＯ）和一氧化氮合成酶（ＮＯＳ）在矽肺发病中的作用和意义。方法：用生化比色法测定９８例各期矽肺患者血清ＮＯ和ＮＯＳ浓度并与正常对照组比较。结果：矽肺患者血清ＮＯ和ＮＯＳ高于对照组（Ｐ〈０．０５）,且矽肺期数越高,血清ＮＯ和ＮＯＳ浓度越高。矽肺Ⅰ－Ⅲ期之间ＮＯ和ＮＯＳ也有差别（Ｐ〈０．０５）。结论：血清ＮＯ和ＮＯＳ水平上升可能参与矽肺的形成和进展,测定ＮＯ和ＮＯＳ的浓度对了解矽肺     

隐睾下降固定术后生殖细胞的凋亡及eNOS和iNOS的表达

目的:探讨隐睾下降固定术后生精细胞的凋亡及内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)在隐睾下降固定后生精细胞中的表达。方法:将雄性SD大鼠(22日龄)随机分为隐睾组和假手术组,建立右侧隐睾模型。术后12天将隐睾组大鼠随机分为隐睾对照组和隐睾固定组,建立隐睾下降固定模型。术后第24天脱颈椎处死大鼠,取血清测定NO含量及一氧化氮合酶(NOS)活性,常规组织学切片观察各组大鼠右侧睾丸生精上皮形态,原位末端标记法(TUNEL)结合流式细胞术(FCM)检测各组睾丸生精细胞凋亡情况,Western blot和免疫组化分别检测各组大鼠右侧睾丸组织eNOS、iNOS蛋白表达的变化。结果:隐睾对照组血清中NO浓度、NOS活性以及生精细胞凋亡率最高,隐睾固定组则高于假手术组。Western blot检测发现隐睾固定组中eNOS和iNOS含量均高于假手术组,免疫组化结果显示在假手术组睾丸生精上皮中仅有eNOS和iNOS的弱表达,而隐睾固定组生精上皮中两者均有较强表达。结论:隐睾下降固定术后睾丸生精功能的改善与生精细胞凋亡减少有关。NO是隐睾下降及固定后生精细胞仍过度凋亡的重要生物活性因子。     

二甲苯对大鼠脑一氧化氮水平及一氧化氮合酶的影响

目的：探讨二甲苯对大鼠脑皮层匀浆上清液一氧化氮（ＮＯ）含量及海马区一氧化氮合酶（ＮＯＳ）活性的影响。方法：采用试剂盒法和ＮＡＤＰＨ组织学方法测定了ＮＯ含量和ＮＯＳ活性。结果：二甲苯接触组大鼠ＮＯ含量明显高于对照组（Ｐ＜０．０５），海马区ＮＯＳ阳性细胞数增加，但与对照组比较无显著性差异。结论：ＮＯ含量升高可能与二甲苯神经毒作用有关。海马区ＮＯＳ阳性细胞没有明显高于对照组而皮层匀浆上清液内ＮＯ含量升高的原因有待进一步阐明。     

染铅大鼠血清NO、NOS、SOD的变化

为探讨染铅大鼠血清中一氧化氮（ＮＯ）浓度、一氧化氮合酶（ＮＯＳ）活力及超氧化物歧化酶（ＳＯＤ）活力的变化,采用钦水染毒制造动物模型,硝酸还原酶法测定血清ＮＯ浓度,ＮＯＳ催化Ｌ－Ａｒｇ法测定血清ＮＯＳ活性,亚硝酸盐显色法测定血清ＳＯＤ活力。数据分析采用ＳＡＳ６．１２统计软件作均数的ｔ检验。结果显示,染铅组ＮＯＳ活力显著低于对照组（Ｐ＜０．０５）,而ＮＯ浓度和ＳＯＤ活力染铅组和对照组差异无显著性（Ｐ＞０．０５）。提示,染铅可以导致大鼠血清ＮＯＳ活力降低,但ＮＯ浓度和ＳＯＤ活力变化及其关系,还需要进一步研究。     

染锰大鼠血清NO、NOS、SOD的变化

为探讨染锰大鼠血清中一氧化氮（ＮＯ）浓度、一氧化氮合酶（ＮＯＳ）活力及超氧化物歧化酶（ＳＯＤ）活力的变化。采用饮水染毒建立动物模型;血清ＮＯ浓度测定采用硝酸还原酶法、血清ＮＯＳ活性测定采用ＮＯＳ催化Ｌ－Ａｒｇ法,血清ＳＯＤ活力测定业硝酸盐显色法;采用ＳＡＳ６．１２统计软件作测定结果均数的ｔ检验。结果显示染锰组ＮＯＳ活力显著低于对照组（Ｐ〈０．０５）,而ＮＯ浓度和ＳＯＤ活力染锰组和对照组无显著性差异     

沙漠热环境徒手行军者血浆NO和NOS与生理应激的关系

目的　探讨沙漠干热环境徒手行军者血浆一氧化氮 (NO)和一氧化氮合酶 (NOS)与生理应激的关系。方法　对在沙漠干热环境中分别以 3 5km/h和 5 0km/h徒手行军 1,2 ,3h试验组 6 0名战士和对照组14名战士血浆NO和NOS、心律增值、肛温增值和积热指数等进行分析。结果　不论是 3 5km/h还是5 0km/h行军 ,各行军时间试验组血浆NO均明显低于对照组 (P <0 0 5 )。3 5km/h行军时 ,行军 3h试验组血浆NO明显低于 1h试验组 (P <0 0 5 )。行军 1h试验组血浆NOS水平明显高于行军 2 ,3h试验组(P <0 0 5 )。各行军时间试验组心率增值、肛温增值和积热指数与对照组比较 ,差异均有显著性 (P <0 0 5 )。行军 3h试验组心率增值明显高于行军 2h试验组 (P <0 0 5 )。5 0km/h行军时 ,各行军时间试验组肛温增值和积热指数与对照组比较 ,差异均有显著性 (P <0 0 5 )。行军 2 ,3h试验组积热指数明显高于行军 1h试验组 (P <0 0 5 ) ,行军 3h试验组明显低于行军 2h试验组 (P <0 0 5 )。行军 2 ,3h试验组心率增值明显高于对照组 (P <0 0 5 )。结论　沙漠干热环境徒手行军者血浆NO和NOS与生理应激相关。     

慢性氟中毒大鼠睾丸组织总抗氧化能力与一氧化氮合酶和一氧化氮水平的变化

目的 通过给实验大鼠饮用不同浓度的氟化钠溶液,造成慢性氟中毒,测定实验大鼠睾丸组织匀浆中总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)与一氧化氮合酶(NOS)活力和一氧化氮(NO)的含量.方法 选用Wistar雄性大鼠24只,分为对照组、低氟组、高氟组,每组8只,染氟组分别自由饮用含氟化钠(NaF)100 mg/L、200mg/L的自来水,对照组自由饮用自来水.20周后处死动物,留取睾丸,制备匀浆.采用比色法检测T-AOC及NOS活力;采用黄嘌呤氧化酶法检测SOD活力;采用硝酸还原酶法检测NO含量.结果 低氟组与对照组比较,T-AOC明显增加(P＜0.01);而高氟组与对照组比较,则明显降低(P＜0.01).SOD活力在各组间比较,差异无统计学意义.与对照组比较,低氟组NOS活力、NO含量均明显减少(P＜0.01);而高氟组NOS活力、NO含量均明显升高(P＜0.01).结论 低剂量氟可能通过抑制NOS活力和NO的合成而使T-AOC代偿性增加;高剂量氟可能使活性氧增加,诱导型一氧化氮合酶(iNOS)开始异常表达而使NO合成增加.     

The Role of L‐Arginine and Inducible Nitric Oxide Synthase in Intestinal Permeability and Bacterial Translocation

Background: Arginine has been shown to have several immunological and trophic properties in stressful diseases. Its metabolites, nitric oxide (NO) and polyamines, are related to arginine's effects. Thus, the aim of this study was to determine the effects of the NO donor L‐arginine and the role of inducible NO synthase (iNOS) on intestinal permeability and bacterial translocation in a model of intestinal obstruction (IO) induced by a simple knot in the terminal ileum. Material and Methods: Male C57BL6/J wild‐type (WT) and iNOS knockout (iNOS–/–) mice were randomized into 6 groups: Sham and Sham–/– (standard chow), IO and IO–/– (standard chow +IO), and Arg and Arg–/– (standard chow supplemented with arginine + IO). After 7 days of treatment with standard or supplemented chows, IO was induced and intestinal permeability and bacterial translocation were evaluated. The small intestine and its contents were harvested for histopathological and morphometric analysis and the determination of polyamine concentration. Results: Pretreatment with arginine maintained intestinal permeability (P > .05; Arg and Arg–/– groups vs Sham and Sham–/– groups), increased polyamine concentration in intestinal content (P < .05; Arg vs IO group), and decreased bacterial translocation in WT animals (Arg group vs IO and IO–/– groups). Absence of iNOS also presented a protective effect on permeability but not on bacterial translocation. Conclusion: Arginine supplementation and synthesis of NO by iNOS are important factors in decreasing bacterial translocation. However, when intestinal permeability was considered, NO had a detrimental role.     

人胃癌组织中一氧化氮合酶的表达及其与血管形成机制的探讨

目的　研究诱导型一氧化氮合酶 (iNOS)在人胃癌组织中的表达及其与胃癌微血管形成的关系。方法　采用免疫组化SP法检测 5 0例原发性胃癌中iNOS的表达 ,同时检测微血管密度 (MVD) ,以CD3 4 标记。结果　iNOS阳性表达率为 70 %,在iNOS阴性表达组MVD均值为 (11 8± 5 9) ,在iNOS阳性表达组中MVD均值分别为 (18 7± 6 3) ,(2 4 5± 5 6 ) ,(30 1± 9 4 ) ,iNOS阴性组和阳性组MVD均值差异有显著统计学意义 (P <0 0 1)。结论　iNOS在胃癌组织中有高表达 (70 %) ,与肿瘤微血管形成有关。     

Mechanisms of Diesel-Induced Endothelial Nitric Oxide Synthase Dysfunction in Coronary Arterioles

Background and objective

Increased air pollutants correlate with increased incidence of cardiovascular disease potentially due to vascular dysfunction. We have reported that acute diesel engine exhaust (DE) exposure enhances vasoconstriction and diminishes acetylcholine (ACh)-induced dilation in coronary arteries in a nitric oxide synthase (NOS)-dependent manner. We hypothesize that acute DE inhalation leads to endothelial dysfunction by uncoupling NOS.

Methods

Rats inhaled fresh DE (300 μg particulate matter/m³) or filtered air for 5 hr. After off-gassing, intraseptal coronary arteries were isolated and dilation to ACh recorded using videomicroscopy.

Results

Arteries from DE-exposed animals dilated less to ACh than arteries from air-exposed animals. NOS inhibition did not affect ACh dilation in control arteries but increased dilation in the DE group, suggesting NOS does not normally contribute to ACh-induced dilation in coronary arteries but does contribute to endothelial dysfunction after DE inhalation. Cyclooxygenase (COX) inhibition did not affect ACh dilation in the DE group, but combined inhibition of NOS and COX diminished dilation in both groups and eliminated intergroup differences, suggesting that the two pathways interact. Superoxide scavenging increased ACh dilation in DE arteries, eliminating differences between groups. Tetrahydrobiopterin (BH₄) supplementation with sepiapterin restored ACh-mediated dilation in the DE group in a NOS-dependent manner. Superoxide generation (dihydroethidium staining) was greater in DE arteries, and superoxide scavenging, BH₄ supplementation, or NOS inhibition reduced the signal in DE but not air arteries.

Conclusion

Acute DE exposure appears to uncouple NOS, increasing reactive oxygen species generation and causing endothelial dysfunction, potentially because of depletion of BH₄ limiting its bioavailability.     

在沙漠干热环境中负重行军者血浆中NO和NOS与生理应激的关系

目的探讨沙漠干热环境负重行军者NO和一氧化氮合酶（NOS）与生理应激的关系。方法60名战士在沙漠干热环境中负重15kg分别以3．5和5．0km／h行军1、2、3h,检测试验组和对照组战士血浆中NO含量和NOS活力、心律增值、肛温增值和积热指数。结果所有行军时间组NO（17．26～23．28μmol／L）含量均明显低于对照组（31．84μmol／L）（P〈0．05）,心率增值（7．6—23．9次／min）均明显高于对照（1．2次／min）（P〈0．05）。15kg负重3．5km／h行军时,行军3h组NO（17．26μmol／L）含量明显低于行军1h组（22．62μmol／L）和2h组（23．10μmol／L）（P〈0．05）;行军1h组NOS（47．35U／L）活力明显高于行军3h组（40．90U／L）和对照组（40．89U／L）（P〈0．05）;行军3h组肛温增值（0．17℃）明显高于行军1h组（0．02oC）和对照组（0．00℃）（P〈0．05）;行军1和2h组积热指数（-18．9±18．31kJ／m2）明显低于行军3h组（22．67kJ／m2）和对照组（0．41kJ／m2）（P〈0．05）,行军3h组积热指数明显高于对照组（P〈0．05）。15kg负重5．0km／h行军时,行军2h组NOS（39．44U／L）活力明显低于对照组（40．89U／L）和其他行军时间组（34．23—40．43U／L）（P〈0．05）;行军1h组（23．9μmin）和3h组（21．3μmin）心率增值明显高于行军2h组（7．60μmin）（P〈0．05）;机体肛温随行军时间的延长而增高;各行军组积热指数（51．04～71．12kJ／m2）明显高于对照组（0．41kJ／m2）。结论在沙漠干热环境中行军者血浆中NO含量和NOS活力与热应激有关,沙漠干热环境劳动强度以不超过重度为宜,持续劳动时间不应超过2h。     

心房利尿钠肽基因多态性与冠心病关系的研究

[目的 ]探讨汉族人群心房利尿钠肽 (atrialnatriureticpeptide ,ANP)T2 2 3 8C基因多态性、血浆中的一氧化氮(nitricoxide ,NO)浓度、一氧化氮合酶 (nitricoxidesynthase ,NOS)活性与冠心病发病的关系。 [方法 ]采用病例 对照研究 ,应用聚合酶链 限制性片段长度多态性 (Polymerasechainrestrictionfragmentlengthpolymorphism ,PCR RFLP)方法检测 12 0例冠心病患者 (包括心绞痛与心肌梗死 )和 13 0名非冠心病对照人群ANPT2 2 3 8C基因多态性 ,应用试剂盒测定血浆中NO含量和NOS的活性。 [结果 ]总研究人群中ANPT2 2 3 8C基因多态性的A1和A2两种等位基因分布频率为 2 5 .46%和74.5 4% ,冠心病组A2A2基因型频率显著高于对照组 ;冠心病患者血浆NO和NOS水平均明显高于对照组 (P <0 .0 1)。在所研究的人群中 ,ANPT2 2 3 8C基因型的分布与血浆NO浓度及NOS活性无相关性。Logistic分析结果提示 ,性别、体重指数 (BMI)、高血压病史、糖尿病史、吸烟史、血浆总胆固醇、NO浓度、NOS活性 ,A2A2ANPT2 2 3 8C基因型为冠心病的独立危险因素。 [结论 ]ANPT2 2 3 8C基因多态性与冠心病发病显著相关 (P <0 .0 5 ) ,将成为冠心病的一种遗传易感性标志物 ,血浆NO和NOS水平与冠心病有密切的关系     

Neuronal Nitric Oxide Synthase Regulates Depression-like Behaviors in Shortening-Induced Obese Mice

Shortening is mainly derived from the partial hydrogenation of palm oil and widely used in fast food. Food processed with shortening contains high levels of industrial trans fatty acids. Studies have shown that there is a correlation between industrial trans fatty acids, obesity, and depression. However, the regulatory effect of neuronal nitric oxide synthase (nNOS) on depression in obese patients is still unknown. The purpose of this study was to explore mood changes in obese mice fed a high shortening diet, and to determine the regulatory effect of nNOS on depressive-like behaviors in obese mice. We used a high shortening diet-induced obesity mouse model to systematically assess the metabolic response, behavioral changes, prefrontal and hippocampal nNOS protein levels, and the effect of nNOS inhibitors (7-nitroindole) on depression-like behavior in obese mice. Interestingly, obese mice on a 9-week high-shortening diet developed short-term spatial working memory impairment and anxiety-like behavior, and obesity may be a risk factor for cognitive impairment and mood disorders. In animals fed a high shortening diet for 12 weeks, obese mice developed depression-like behavior and had significantly elevated levels of nNOS protein expression in the hippocampus and prefrontal lobe. Administration of the nNOS inhibitor 7-nitroindole could improve depression-like behaviors in obese mice, further suggesting that inhibition of nNOS is helpful for depression associated with obesity.     

Monomethylarsonous Acid Induced Cytotoxicity and Endothelial Nitric Oxide Synthase Phosphorylation in Endothelial Cells

Chronic arsenic poisoning is reported to be associated with peripheral and cardiovascular disease, arteriosclerosis, Raynaud’s syndrome, hypertension, and Blackfoot disease. Monomethylarsonous acid (MMA^III) is a reactive metabolite of inorganic arsenic and a potent inhibitor of endothelial nitric oxide synthase (eNOS). Arsenic is also reported to phosphorylate eNOS in cultured keratinocyte and Human T cell leukemia Jurkat cells, respectively. In the present study, we examined the cytotoxicity and eNOS phosphorylation by MMA^III exposure in cultured bovine aortic endothelial cells (BAEC). Results showed that MMA^III is more toxic than arsenite in BAEC cells. The IC₅₀ values for MMA^III and arsenite were determined to be approximately 1.7 and 24.1 μmol/L, respectively. Exposure of BAEC to MMA^III (0.75 μmol/L) caused a significant eNOS phosphorylation 15 min after MMA^III exposure. However, a complex of MMA^III with dithiothreitol (DTT) that lacks the reactivity with vicinal thiols unaffected eNOS phosphorylation. The present study shows that MMA^III generated during biomethylation of arsenic is highly toxic in BAEC. Our study also suggests that MMA^III could induce the eNOS phosphorylation through modification to cellular thiols of the eNOS enzyme. And the initial up-regulation of eNOS phosphorylation by MMA^III seems to be an adaptive response against disruption of eNOS bioactivity during arsenic exposure.     

铅对大鼠脑细胞一氧化氮合酶表达的影响

目的观察实验性铅中毒对大鼠脑细胞一氧化氮合酶(NOS)表达的影响,为进一步揭示铅的神经毒作用机制提供科学依据。方法取健康成年雄性SD大鼠24只,随机分为4组,每组6只,经腹腔注射醋酸铅连续染毒5d,剂量分别为25、50、100mg/kg体重,分别取海马、皮层部位脑组织,用免疫组化方法分别测定海马、皮层组织中神经元型一氧化氮合酶(nNOS)和依赖型一氧化氮合酶(iNOS)的蛋白含量。结果各剂量染铅组皮层、海马组织中iNOS表达与对照组相比,明显升高(P均<0.05),并有良好的剂量-反应关系(r=-0.727,P<0.05)。各剂量染毒组海马nNOS表达明显升高(P均<0.05),并有良好的线性关系(r=0.847,P<0.05),皮层组织nNOS表达无明显变化(P均>0.05)。结论铅所引起的神经细胞毒性可能通过铅诱导NOS的高表达,使得NO生成过多进而造成神经损害。     

2型糖尿病小型猪勃起功能障碍及NOS变化

目的观察一氧化氮合酶(NOS)在糖尿病性勃起功能障碍中的作用。方法采用高脂高糖饮食喂养的方法建立广西巴马小型猪糖尿病性阴茎勃起功能障碍模型(DMED),对正常对照组(CD)和高脂高糖组(HFSD)动物于造模第12月后进行阿朴吗啡阴茎勃起实验,用酶联免疫吸附试验(ELISA)检测阴茎海绵体组织中NOS活性。结果 HFSD组动物空腹血糖和血清总胆固醇明显升高(P0.01),HFSD组动物阴茎勃起率较正常组明显降低(P0.01),NOS活性亦显著降低(P0.05)。结论糖尿病严重影响小型猪勃起功能,阴茎海绵体组织NOS活性的降低可能是其机理之一。     

氟对大鼠脑组织中一氧化氮合成酶活性的影响

本文利用化学发光分析技术测定大鼠脑组织中的一氧化氮合成酶的活性，研究氟对神经系统的作用机理。结果表明，无论在体内还是在体外，氟能使一氧化氮合成酶的活性增高，而且这种增强作用能被一氧化氮合成酶的抑制剂L－硝基精氨酸所阻断。     

电焊作业对工人血清一氧化氮合酶活力的影响

目的探讨电焊作业对工人血清中一氧化氮合酶(NOS)活力的影响,进一步了解电焊作业对工人健康损害的机制,为保护电焊作业工人身体健康提供理论依据。方法以某金属结构厂54名电焊作业工人为接触组,不接触毒物的59名非电焊工人为对照组,采用NOS催化L-Arg法测定血清中NOS活力;血锰含量测定采用石墨炉原子吸收法,血中铜、铁、锌、镁、钙含量测定采用火焰原子吸收法。结果接触组工人血清中总NOS活力为(27.88±7.49)U/ml,低于对照组(30.48±4.69)U/ml,差异有显著性(P<0.05),且接触组工人血清中诱导型NOS(iNOS)活力为(16.18±6.70)U/ml,亦低于对照组(19.71±4.26)U/ml,差异有显著性(P<0.05);血锰接触组为(42.73±21.63)μg/L,明显高于对照组(29.97±17.62)μg/L,差异有显著性(P<0.01);血锌接触组和对照组分别为(9.02±3.47)mg/L和(12.72±3.89)mg/L,两组间差异有显著性(P<0.05);接触组和对照组血镁分别为(47.99±9.86)mg/L和(35.82±15.08)mg/L,两组间差异有显著性(P<0.05);两组间血铜、血铁和血钙含量比较,差异均无显著性(P>0.05)。结论电焊作业可能导致工人血锰含量增加,而引起血清NOS活力降低;同时还可使血锌含量下降和血镁含量升高。     

一氧化氮在急性肝衰竭中的作用

为探讨ＮＯ在急性肝衰竭中的作用，采用Ｄ－ＧａｌＮ（８００ｍｇ／ｋｇ）和ＬＰＳ（８μｇ／鼠）腹腔注射复制大鼠急性肝衰竭模型，用氨胍（ＡＧ，１００ｍｇ·ｋｇ－１·ｄ－１）和左旋精氨酸（ＬＡ，４００ｍｇ·ｋｇ－１·ｄ－１）皮下注射３ｄ，分别抑制和促进ＮＯ的合成，注射Ｄ－ＧａｌＮ和ＬＰＳ后２４ｈ处死，留血清测定ＮＯ、ＡＬＴ和ＡＳＴ的水平，肝组织测定诱导型ＮＯ合酶（ｉＮＯＳ）的活性并作组织学观察。结果发现急性肝衰竭时ＮＯ和ｉＮＯＳ的水平升高（Ｐ＜００５），与ＡＬＴ和ＡＳＴ的升高相一致（Ｐ＜００５），抑制ｉＮＯＳ的活性或促进ＮＯ的合成，则ＮＯ、ＡＬＴ和ＡＳＴ的水平降低（Ｐ＜００５）或升高（Ｐ＜００５），组织学观察证实了上述结果。说明ＮＯ及ｉＮＯＳ参与急性肝衰竭，抑制ＮＯ的合成对急性肝衰竭有保护作用。     

锰致神经细胞损伤中诱导型一氧化氮合酶及其基因的变化

[目的]观察不同浓度锰对大鼠脑片神经细胞的损伤情况,探讨诱导型一氧化氮合酶(iNOS)在锰诱导神经细胞损伤中的变化. [方法]培养出生后4～7 d大鼠脑片,培养液为50％高糖杜尔伯科改良伊格尔培养基,25％Hank平衡盐溶液,24％热灭活马血清,1％青霉素和链霉素.待第15天脑片神经细胞生长状态最佳时加入0、25、100、400 μmol/L MnC12.培养24h后,测定培养液中乳酸脱氢酶(LDH)活性,脑片细胞悬液中细胞凋亡率、一氧化氮生成量和iNOS活性,mRNA和蛋白表达水平. [结果]不同浓度锰处理脑片24h后,脑组织切片神经细胞发生明显损伤.随着锰处理浓度升高,LDH活性升高,100和400 μmol/L锰处理组是对照组的1.71、2.76倍.细胞凋亡率和一氧化氮生成量升高增加,25、100和400 μmol/L锰处理组分别是对照组的3.31、4.50和6.97倍和1.98、2.79和4.02倍.iNOS活性增强,100和400 μmol/L锰处理组分别是对照组的2.12和2.64倍.iNOS mRNA和蛋白表达水平明显升高,25、100和400 μmol/L锰处理组iNOS mRNA表达水平是对照组的1.27、1.43和1.86倍.100和400 μmol/L锰处理组iNOS蛋白表达水平分别是对照组的4.17和5.50倍. [结论]锰可致大鼠脑片神经细胞一氧化氮生成量和iNOS表达升高,进一步导致细胞凋亡率增加.