Effects of Selenium and Zinc on Renal Oxidative Stress and Apoptosis Induced by Fluoride in Rats

To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride. Methods Wistar rats were given distilled water containing sodium fluoride (50 mg/L NaF) and were gavaged with different doses of selenium-zinc preparation for six months. Four groups were used and each group had eight animals (four males and four females). Group one, sham-handled control; group two, 50 mg/L NaF; group three, 50 mg/L NaF with a low dose of selenium-zinc preparation (0.1 mg/kg Na2 SeO3 and 14.8 mg/kg ZnSO4·7H2O); and group four, 50 mg/L NaF with a high dose of selenium-zinc preparation (0.2 mg/kg Na2 SeO3 and 29.6 mg/kg ZnSO4·7H2O). The activities of serum glutathione peroxidase (GSH-Px), kidney superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and glutathione (GSH) in the kidney were measured to assess the oxidative stress. Kidney cell apoptosis and cell cycle were detected by flow cytometry. Results NaF at the dose of 50 mg/L increased excretion of fluoride in urine, promoted activity of urineγ-glutamyl transpeptidase (γ-GT), inhibited activity of serum GSH-PX and kidney SOD, reduce kidney GSH content, and increased kidney MDA. NaF at the dose of 50 mg/L also induced rat renal apoptosis, reduced the cell number of G2/M phase in cell cycle, and decreased DNA relative content significantly. Selenium and zinc inhibited effects of NaF on oxidative stress and apoptosis, promoted the cell number of G2/M phase in cell cycle, but failed to increase relative DNA content significantly. Conclusion Sodium fluoride administered at the dose of 50 mg/L for six months induced oxidative stress and apoptosis, and changes the cell cycle in rat renal cells. Selenium and zinc antagonize oxidative stress, apoptosis, and cell cycle changes induced by excess fluoride.     

Homeopathic Thuja 30C ameliorates benzo（a）pyrene- induced DNA damage,stress and viability of perfused lung cells of mice in vitro

OBJECTIVE： To examine if the ultra-highly diluted homeopathic remedy Thuja 30C can ameliorate benzo（a）pyrene （BaP）-induced DNA damage, stress and viability of perfused lung cells of Swiss albino mice in vitro. METHODS： Perfused normal lung cells from mice were cultured in 5% Roswell Park Memorial Institute medium and exposed to BaP, a potent carcinogen, at the half maximal inhibitory concentration dose （2.2 μmol/L） for 24 h. Thereafter, the intoxicated cells were either treated with Thuja 30C （used against tumor or cancer） or its vehicle media, succussed alcohol 30C. Relevant parameters of study involving reactive oxygen species （ROS） accumulation, total glutathione （GSH） content, and generations of heat shock protein （hsp）-90 were measured; the cell viability and other test parameters were measured after treatment with either Thuja 30C or its vehicle media. Circular dichroism spectroscopy was performed to examine if Thuja 30C directly interacted with calf thymus DNA as target. For ascertaining if DNA damaged by BaP could be partially repaired and restituted by the remedy, 4＇,6-diamidino-2-phenylindole staining was performed. RESULTS： Thuja 30C increased cell viability of BaP-intoxicated cells significantly, as compared to drug-untreated or drug-vehicle control. A minimal dose of Thuja 30C significantly inhibited BaP-induced stress level, by down-regulating ROS and hsp-90, and increasing GSH content. Thuja 30C itself had no DNA-damaging effect, and no direct drug-DNA interaction. However, it showed quite striking ability to repair DNA damage caused by BaP. CONCLUSION： Thuja 30C ameliorates BaP-induced toxicity, stress and DNA damage in perfused lung cells of mice and it apparently has no effect on normal lung cells.     

Effect and Mechanism of Epidermal Growth Factor on Proliferation of GL15 Gliomas Cell Line

The effects of epidermal growth factor (EGF) on proliferation of G15 glioma cells and the possible mechanisms were investigated. GFAP and EGFR expression was detected by immunohisto-chemical method. After the cells were treated with EGF at different concentrations, cell count method was used to determine the proliferation of glioma cells, cell cycle and apoptosis were analyzed by flow cytometry (FCM), and laser scan confocal microscope (LSCM) was used to measure the cyto-plasmic free calcium. The results showed that GFAP was diffusedly expressed in GL15 cells and EGFR was over-expressed. EGF at doses of≤1 ng/mL could significantly stimulate cell proliferation, cells in phase G0/G1 decreased, and those in phase S increased. EGF at doses of 10 and 100ng/ml could inhibit the cell proliferation significantly, and the apoptosis ratio in high dose of EGF group was higher than in control group. EGF could significantly induce a quick rise of intracellular free calcium, but the peak value of intracellular free calcium activated by high dose of EGF was higher than by low dose of EGF. It was suggested that EGF had a dual effect on gliomas: low dose of EGF could stimulate the cell proliferation of gliomas, but high dose of EGF could induce the cell apoptosis and inhibit the proliferation of gliomas, which might be contributed to the difference of intracellular free calcium.     

Possible role of DNA polymerase beta in protecting human bronchial epithelial cells against cytotoxicity of hydroquinone

Objective To explore the toxicological mechanism of hydroquinone in human bronchial epithelial cells and to investigate whether DNA polymerase beta is involved in protecting cells from damage caused by hydroquinone. Methods DNA polymerase beta knock-down cell line was established via RNA interference as an experimental group. Normal human bronchial epithelial cells and cells transfected with the empty vector of pEGFP-C1 were used as controls. Cells were treated with different concentrations of hydroquinone(ranged from 10 μmol/L to 120 μmol/L) for 4 hours. MTT assay and Comet assay [single-cell gel electrophoresis(SCGE)] were performed respectively to detect the toxicity of hydroquinone. Results MTT assay showed that DNA polymerase beta knock-down cells treated with different concentrations of hydroquinone had a lower absorbance value at 490 nm than the control cells in a dose-dependant manner. Comet assay revealed that different concentrations of hydroquinone caused more severe DNA damage in DNA polymerase beta knock-down cell line than in control cells and there was no significant difference in the two control groups. Conclusions Hydroquinone has significant toxicity to human bronchial epithelial cells and causes DNA damage. DNA polymerase beta knock-down cell line appears more sensitive to hydroquinone than the control cells. The results suggest that DNA polymerase beta is involved in protecting cells from damage caused by hydroquinone.     

Barrientosiimonas humi ethyl acetate extract exerts cytotoxicity against MCF-7 and MDA-MB-231 cells via induction of apoptosis and cell cycle arrest

Objective:To elucidate the cytotoxic effect of the secondary metabolites of Barrientosiimonas humi(B.humi)onMCF-7and MDA-MB-231 human breast cancer cells and itsunderlying mechanisms of action.Methods:The extract was obtained from the fermentation of B.humi and fractionation of the crude extract was conducted via column chromatography.Cytotoxicity of theB.humi extract was determined by using MTT assay and real-time cellular analysis.Morphological changes,cell cycle profiles,mode of cell death,and caspase expressions of control and treated breast cancer cells were determined.Results:The ethyl acetate extract isolated from B.humi was cytotoxicagainst MCF-7 and MDA-MB-231celllines.Oneof thedichloromethane(DCM)fractions,designatedasDCM-F2,exhibited the strongest activity among all the fractions and thereby was selected for further studies.DCM-F2 had selective cytotoxicity on target cells by inducing apoptosis,particularly in the early stage,and cell cycle arrest.Treated cells caused inhibition of cell cycle progression at 72 h leading to a significant increase(P<0.05)in the G0/G1 population.DCM-F2 treated MDA-MB-231 cells showed caspase-dependent apoptosis,whereas DCM-F2 treated MCF-7 cells showed a caspase-independent apoptosis pathway.Five compounds were successfully isolated from B.humi.Cyclo(Pro-Tyr)was the most cytotoxic and selective compound against MCF-7 cells.Conclusions:B.humi ethyl acetate extract exhibits significant cytotoxicity against MCF-7 and MDA-MB-231 cells via induction of apoptosis and cell cycle arrest.     

Edaravone rescues the lung by inhibiting lipid peroxidation and pro-inflammatory cytokines in a rat model

Acute lung injury/acute respiratory distress syndrome （ALI/ARDS） is a frequent complication in critically ill patients and cause significant mortality.1 Effects of reactive oxygen species （ROS） on alveolar epithelial cells are involved in the pathophysiology of ALI/ARDS.ROS can provoke DNA damage,lipid peroxidation,and activation of various genes coding for proteins involved in inflammation and cell damage.     

6-OHDA induces cycle reentry and apoptosis of PC12 cells through activation of ERK1/2 signaling pathway

This study investigated the effect and mechanism of cell cycle reentry induced by 6-hydrodopamine （6-OHDA） in PC12 cells. By using neural differentiated PC12 cells treated with 6-OHDA, the apoptosis model of dopaminergic neurons was established. Cell viability was measured by MTT. Cell apoptosis and the distribution of cell cycle were assessed by flow cytometry. Western blot was used to detect the activation of extracellular regulator kinasel/2 （ERK1/2） pathway and the phosphorylation of retinoblastoma protein （RB）. Our results showed that after PC12 cells were treated wtih 6-OHDA, the viability of PC12 cells was declined in a concentration-dependent manner. Flow cytornetry revealed that 6-OHDA could increase the apoptosis ratio of PC12 cells in a time-dependent manner. The percentage of ceils in G0/G1 phase of cell cycle was decreased and that in S phase and G2/M phase increased. Simultaneously, ERK1/2 pathway was activated and phosphorylated RB increased. It was concluded that 6-OHDA could induce cell cycle reentry of dopaminergic neurons through the activation of ERK1/2 pathway and RB phosphorylation. The aberrant cell cycle reentry contributes to the apoptosis of dopaminergic neurons.     

Growth inhibition and gene induction in human hepatocellular carcinoma cell exposed to sodium 4-phenylbutanoate

Background Sodium 4-phenylbutanoate （NaPB） can induce cellular differentiation and cell cycle arrest. However, its potential anticancer properties in hepatocellular carcinoma and influence on normal liver cell are still unclear. We observed the effects of NaPB on growth inhibition, including differentiation and phase growth arrest in normal liver cell line L-02 and hepatocellular carcinoma cell line Bel-7402. Furthermore, we investigated its mechanism in Bel-7402. Methods Hepatocellular carcinoma cells Bel-7402 and normal liver cell line L-02 were treated with NaPB at different concentrations. Light microscopy was used to find morphological change in cells. Cell cycle was detected by flow cytometry. Expression of acetylating histone H4 and of histones deacetylase 4 （HDAC4） were determined by Western blot. The expression of P21WAF1/CIP1 and E-cadherin were observed through immunocytochemistry. Results NaPB treatment led to time dependent growth inhibition in hepatocellular carcinoma cells Bel-7402. NaPB treatment caused a significant decline in the fraction of S phase cells and a significant increase in Go/G1 cells. NaPB increased the expression of P21wAFVCIP1 and E-cadherin in Bel-7402 and significantly decreased the level of HDAC4 in Bel-7402. NaPB significantly improved the level of acetylating histone H4. The normal liver cell line L-02 showed no distinct changes under treatment with NaPB. Conclusions NaPB inhibited the growth of hepatocellular carcinoma cells Bel-7402 and induced partial differentiation through enhancing the acetylating histones. In Bel-7402, the expressions of P21WAF1/CIP1 and E-cadherin may be related to level of acetylating histones and inhibition of cellular growth. NaPB showed no significant effect on normal liver cells.     

The effects on cell growth of tea polyphenols acting as a strong anti-peroxidatant and an inhibitor of apoptosis in primary cultured rat skin cells

Studies during the past few years have indicated an inhibitory effect of green tea or tea polyphenols on tumorigenesis in animal and even in human.The purpose of this study was to observe the possible effects of tea polyphenols on skin cell growth and on apoptosis in rat priary cultured keratinocytes and fibroblasts.The release of a cell plasma enzyma enzyme(LDH),lipid peroxidation products (MDA production),and GSH-Px(glutathione peroxidase)into the medium in cultrued cells was determined after treatment with tea polyphenols in a primary culture of skin cells,The percentage of cells in each cell cycle phase and in apoptosis were assayed by flow cytometry(FCM),Tea polyphenols may have a beneficial effect on skin cells at concentrations from 0.05% to 0.1%,showing a dose-dependent decrease in LDH,MDA(malondialdehyde)production,and a significant dose -de -pendent increase in GSH-Px and cell number,These effects were more obvious after exposure for 24h than after 12h,The results indicate that tea polyphenols may stabliize and protect the cell membrane against the release of cell plasma enzyme LDH,and its anti-peroxidation effect is also important for cell growth,FCM analysis revealed that treatment with 0.01% to 0.1% tea polyphenols dereased the percentage of cells in the G1/G0(quiescent)phase from 81.32%to 74.38%,and increased the percentage of cells in S and G2/M phase from 9.87% to 15.26%,and from 6.51% to 10.36%,respectively,Tea polyphenols also increased the value of PI(proliferation index) from 18.17 to 25.62,At the same time it decreased the percentage of apoptosis from 27.10% to 17.97%,which indicates that green tea stimulates cell growth and inhibits the occureeence of apoptosis,Our results indicate that tea polyphenols are effective anti-oxidants and also inhibit apoptosis ,which may improve the proliferative capacity of primary skin cells in vitro.     

Copper ions stimulate the proliferation of hepatic stellate cells via oxygen stress in vitro

This study examined the effect of copper ions on the proliferation of hepatic stellate cells (HSCs) and the role of oxidative stress in this process in order to gain insight into the mechanism of hepatic fibrosis in Wilson’s disease. LX-2 cells, a cell line of human HSCs, were cultured in vitro and treated with different agents including copper sulfate, N-acetyl cysteine (NAC) and buthionine sulfoximine (BSO) for different time. The proliferation of LX-2 cells was measured by non-radioactive cell proliferation assay. Real-time PCR and Western blotting were used to detect the mRNA and protein expression of platelet-derived growth factor receptor β subunit (PDGFβR), ELISA to determine the level of glutathione (GSH) and oxidized glutathione (GSSG), dichlorofluorescein assay to measure the level of reactive oxygen species (ROS), and lipid hydroperoxide assay to quantify the level of lipid peroxide (LPO). The results showed that copper sulfate over a certain concentration range could promote the pro- liferation of LX-2 cells in a time- and dose-dependent manner. The effect was most manifest when LX-2 cells were treated with copper sulfate at a concentration of 100 μmol/L for 24h. Additionally, copper sulfate could dose-dependently increase the levels of ROS and LPO, and decrease the ratio of GSH/GSSG in LX-2 cells. The copper-induced increase in mRNA and protein expression of PDGFβR was significantly inhibited in LX-2 cells pre-treated with NAC, a precursor of GSH, and this phenome- non could be reversed by the intervention of BSO, an inhibitor of NAC. It was concluded that copper ions may directly stimulate the proliferation of HSCs via oxidative stress. Anti-oxidative stress therapies may help suppress the copper-induced activation and proliferation of HSCs.     

氟对人胎肝细胞细胞周期、凋亡及p53表达的影响

目的　研究氟对人胎肝细胞 (L 0 2细胞 )细胞周期、凋亡及p5 3表达的影响。方法　体外培养的人胎肝细胞接触 4 0、 80、 16 0 μg/ml氟化钠 2 4h后 ,MTT法检测L 0 2细胞存活率 ,流式细胞术检测细胞凋亡率和周期构成比 ,Westernblot检测P5 3蛋白的表达水平。结果　高剂量氟染毒组细胞存活率显著低于对照组 (P <0 0 1) ;各染氟组S期细胞数与对照组相比均明显增多 (P <0 0 1) ,中、高剂量氟染毒组细胞凋亡率和p5 3蛋白表达量均显著高于对照组 (P <0 0 1)。结论　氟可使L 0 2细胞S期细胞数增多 ,诱导人胎肝细胞凋亡和 p5 3表达 ,并呈剂量 效应关系。     

氟砷染毒大鼠其子代脾脏氧化性损伤的研究

目的：揭示氟砷共存时对子代健康影响。方法：采用两代一窝繁殖实验 的方法,测定Wistar大鼠暴露于氟砷后其子代脾脏中氟砷的蓄积水平、脂质过氧化水平和抗氧化能力,以及病理组织学检查。结果：随着暴露剂量的增加脾脏中氟、砷含量显著增加,SOD和GSH－Px活性随之降低, 而LPO含量却逐渐增加;停止氟砷暴露8周后,脾脏中氟砷含量显著降低,酶的活性有所恢复,而LPO含量明显减少。结论：氟砷联合染毒可导致大鼠子代脾脏的氧化性损伤。     

二氢杨梅素的体外护肝作用：基于脂噬介导的LO2细胞脂质蓄积及HepG2细胞增殖

目的 基于脂噬途径研究二氢杨梅素（DMY）对LO2细胞脂质蓄积的防治效果及其机制,并探索其对HepG2细胞的增殖抑制。方法 FBS诱导LO2细胞建立脂肪变性模型,研究分别设置对照组：10%FBS-DMEM正常培养;模型组：50%FBS-DMEM;阳性对照组：100 μg/mL DMY+10%FBS-DMEM;处理组（L-DMY组：50 μg/mL DMY+50%FBS-DMEM;M-DMY组：100 μg/mLDMY+50%FBS-DMEM;H-DMY组：200 μg/mL DMY+50%FBS-DMEM）及恢复对照组：先50% FBS-DMEM培养,后10%FBS-DMEM培养。油红O染色测定脂滴累积。试剂盒测定TC、TG、LDL水平和AST、ALT和LDH酶活性。AO染色观察自噬溶酶体数量,透射电镜观察自噬体数量。Western blot检测自噬蛋白LC3表达量。MDC染色观察自噬体形成情况,q-PCR测定LC3、ATG7、AMPK、mTOR、p62和Beclin1的mRNA表达水平。细胞周期阻滞实验分析HepG2细胞周期比例,流式细胞术检测HepG2细胞凋亡情况,细胞DNA断裂实验检测HepG2细胞DNA的完整情况。结果 DMY干预和预处理可抑制LO2细胞的脂质蓄积,并且降低TC、TG、LDL水平和AST、ALT和LDH酶活性,差异具有统计学意义（P<0.05）;DMY可促进LO2细胞的自噬体和自噬溶酶体的形成,并促进自噬蛋白LC3的表达;DMY可减轻高FBS诱导的LO2细胞自噬体形成抑制,并上调LC3（P< 0.01）、ATG7（P<0.01）、Beclin1（P<0.05）和AMPK（P<0.001）的mRNA水平,下调p62（P<0.001）和mTOR（P<0.001）的mRNA水 平。DMY可阻滞HepG2细胞的有丝分裂和细胞增殖（53.90% vs 14.62%; 32.31% vs 70.17%）,诱导HepG2细胞的晚期凋亡（4.74% vs 57.86%）和DNA断裂。结论 DMY通过调节AMPK/mTOR介导的脂噬途径减少LO2细胞的脂质累积,通过阻滞细胞周期和促进凋亡抑制HepG2增殖,发挥体外护肝作用。     

高浓度花生四烯酸诱导小鼠成纤维细胞L929凋亡的研究

目的　探讨花生四烯酸是否能诱导小鼠成纤维细胞L92 9凋亡及其可能机制。方法　用四甲基偶氮唑盐(MTT)法和乳酸脱氢酶 (LDH)释放率测定细胞存活率及损伤程度 ,比色法测定细胞脂质过氧化产物丙二醛 (MDA)含量 ,Hoechst 3 3 2 58染色观察凋亡细胞核形态变化 ,DNA琼脂糖凝胶电泳检测DNA降解情况。结果　L92 9细胞在低浓度花生四烯酸 (40～ 160 μmol·L- 1)作用 2 4h后 ,细胞存活率明显下降 ,LDH释放率和细胞MDA含量显著增加 (P <0 .0 1)。经 160 μmol·L- 1花生四烯酸处理后的L92 9细胞呈现典型的凋亡核固缩表现。琼脂糖凝胶电泳显示DNA凋亡梯带。结论　高浓度花生四烯酸 (80～ 160 μmol·L- 1)能诱导小鼠成纤维细胞L92 9凋亡 ,其中促脂质过氧化作用可能是一个关键因素     

唐古特大黄多糖组分1对小肠上皮细胞辐射损伤的保护作用

目的探讨唐古特大黄多糖组分1（RTP1）对电离辐射所致肠上皮细胞损伤的保护作用。方法采用大鼠空肠上皮细胞（IEC-6细胞株）,共分为5组,正常对照组（normal control,NC）、辐射对照组（irradiation control,IC）以及RTP1低剂量组（10μg/mL）、中剂量组（30μg/mL）和高剂量组（100μg/mL）,以6.0 Gy 60Coγ射线一次性照射损伤细胞,损伤前用RTP1预处理细胞48 h。采用MTT比色法测定细胞活力,流式细胞术检测细胞凋亡情况并对细胞周期进行检测。结果与IC组比较,RTP1可显著提高IEC-6细胞的增殖能力,减少受照射细胞的凋亡和坏死,降低G1期细胞数量,增加S期细胞数量。结论 RTP1对辐射损伤的肠上皮细胞具有一定的保护作用。     

CaN抑制剂对H2O2诱导的大鼠H9c2心肌细胞凋亡的影响

目的：探讨过氧化氢（H₂O₂）诱导的大鼠H9c2心肌细胞凋亡以及钙调神经磷酸酶（CaN）抑制剂他罗利姆（FK506）对细胞的保护作用,为心肌缺血/再灌注所致的心肌损伤及拮抗机制提供实验依据。方法：将大鼠H9c2心肌细胞株体外培养进行实验,实验分为正常对照组（n=6）和H₂O₂各处理组（n=6）。正常对照组采用生理盐水,实验各组分别用50、100、200和400 μmol•L^-1 H₂O₂处理1、 6和24 h后,用罗丹明（Rhodamme-123）荧光探针检测心肌细胞线粒体膜电位(Δψmt)变化,用Annexin-Ⅴ/PI双染流式细胞术检测心肌细胞凋亡率;并采用100 μmol•L^-1 H₂O₂处理6 h建立大鼠心肌细胞凋亡的损伤模型,给予高、低剂量FK506（0.60和0.15 μmol•L^-1）干预,流式细胞术检测心肌细胞凋亡率。结果：①100、200和400 μmol•L^-1 H₂O₂处理组1 h 时线粒体膜电位均较对照组显著升高（P<0.01）, 6和24 h时,200和400 μmol•L^-1组Δψmt值均低于100 μmol•L^-1 组（P<0.05）,且400 μmol•L^-1组低于200 μmol•L^-1组（P<0.05）;②200和400 μmol•L^-1 H₂O₂处理组1　h 时心肌细胞凋亡率和坏死率均较对照组显著增加（P<0.05）,24　h达高峰。③ 高、低剂量FK506干预组与单纯100 μmol•L^-1H₂O₂处理组比较,心肌细胞凋亡率均明显降低（P<0.01）,高、低剂量组比较差异无显著性（P>0.05）。结论：H₂O₂可损伤心肌细胞线粒体,引起线粒体膜电位下降,导致细胞凋亡。CaN抑制剂对H₂O₂诱导的大鼠H9c2心肌细胞凋亡具有保护作用。     

4-羟苯基维胺脂对宫颈癌HeLa细胞系的放射增敏作用

目的探讨4-羟苯基维胺脂(4-HPR)对HeLa细胞生长抑制和凋亡的影响;研究小剂量4-HPR对HeLa细胞的放射增敏效应。方法用四甲基偶氮唑蓝比色法(MTT)观察4-HPR对HeLa细胞的生长抑制情况;电镜观察4-HPR、放疗处理后HeLa细胞超微结构的改变;流式细胞仪检测单用4-HPR、γ-射线以及2者联合使用时HeLa细胞凋亡率和细胞周期变化。结果4-HPR和2 Gy60Co照射单独作用均可引起HeLa细胞超微结构改变,发生早期凋亡,4-HPR低剂量组(1μmol.L-1,2μmol.L-1)、单纯放射组与无药对照组凋亡率比较无统计学差异(P>0.05);4-HPR 4μmol.L-1组与无药对照组有显著性差异(P<0.01)。2 Gy60Co照射和4-HPR(2μmol.L-1,4μmol.L-1)联合使用细胞凋亡率较单纯放射组凋亡率有显著性差异(P<0.05,P<0.01);4-HPR作用后,HeLa细胞周期发生变化,表现为G1期减少,S期增加。结论4-HPR可诱导肿瘤细胞凋亡,小剂量4-HPR可增加HeLa细胞对放疗的敏感性。     

氟、砷及氟砷联合作用对小鼠肝、脑、肾氧化损伤的实验研究

目的　探讨氟、砷及氟砷联合作用对肝、脑、肾损害的机理。方法　用高氟、高砷、高氟高砷饲料分别饲养小鼠 12mo ,分别检测肝、脑、肾的LPO和GSH含量和SOD及GSH Px活性。结果　与对照组比较 ,氟组、砷组及氟砷联合组GSH含量均显著降低 ;各组SOD活力显著降低 ;除脑组织GSH PX降低不明显外 ,其余各组均显著降低。结论　氟、砷及氟砷联合作用均可使小鼠肝、脑、肾LPO增强 ,抗氧化能力降低 ,而且发现氟砷联合拮抗作用并不明显。     

银杏内酯B对H_2O_2诱导PC12细胞氧化损伤的影响

目的 :探讨银杏内酯B(ginkgolideB)对过氧化氢 (Hydrogenperoxide ,H2 O2 )引起PC12细胞氧化损伤的保护作用。方法 :用噻唑兰 (MTT)检测PC12细胞的存活率 ;乳酸脱氢酶法检测PC12细胞损伤 ;用硫代巴比妥酸法测定细胞脂质过氧化物 ;同时检测细胞内抗氧化酶的活性。结果 :PC12细胞在 5 0～ 30 0 μmol LH2 O2 作用 3h后 ,细胞的死亡率及乳酸脱氢酶 (LDH)释放明显增加 ,抗氧化酶如超氧化物歧化酶 (superoxidedismutase ,SOD)、谷胱甘肽过氧化酶 (glutathioneperoxidase ,GSH Px)活性显著降低 ,而脂质过氧化物生成增多。银杏内酯B 10～ 10 0 μmol L能显著降低细胞死亡率、LDH释放及丙二醛 (MDA)的生成 ,且能明显提高抗氧化酶的活性。结论 :银杏内酯B可拮抗H2 O2 引起的PC12细胞损伤 ,其机理可能与银杏内酯B减少脂质过氧化物的生成 ,提高抗氧化酶的活性有关