Hydroxytyrosol protects against oxidative DNA damage in human breast cells

Over recent years, several studies have related olive oil ingestion to a low incidence of several diseases, including breast cancer. Hydroxytyrosol and tyrosol are two of the major phenols present in virgin olive oils. Despite the fact that they have been linked to cancer prevention, there is no evidence that clarifies their effect in human breast tumor and non-tumor cells. In the present work, we present hydroxytyrosol and tyrosol's effects in human breast cell lines. Our results show that hydroxytyrosol acts as a more efficient free radical scavenger than tyrosol, but both fail to affect cell proliferation rates, cell cycle profile or cell apoptosis in human mammary epithelial cells (MCF10A) or breast cancer cells (MDA-MB-231 and MCF7). We found that hydroxytyrosol decreases the intracellular reactive oxygen species (ROS) level in MCF10A cells but not in MCF7 or MDA-MB-231 cells while very high amounts of tyrosol is needed to decrease the ROS level in MCF10A cells. Interestingly, hydroxytyrosol prevents oxidative DNA damage in the three breast cell lines. Therefore, our data suggest that simple phenol hydroxytyrosol could contribute to a lower incidence of breast cancer in populations that consume virgin olive oil due to its antioxidant activity and its protection against oxidative DNA damage in mammary cells.     

硒对氧化损伤大鼠肝细胞糖代谢关键酶影响

目的 研究硒对氧化损伤大鼠肝细胞糖代谢关键酶表达的影响,并初步探讨其作用机制.方法 采用0.1 mmol/L的H₂O₂建立氧化损伤细胞模型,并施加不同剂量硒干预,通过实时定量PCR技术检测葡萄糖激酶(glu-cok inse,GK)、糖原合成酶(glycogen synthase,GS)和蛋白激酶B(protein kinase B,PKB/Akt)的mRNA表达,并采用蛋白免疫印迹(Western-blot)方法检测Akt的蛋白表达水平.结果 补硒各组GK的mRNA表达量为(9.692~16.588)×10^-6,均高于H₂O₂损伤组(P<0.05);高剂量补硒组GS和Akt的mRNA表达量分别为57.618×10^-6和0.2398×10^-3,均高于H₂O₂损伤组(P<0.05);补硒各组Akt的蛋白表达量为(0.3343~0.4346)×10^-3,均高于H₂O₂损伤组(P<0.05).结论 补硒可以在一定程度上改善氧化损伤对肝细胞糖代谢关键酶GK、GS的影响,其机制可能与上调胰岛素信号传导通路的关键信号分子Akt的表达有关.     

Suppression of oxidative stress by grape seed supplementation in rats

Polyphenol-rich grape seeds have a beneficial effect on human health. The present study was performed to investigate the effects of grape seeds on antioxidant activities in rats. Male Sprague-Dawley rats were randomly divided into a control diet group (C), a high-fat diet group (HF), a 5% grape seed-supplemented control diet group (G), and a 5% grape seed-supplemented high-fat diet group (HG). Dietary supplementation with grape seeds reduced serum concentrations of lipid peroxides compared with those in the C and HF groups. The hepatic level of lipid peroxides decreased significantly in the grape seed groups compared with that in the C and HF groups. Superoxide dismutase activity in the G group increased significantly compared with that in the C group. Catalase activity tended to be higher by feeding grape seeds. The grape seed diet increased glutathione peroxidase activity in the C group. Glutathione-S-transferase activity increased significantly in the G group compared with that in the C group. Hepatic content of total glutathione increased significantly in the HG group but decreased significantly in the HF group. The ratio of reduced glutathione and oxidized glutathione increased by feeding the grape seed diet. Total vitamin A concentration was significantly higher in HG group than in other groups. Liver tocopherol content of the G and HG groups was significantly higher than that of the control groups. These results suggest that dietary supplementation with grape seeds is beneficial for suppressing lipid peroxidation in high fat-fed rats.     

微囊藻毒素-LR致HT17细胞毒性及DNA损伤

目的比较微囊藻毒素-LR(MCLR)对2种人肝癌细胞系HT17和HepG2的细胞毒性差异,研究MCLR对HT17细胞的氧化性DNA损伤作用。方法应用四甲基偶氮噻唑蓝法检测细胞毒性,免疫酶染色法检测细胞内8-羟基脱氧鸟嘌呤核苷(8-OHdG)水平。结果当剂量增加到1μg/ml时,MCLR对HT17细胞产生明显的细胞毒性,细胞存活率随着处理剂量的增加而降低。HT17细胞对MCLR的敏感性高于HepG2细胞。非毒性剂量的MCLR处理HT17细胞引起8-OHdG水平升高,处理剂量与8-OHdG水平之间呈现剂量-反应关系。结论HT17细胞对MCLR的毒性更敏感,可能与HT17细胞表达有机阴离子转运多肽(OATP)1B1有关。非毒性剂量的MCLR引起氧化性DNA损伤提示长期少量接触MCLR可能对人类健康产生潜在的远期危害。     

亚硒酸钠对神经皮质细胞氧化损伤作用

目的研究不同剂量亚硒酸钠对小鼠大脑皮层神经皮质细胞的损伤作用。方法选用24h龄ICR小鼠，培养大脑神经皮质细胞，48h后加入不同浓度的亚硒酸钠（0．004，0．020，0．100，0．500μmol／L），四甲基偶氮噻唑蓝试验检测细胞活性、激光共聚焦显微镜检测线粒体膜电位，慧星试验检测细胞DNA损伤。结果高剂量亚硒酸钠（0．1和0．5umol／L）明显抑制皮质神经细胞生长、降低线粒体膜电位、并严重损伤DNA，且呈现剂量效应关系（P〈0．05）。与对照组比较，低剂量亚硒酸钠（0．004和0．020μmol／L）虽然呈现一定毒性作用，但差异无统计学意义（P〉0．05）。结论高浓度亚硒酸钠可引起细胞损伤，降低细胞活力，其机制可能与细胞线粒体结构和功能改变以及DNA结构榻伤有关．     

Curcumin protects against the oxidative damage induced by the pesticide parathion in the hippocampus of the rat brain

Abstract

One of the main concerns regarding organophosphate pesticides (OP) is their possible toxic effects. Doses that do not produce acute toxicity are capable of altering the structure and biochemistry of different tissues and organs by production of reactive oxygen species (ROS). Curcumin (CUR) is the main substance in Curcuma longa (Zingiberacea) rhizome that has strong antioxidant activity. However, the neuroprotective properties of curcumin against oxidative stress induced by prolonged exposure to parathion (PAR) is not clear.

Objective

The present work evaluated the protective effect of curcumin against the oxidative damage induced in the rat hippocampus by the OP PAR.

Methods

Forty female Wistar rats were distributed in four groups as follows: exposed to PAR by inhalation (PAR group); pre-treated with CUR and then exposed to PAR by inhalation, (CUR + PAR group); exposed to environmental air and treated with CUR in the food (CUR group); and exposed to environmental air (the control group). At the end of the handling process, the concentration of erythrocyte cholinesterase was monitored, as indicator of PAR intoxication and lipoperoxidation, immunohistochemistry for astrocytes, and activated microglia and apoptosis was determined in the hippocampus.

Results

In the present study, we show that the administration of CUR (200 mg/kg body weight) significantly diminished the oxidative damage in the hippocampus of rats exposed to the OP PAR.

Discussion

These data suggest that CUR may be an alternative to prevent neurodegenerative damage after pesticide exposure.     

茶多酚对甲基汞致大鼠大脑皮质神经元氧化损伤的防护作用

目的探讨茶多酚(tea polypheonols,TP)对甲基汞(methylmercury,MeHg)所致大鼠大脑皮质神经元氧化损伤的防护作用及机制。方法进行大鼠大脑皮质神经元原代培养,细胞成熟后给予0.01、0.1、1、2μmol/L MeHg分别处理0.5、1、3、6、12 h,通过测定培养液中乳酸脱氢酶(lactate dehydrogenase,LDH)活力来进行MeHg细胞毒性分析;根据测定结果选择最具代表性的1μmol/L MeHg暴露6 h作为MeHg染毒组。应用同样方法进行TP预处理组选定,向培养液中分别加入终浓度为5、10、20及40μmol/L TP,分别预处理0.5、1、3及6 h后,再加入终浓度为1μmol/L MeHg,继续培养6 h后测定培养液LDH漏出,根据实验结果选定5、10、20μmol/L预处理3 h作为TP预处理剂量及时间;细胞经各剂量TP预处理后,再暴露于1μmol/L MeHg 6 h,测定神经元细胞凋亡率、非蛋白巯基(non-protein sulfhydryl,NPSH)含量、活性氧簇(reactive oxygen species,ROS)水平及Na+-K+-ATPase和Ca2+-ATPase活力。结果与对照组比较,随着染MeHg剂量的升高,培养液中LDH活力逐渐升高,呈现剂量和时间依赖性的效应关系。TP预处理后,LDH活力逐渐降低,在10、20μmol/L TP预处理组显著降低(P0.05或P0.01);1μmol/L MeHg导致神经元凋亡率显著升高,NPSH含量显著降低,ROS水平显著升高,Na+-K+-ATPase和Ca2+-ATPase活力显著降低,差异均有统计学意义(P0.01),TP预处理对上述指标的拮抗作用呈现剂量-效应关系,差异均有统计学意义(P0.05或P0.01)。结论 TP对MeHg所致大鼠大脑皮质神经元氧化损伤具有一定的防护作用。     

抗坏血酸对染砷小鼠肝脏氧化损伤拮抗作用

目的 研究抗坏血酸(VC)对砷中毒小鼠肝脏中丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽(GSH)的影响。方法 用硫代巴比妥酸法测定丙二醛(MDA)含量;用Nitrite-kit法检测SOD活性;用二硫双硝基苯酸(DTNB)比色法测定GSH含量。结果 对照组MDA含量为14.87 nmol/(mg·prot),SOD活力为167.49NU/(mg·prot),GSH含量为51.27 nmol/(mg·prot);20μmol/L染砷组小鼠肝脏中MDS含量明显增高,为18.48nmol/(mg·prot),SOD活力明显下降,为125.97 NU/(mg·prot),GSH含量也显著降低,为34.87 nmol/(mg·prot);而抗坏血酸拮抗组小鼠肝脏中MDS含量与单纯染砷组相比明显下降,为16.24 nmol/(mg·prot),但未达到对照组水平;SOD活力明显增高,为138.94 NU/(mg·prot),但未达到对照组水平,GSH含量显著增高,为50.39 nmol/(mg·prot),与对照组比较差异无统计学意义。结论 抗坏血酸可拮抗砷对小鼠肝脏的氧化损伤。     

线粒体损伤在镉诱导肝细胞凋亡和DNA损伤中的作用

目的探讨活性氧(reactive oxidative species, ROS)介导的线粒体损伤在镉(cadmium, Cd)暴露诱导肝L02细胞凋亡和DNA损伤中的作用。方法以肝L02细胞为研究对象,利用0～90μmol/L的Cd处理细胞24 h,采用噻唑兰法检测Cd暴露对细胞生存率的影响;以0、20和40μmol/L的Cd染毒细胞24 h,分别采用克隆形成实验、流式细胞术、彗星实验、2′,7′-二氯荧光黄双乙酸盐非标记性氧化敏感的荧光探针、线粒体红色荧光探针(Mitotracker Red CMXRos)和10-N-壬基-吖啶橙等荧光探针标记、线粒体膜电位检测试剂盒(JC-1)、ATP测定试剂盒以及Western Blot等方法,检测Cd暴露对细胞克隆形成能力、细胞凋亡、DNA损伤、ROS水平、线粒体形态、线粒体膜电位(mitochondrial membrane potential, MMP/Δψm)、线粒体质量、ATP含量及相关蛋白的影响;利用90μmol/L抗氧化剂维生素C预处理细胞1 h后给予40μmol/L Cd处理细胞24 h,检测ROS水平、Δψm、线粒体质量、ATP...     

姜黄素对甲醛致A549细胞氧化损伤拮抗作用

目的 探讨姜黄素对甲醛致细胞氧化损伤的拮抗效应。方法 采用A549细胞株作为实验材料,实验设对照组、0.1 mmol/L甲醛染毒组,姜黄素组(0.1 mmol/L甲醛+2.5～20.0 mg/L姜黄素),检测A549细胞中一氧化氮合酶(NOS),丙二醛(MDA),超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px)活性。结果 甲醛染毒组A549细胞SOD、NOS和GSH-Px活性分别为(21.79±1.13)、(1.88±0.16)与(27.83±0.2)U/mgprot,与对照组比较,SOD、NOS和GSH-Px活性明显下降(P<0.05),MDA含量[(3.87±0.153.87)nmol/mgprot]明显升高(P<0.05)。与甲醛染毒组比较,各姜黄素组GSH-Px活性上升、MDA含量下降(P<0.05),与对照组比较,40 mg/L姜黄素组GSH-Px活性、MDA含量差异无统计学意义(P>0.05)。结论 姜黄素可提高A549细胞抗氧化酶活性,并存在剂量效应关系。     

精浆生物大分子氧化损伤与精液参数的相关性研究

目的:探讨精浆中生物大分子氧化损伤与精液参数的相关性。方法:收集96名因不孕不育就诊的男性为研究对象,经过培训的调查员使用结构式调查表对就诊男性进行面对面询问调查。手淫法采集精液样本,用计算机辅助精子分析系统进行精液常规分析。采用酶联免疫吸附试验检测精浆中的羰基衍生物(PC)浓度及8-异前列腺素F2α(8-iso-PGF2α)浓度以反映蛋白质氧化损伤及脂质氧化损伤。根据精子浓度、前向运动精子率和畸形精子率是否正常,将研究对象分为正常组和异常组,研究精液常规指标与氧化损伤指标的关系。结果:异常组8-iso-PGF2α水平高于正常组(P0.05),PC水平差异两组间无统计学意义(P0.05)。前向运动精子率及畸形精子率正常组和异常组间8-iso-PGF2α和PC水平差异均无统计学意义。Pearson相关分析显示,8-iso-PGF2α与精子浓度负相关(r=-0.254,P=0.018),与其他精液参数无统计学相关性;PC水平与各精液参数无统计学相关性。多重线性回归分析显示,8-iso-PGF2α水平每增加1ng/ml,精子浓度平均减少7×10~4/ml。结论:精子浓度低可能与脂质氧化损伤有关。     

八氯二丙醚生产工人p53蛋白及氧化损伤检测

目的检测八氯二丙醚生产工人氧化损伤及血清p53蛋白表达情况。方法选择暴露于八氯二丙醚工人21名为研究对象，另选21名非暴露者为对照，进行血清p53蛋白及丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）的测定。结果暴露于八氯二丙醚工人血清p53蛋白水平略高于对照组，但工龄〉8年组血清p53蛋白的水平显著高于工龄〈8年组。差异有统计学意义（P〈0．01）；SOD、GSH—Px酶活性略低于对照组，MDA水平则显示升高（P〈0．01）。结论长期暴露接触于八氯二丙醚作业工人可有p53基因异常的危险性，以及对氧化性应激的易感性。     

Kiwifruit protects against oxidative DNA damage in human cells and in vitro

Antioxidant micronutrients may account for the beneficial effects of fruits on human health. A direct demonstration that consumption of fruit decreases oxidative DNA damage in human cells would support this hypothesis. Kiwifruit was taken as an example of a food with putative antioxidant properties, and its effectiveness at decreasing oxidative DNA damage was assessed in ex vivo as well as in vitro tests. The comet assay (single-cell gel electrophoresis) was used to measure DNA damage in lymphocytes collected during a human supplementation trial with a single 0.5-liter drink of kiwifruit juice (with water as a control). The comet assay was also modified to assess the antioxidant effect of kiwifruit in vitro by measuring the ability of an extract to interfere with oxidative damage to DNA induced by H2O2. Ex vivo, consumption of kiwifruit led to an increased resistance of DNA to oxidative damage induced by H2O2 in isolated lymphocytes, in comparison with lymphocytes collected after a control drink of water. No effect was seen on endogenous DNA damage. In vitro, a simple extract of kiwifruit, buffered to pH 7, was more effective than a solution of vitamin C (of equivalent concentration) at protecting DNA from damage, whereas at the highest concentrations tested, neither kiwi extract nor vitamin C had a protective effect. We have demonstrated significant antioxidant activity of kiwifruit ex vivo and in vitro, not attributable entirely to the vitamin C content of the fruit. Our dual approach is appropriate for testing other fruit and vegetable products for potential antioxidant effects.     

葡萄籽原花青素对镉致肝损伤保护作用的研究

目的 探讨葡萄籽原花青素(GSP)对氯化镉(CdCl2)诱导大鼠肝氧化损伤的保护作用.方法 40只SPF级SD大鼠,雌雄各半,随机分为对照组(腹腔注射生理盐水和灌胃生理盐水)、染镉组(腹腔注射1.5 mg/kg的CdCl2和灌胃生理盐水)、GSP低、中、高剂量干预组(均腹腔注射1.5 mg/kg CdCl2,同时分别灌胃20、40、80 mg/kg GSP),采用硫代巴比妥酸法和单细胞凝胶电泳技术(SCGE)分别检测肝细胞中丙二醛(MDA)的含量和DNA损伤情况.结果 染镉组肝细胞MDA含量和细胞彗尾长、Olive尾矩均明显高于对照组,表明1.5 mg/kg CdCl2可引发大鼠肝脏出现明显的脂质过氧化损伤.GSP抑制染镉大鼠肝细胞MDA的产生,呈明显的剂最-效应关系,GSP低、中、高剂量组MDA清除率分别为12.74％、24.22％、43.65％.GSP低、中、高剂量干预组中肝脏细胞的彗尾长、Olive尾矩均低于染镉组的,表明GSP具有一定抑制DNA损伤和促进DNA修复的生物学作用.结论 GSP对镉致肝组织脂质过氧化和DNA损伤有一定的保护作用.     

污灌玉米有机提取物致小鼠肝肾氧化损伤作用

目的 研究某污灌区玉米中有机污染物对小鼠肝肾组织的氧化损伤作用。方法 采用超声振荡法提取某污灌区农田生产的玉米中的有机污染物,对小鼠进行灌胃染毒2周;测定肝、肾组织的总超氧化物歧化酶(T-SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)。结果 污灌区低、高剂量组肝组织的T-SOD活性分别为(32.44±7.93),(30.92±9.29)U/(mg.prot);肾组织的GSH-PX活性分别为(67.28±27.21),(66.52±15.19)U/(mg.prot),与对照组比较均明显降低(P<0.05或P<0.01)。结论 该污灌区玉米有机提取物中含有致小鼠肝肾组织氧化损伤的有机污染物;对照区玉米中的有机污染物很可能来源于被污染的大气。     

番茄红素对大鼠肺氧化损伤的影响

目的　观察臭氧对大鼠造成的氧化损伤和番茄红素 (LP)对损伤的影响。方法　利用臭氧吸入造成氧化损伤模型 ,以黄嘌呤氧化酶法测定血清和肺匀浆的SOD活性 ,硫代巴比妥显色法测定MDA含量 ,DTNB比色法测定GSH Px活力。结果　各番茄红素给药组的大鼠血清和肺组织的SOD活性、GSH Px活力上升 ,MDA含量降低 ,与模型组相比差异有显著性 (P <0 0 5 )。结论　番茄红素可以保护臭氧造成的大鼠氧化损伤     

多壁碳纳米管致RAW264.7巨噬细胞毒性与氧化损伤研究

目的探讨多壁碳纳米管(MWCNTs)对小鼠巨噬细胞株RAW264.7细胞的体外细胞毒性和氧化损伤作用。方法用DNA钠盐提高MWCNTs的分散度,设4个浓度组(2.5、10、25和100μg/ml)、DNA钠盐溶剂对照组和生理盐水对照组,染毒24h后,用四甲基偶氮唑盐(MTT)方法观察细胞毒性,并根据染毒后细胞的总蛋白(TP)、乳酸脱氢酶(LDH)、一氧化氮(NO)、谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和丙二醛(MDA)的变化情况分析MWCNTs的细胞毒性和氧化损伤作用。结果25μg/ml和100μg/ml浓度组细胞存活率及细胞毒性和氧化损伤指标均有不同程度的改变,呈一定的浓度-反应关系;随着染毒浓度的升高,细胞和其上清液中TP、LDH、NO和MDA含量随之升高,而GSH和SOD含量随之降低,且呈一定的暴露-反应关系;且与细胞发生融解破碎,间隙加大等形态学改变情况相符。结论MWCNTs对体外培养巨噬细胞株RAW264.7细胞具有细胞毒性和氧化损伤作用,且随剂量的增大而增强。     

Vitamin C supplementation decreases oxidative DNA damage in mononuclear blood cells of smokers

Summary. Background: Antioxidants, in particular vitamin C, have been suggested to decrease oxidative DNA damage. Such effects have been shown in mononuclear blood cells in the first few hours after ingestion, whereas studies of longer-term effects in well-nourished humans have been mainly negative. Aim: To investigate the antioxidant effect of vitamin C in terms of oxidative DNA damage measured by the comet assay and DNA repair measured by expression of OGG1 mRNA in blood cells of male smokers given 2 × 250 mg vitamin C daily as plain or slow release tablets combined with plain release vitamin E 2 × 91mg, or placebo for 4 wk. Results: This study showed a difference in DNA protective effects between a slow release and a plain release vitamin C formulation. Ingestion of slow release vitamin C formulation was associated with fewer endonuclease III and formamidopyrimidine DNA glycosylase sensitive sites measured by the comet assay in mononuclear blood cells obtained 4 h and 8 h after a single tablet and 4 wk after two tablets a day. Ingestion of the vitamin formulation with plain release only indicated a damage-reducing effect 4 h after intake of a single tablet, and the effect was more apparent on endonuclease III than formamidopyrimidine DNA glycosylase sites. Overall the slow release tablets of vitamin C formulation had a more pronounced and a sustained protective effect on base damage compared with the plain release tablets. Plasma vitamin E was unaltered in the first 12 h after ingestion of a single tablet, suggesting that the antioxidant effect was mediated by vitamin C. Differences in plasma vitamin C levels at steady state could not explain the difference between the two vitamin C formulations, whereas wider amplitudes of plasma vitamin C were seen after ingestion of plain release formulation compared to slow release formulation. Assessment of OGG1 mRNA levels by RT-PCR did not indicate increased expression of this DNA repair gene after 4 wk of vitamin supplementation. Conclusion: This study suggests that long-term vitamin C supplementation at high dose, i. e. 500 mg together with vitamin E in moderate dose, 182mg, decreases the steady-state level of oxidative DNA damage in mononuclear blood cells of smokers.     

葡萄籽提取物的体外抗脂质过氧化作用

以大鼠肝、脑组织匀浆为材料研究葡萄籽提取物 (GSE)的抗氧化作用。组织匀浆与GSE共浴后 ,比色法测定丙二醛 (MDA)生成量。组织匀浆与GSE共浴后 ,分别以自由基诱导剂CCl4、H2 O2 和铁离子 -抗坏血酸 (Fe2 + VC)激发脂质过氧化作用 ,以MDA产生和还原型谷胱甘肽 (GSH)耗竭作为脂质过氧化作用程度指标。结果表明 ,GSE可明显降低大鼠肝、脑组织自发性MDA的生成 ,减轻CCl4、H2 O2 、Fe2 + VC所致的肝脏脂质过氧化反应 ,减轻肝组织GSH耗竭。提示GSE具有良好的抗脂质过氧化作用。     

亚急性1,2-二氯乙烷染毒致小鼠肝组织氧化损伤的研究

本研究的目的是探讨亚急性1,2-二氯乙烷(1,2-DCE)中毒致肝脏氧化损伤情况,为阐明1,2-DCE中毒性肝损伤的机制提供参考依据。将昆明种小鼠随机分成对照组和不同剂量1,2-DCE染毒组(0.35、0.7、1.2 mg/L),采用静式吸入方式染毒1周;然后,取血和肝组织,分别检测血中总胆红素(TB)和谷胱甘肽(GSH)含量,肝组织中丙二醛(MDA)、GSH含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性。结果中、高剂量染毒组小鼠的血浆中TB含量显著高于对照组小鼠;而中、高剂量染毒组小鼠的肝组织中GSH-Px活性和GSH含量及高剂量组的SOD活性显著低于对照组,高剂量染毒组小鼠的肝组织中MDA含量显著高于对照组。提示亚急性1,2-DCE中毒可引起肝组织的氧化性损伤。