Dichloroacetate- and trichloroacetate-induced modulation of superoxide dismutase,catalase, and glutathione peroxidase activities and glutathione level in the livers of mice after subacute and subchronic exposures

Dichloroacetate (DCA) and trichloroacetate (TCA) were previously found to induce various levels of oxidative stress in the hepatic tissues of mice after subacute and subchronic exposures. The cells are known to have several protective mechanisms against production of oxidative stress by different xenobiotics. To assess the roles of the antioxidant enzymes and glutathione (GSH) in DCA- and TCA-induced oxidative stress, groups of B6C3F1 mice were administered either DCA or TCA at doses of 7.7, 77, 154, and 410 mg kg^?1 day^?1, by gavage for 4 weeks (4-W) and 13 weeks (13-W), and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as GSH were determined in the hepatic tissues. DCA at doses ranging between 7.7–410, and 7.7–77 mg kg^?1 day^?1, given for 4-W and 13-W, respectively, resulted in either suppression or no change in SOD, CAT, and GSH-Px activities, but doses of 154–410 mg DCA kg^?1 day^?1 administered for 13-W were found to result in a significant induction of the three enzyme activities. TCA administration on the other hand, resulted in increases in the SOD and CAT activities, but caused suppression of GSH-Px activity in both the periods. Except for the DCA doses of 77–154 mg kg^?1 day^?1 administered for 13-W that resulted in a significant reduction in the GSH levels, all other DCA as well as TCA treatments produced no changes in GSH. Since these enzymes are involved in the detoxification of the reactive oxygen species (ROS), superoxide anion (SA), and H₂O₂, it is concluded that SA is the main contributor to DCA-induced oxidative stress, while both ROS contribute to that of TCA. The increase in the enzyme activities associated with 154–410 mg DCA kg^1? day^?1 in the 13-W period suggest their role as protective mechanisms contributing to the survival of cells modified in response to those treatments.     

甲醛暴露时间延长加剧小鼠哮喘模型肺氧化损伤并促进IL-17表达

为了探究不同暴露时间甲醛对小鼠哮喘模型肺氧化应激及IL-17表达的影响,用浓度为3.0 mg·m~(-3)的甲醛气体吸入染毒,同时将48只雄性Balb/c小鼠随机分为6组:(1)对照组(生理盐水组);(2)ovalbumin(OVA)致敏组;(3)0.5 h甲醛+OVA组;(4)1h甲醛+OVA组;(5)1.5 h甲醛+OVA组;(6)2 h甲醛+OVA组,以不同时间长度进行甲醛暴露,连续35 d。OVA致敏组、0.5 h甲醛+OVA组、1 h甲醛+OVA组、1.5 h甲醛+OVA组、2 h甲醛+OVA组均在第11、18及25天腹腔注射OVA致敏液(5 mg OVA+175 mg Al(OH)_3+30 mL生理盐水),第29~35天(共计1周)进行1%OVA雾化(30 min·d~(-1)),每日1次,诱发哮喘。第36天进行以下操作:取肺组织测定肺系数并制作肺匀浆,检测肺组织中活性氧自由基(ROS)、丙二醛(MDA)和还原型谷胱甘肽(GSH)的含量,并采用ELISA法检测肺组织中IL-17的水平。同时,采用HE染色法观察小鼠肺部气道的病理学变化。结果显示,在浓度为3.0 mg·m~(-3)的甲醛气体吸入染毒条件下,与对照组相比,1.5 h甲醛+OVA染毒组、2 h甲醛+OVA染毒组ROS、MDA、IL-17含量上升,具有统计学意义(P0.01)。同时,随着暴露时间长度的增加,小鼠肺部气道出现明显病理学变化。综上所述,每天2 h甲醛+OVA染毒能对小鼠肺造成损伤并恶化OVA对小鼠肺的损伤,产生炎症反应,并通过氧化应激反应介导。     

Effects of subchronic exposure to carbofuran on antioxidant defence system and malondialdehyde levels in common carp (Cyprinus carpio L.)

The present study focused on the assessment of oxidative stress induction by pesticides such as carbamates which are widely used as insecticides and nematicides and contaminate aquatic ecosystems on certain biomarkers in liver of common carp (Cyprinus carpio L.). Biomarkers selected for stress monitoring were malondialdehyde (MDA), an index of lipid peroxidation, and antioxidant defence system enzymes, mainly catalase (CAT), glutathione reductase (GR), and glutathione-S-transferase (GST) activities in liver of fish exposed to 0, 10, 50, or 100?µg?L^?1 of carbofuran for 4, 15, or 30 days. Oxidative stress was found in liver of common carp exposed to carbofuran which was manifested by a decrease in CAT and GR activities after 4 and 30 days of exposure. An adaptive response was probably produced since at day 15 no modifications in the CAT activity and increased GR activity were observed. In addition, a decrease in MDA content with the highest concentration of carbofuran used was found after 30 days of exposure. However, no significant changes were found in GST activity showing a varied response. The results concerning oxidative and antioxidant profiles indicate that subchronic exposure to the insecticide carbofuran is capable of inducing oxidative stress in fish.     

Alteration of body total antioxidant capacity and thiol molecules in human chronic exposure to aluminum

The physiological role of aluminum (Al) is not yet known. Exposure to Al may cause many human disorders. The aim of this study was to explore how occupational human exposure to Al might affect the body oxidative stress. The relation between Al toxicity and oxidative stress was studied in blood samples obtained from 45 primary Al production workers, with a minimum work history of three years in the age range of 29–52 years. They were evaluated for oxidative stress biomarkers including thiobarbituric acid reactive substances (TBARS) indicator of lipid peroxidation, ferric reducing ability of plasma (FRAP) indicator of total antioxidant capacity, total thiol molecules and Al level in blood. The results showed that workers have significantly higher blood Al levels and concomitant lower blood FRAP and total thiol molecules in comparison to controls. Smokers had lower total thiol molecules than non-smokers. The subjects who had a previous history of disease had lower FRAP levels. It is concluded that Al induces oxidative stress in primary Al production workers. Supplementation of workers with antioxidants may have beneficial effects.     

GO通过氧化损伤激活秀丽线虫未折叠蛋白反应

以秀丽线虫为受试生物,探讨氧化石墨烯(GO)对秀丽线虫未折叠蛋白应答的激活及其与氧化应激的关系。将L4幼虫暴露于GO中24 h,通过检测活性氧(ROS)水平、乳酸脱氢酶(LDH)、丙二醛(MDA)、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)等指标评估GO对秀丽线虫所致氧化损伤;以hsp-4和hsp-6分别作为秀丽线虫内质网和线粒体未折叠蛋白反应(UPR)的报告基因评价GO对秀丽线虫UPR应答的激活;同时以谷胱甘肽(GSH)作为抗氧化剂探讨GO所致UPR应答与氧化应激的关系。研究结果显示,GO暴露后秀丽线虫体内ROS、LDH和MDA水平升高,抗氧化酶活性上升;内质网和线粒体UPR反应增强,GSH预处理可以降低内质网和线粒体UPR应答。研究表明,GO短期暴露可以诱导秀丽线虫机体氧化应激进而激活UPR应答,抗氧化保护可以降低UPR应答反应。     

三种典型纳米颗粒物造成的人体肺细胞氧化应激和炎症效应(Oxidative Stress and Inflammatory Effect on A549 Cell Line Induced by Three Typical Nano-Particles )

采用体外细胞暴露实验研究了人肺腺癌细胞系(A549)单层细胞暴露于50和500μg·mL-1两种浓度纳米氧化钛、纳米氧化硅、碳纳米管和晶体石英砂等四种颗粒物后产生的氧化应激和炎症反应.用细胞活度、细胞内活性氧总量和细胞上清液中白细胞介素8(IL-8)表达量表征暴露效应.研究结果表明,纳米氧化钛、纳米氧化硅和碳纳米管在体外暴露实验过程中均发生不同程度的聚集;细胞暴露48h后,三种纳米颗粒物均使A549细胞活度下降,诱导细胞产生过量活性氧,同时刺激细胞IL-8表达量增高;三种纳米颗粒物中,纳米氧化钛和纳米氧化硅对细胞活度影响较大,碳纳米管诱发的炎症效应较另两种纳米材料强.     

微囊藻毒素对束丝藻细胞生长和抗氧化系统的影响

为从活性氧(ROS)角度探讨微囊藻毒素(MC)导致藻类细胞死亡的机理及揭示藻细胞对MC诱发的氧化胁迫的响应机制,采用50和500μg·L-1的微囊藻毒素LR(MC-LR)处理束丝藻(Aphanizomenon sp. DC01)细胞,测定了细胞生长、细胞内活性氧(ROS)含量及抗氧化系统的变化.结果表明,50μg·L-1的MC-LR处理对藻细胞的生长无显著影响,而500μg·L-1的MC-LR处理可诱导藻细胞死亡.50μg·L-1的MC-LR处理的藻细胞ROS含量在处理第2d显著高于对照;但藻细胞能通过还原型谷胱甘肽(GSH)含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPX)活性改变修复氧化损伤,使ROS水平在处理第3d恢复到对照水平.500μg·L-1的MC-LR处理可显著降低藻细胞GSH含量和SOD与GPX活性,刺激藻细胞生成过量的ROS;ROS在毒素处理4d后突然暴发,过量的ROS引起膜质过氧化,并最终导致藻细胞死亡。     

ROS介导的氧化应激在INH诱导的细胞毒性中的作用及槲皮素的干预

为探讨ROS介导的氧化应激在异烟肼(INH)诱导L-02细胞毒性中的作用及槲皮素的干预作用,建立体外培养INH诱导L-02细胞氧化损伤模型,实验分为对照组(A)、INH组(B)、槲皮素低剂量组(C)及槲皮素高剂量组(D)。采用生化分析法检测L-02细胞培养液中天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)的活性;利用荧光探针检测L-02细胞线粒体内活性氧(ROS)水平;应用比色法检测L-02细胞内丙二醛(MDA)、谷胱甘肽(GSH)的含量以及主要抗氧化物酶的活性。结果表明,与对照组相比,INH能显著增加L-02细胞培养液中AST和ALT的活性、细胞线粒体内ROS水平及细胞内MDA的含量(P0.01),并显著减少L-02细胞内GSH的含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性(P0.01)。与INH组比较,槲皮素低剂量组L-02细胞培养液中AST的活性、线粒体内ROS水平及细胞内MDA的含量明显降低(P0.05),而细胞内SOD的活性明显增加(P0.05);高剂量槲皮素能显著降低L-02细胞培养液中AST和ALT的活性、细胞线粒体内ROS水平及细胞内MDA的含量(P0.01),并能显著增高L-02细胞内GSH的含量和主要抗氧化物酶的活性(P0.01)。与槲皮素低剂量组相比,槲皮素高剂量组的保护效应更明显(P0.05)。可见,ROS介导的氧化应激在INH诱导的L-02细胞毒性中发挥了重要作用,且槲皮素对INH诱导的L-02细胞氧化损伤具有保护作用。     

Fecundity and survival in relation to resistance to oxidative stress in a free-living bird

Major life history traits, such as fecundity and survival, have been consistently demonstrated to covary positively in nature, some individuals having more resources than others to allocate to all aspects of their life history. Yet, little is known about which resources (or state variables) may account for such covariation. Reactive oxygen species (ROS) are natural by-products of metabolism and, when ROS production exceeds antioxidant defenses, organisms are exposed to oxidative stress that can have deleterious effects on their fecundity and survival. Using a wild, long-lived bird, the Alpine Swift (Apus melba), we examined whether individual red cell resistance to oxidative stress covaried with fecundity and survival. We found that males that survived to the next breeding season tended to be more resistant to oxidative stress, and females with higher resistance to oxidative stress laid larger clutches. Furthermore, the eggs of females with low resistance to oxidative stress were less likely to hatch than those of females with high resistance to oxidative stress. By swapping entire clutches at clutch completion, we then demonstrated that hatching failure was related to the production of low-quality eggs by females with low resistance to oxidative stress, rather than to inadequate parental care during incubation. Although male and female resistance to oxidative stress covaried with age, the relationships among oxidative stress, survival, and fecundity occurred independently of chronological age. Overall, our study suggests that oxidative stress may play a significant role in shaping fecundity and survival in the wild. It further suggests that the nature of the covariation between resistance to oxidative stress and life history traits is sex specific, high resistance to oxidative stress covarying primarily with fecundity in females and with survival in males.     

Effects of salinity stress on neurotransmission, energy metabolism, and anti-oxidant biomarkers of Carcinus maenas from two estuaries of the NW Iberian Peninsula

This study investigated the effects of salinity on biomarkers of oxidative stress, energy metabolism, and neurotransmission of Carcinus maenas from an estuary low impacted by pollution and from an estuary under chemical stress in the NW Iberian Peninsula. Crabs were collected in the field and, following an acclimation period, they were exposed for 7 days to five salinity levels ranging from 4 to 45 psu. At the end of the exposure period, stress biomarkers were determined in samples of muscle and digestive gland. The biomarkers assessed in the muscle were the activities of the enzymes cholinesterases (ChE), of which acetylcholinesterase is involved in neurotransmission, and lactate dehydrogenase (LDH) and isocitrate dehydrogenase (IDH) that are involved in energy metabolism. The biomarkers assessed in the digestive gland were (1) the activities of the enzymes glutathione S-transferases (GST), glutathione reductase (GR), and glutathione peroxidase (GPx), involved in phase II biotransformation and the anti-oxidant defence system; (2) the levels of total glutathiones (TG), also belonging to the anti-oxidant system; and (3) the levels of lipid peroxidation as a measure of oxidative damage. The results showed a significant influence of salinity on neurotransmission, energy metabolism, anti-oxidant status, and oxidative damage of C. maenas. For some biomarkers, this influence was dependent on whether the crabs were collected at the low-polluted estuary or at the contaminated estuary. In particular, crabs collected at the low-polluted estuary showed altered neurotransmission and anti-oxidant defences (GR). Crabs collected at the impacted estuary showed alterations in neurotransmission, energy metabolism (IDH and LDH), biotransformation, and anti-oxidant defences (GST, GR, GPx, and TG), as well as in oxidative damage, indicating that salinity change superimposes higher stress on these organisms. For ChE, IDH, and TG, altered responses were induced by both hypo- and hypersalinity.     

原花青素对镉引起的鸡胚睾丸氧化损伤的缓解作用

为探索原花青素对镉引起的鸡胚睾丸氧化损伤的缓解作用,本实验设置了对照组、镉、葡萄籽提取物原花青素(grape seed proanthocyanidin extract,GSPE)和镉+GSPE组,在胚胎期第6.5天(E6.5)注射0.05 mg·kg-1镉或2.5 mg·kg-1GSPE,统计孵化率和睾丸指数,并在E17.5检测睾丸形态、氧化指标、细胞凋亡和内质网应激相关基因的表达情况。结果表明:与对照组相比,镉处理组孵化率和睾丸指数均显著降低;睾丸组织结构出现了细胞核固缩、空泡化和染色质周缘化等变化,过氧化氢和丙二醛水平升高、超氧化物歧化酶活性显著降低、谷胱甘肽含量明显减少,凋亡细胞显著增多;睾丸中抗凋亡基因Bcl-2 mRNA表达水平下降,同时促凋亡基因Caspase3和内质网应激相关基因(XBP-1和HO-1)mRNA表达水平显著上升。然而,GSPE联合处理,明显缓解了镉引起的睾丸损伤,使孵化率和睾丸指数回升,抗氧化水平和内质网应激得到改善,凋亡细胞显著减少,睾丸形态趋于正常。结果表明:GSPE可通过其抗氧化作用降低XBP-1相关的内质网应激基因的表达,从而缓解镉引起的鸡胚睾丸生殖毒性。     

DNA fragmentation,apoptosis and cell cycle arrest induced by sodium arsenite in cultured murine Sertoli cells: prevention by curcumin

Arsenic is a significant environmental concern worldwide, primarily due to geo physiochemical contamination of drinking water, and a major public health hazard in both developing and developed countries. The present study was aimed to investigate ameliorative effects of curcumin (Cur) against sodium arsenite (SA)-induced toxicity in cultured murine Sertoli cells. The cells were treated with SA (5 μM) and Cur (5 μg/ml and 10 μg/ml) alone or in combination for 12 hr. The SA treatment decreased cell viability, produced oxidative stress, and induced apoptosis as reflected by reactive oxygen species (ROS) generation, loss of mitochondrial transmembrane potential, DNA fragmentation, and apoptotic cells. Moreover, the SA-induced cell cycle arrest in the cells is characterized by a rise in the number of cells in the sub G1 phase of the cell cycle. The Cur was found to be effective in reversing all these arsenic (As)-induced cellular events. Data suggest that Cur modulates As-mediated oxidative stress, apoptosis, DNA fragmentation, and cell cycle arrest through suppression of excessive ROS generation. Evidence indicates that Cur may emerge as a useful protective agent against As-induced Sertoli cells toxicity by inhibiting As-induced damage in testes.     

铅与纳米SiO2联合染毒对A549细胞氧化损伤的影响

为了研究铅与纳米SiO2联合染毒所致的细胞损伤特征,并从氧化应激方面探讨其可能的作用机制。用铅和SiO2处理A549细胞,采用四唑盐(MTT)比色法检测细胞存活率,评价铅和SiO2联合染毒所致的细胞损伤特征;采用硫代巴比妥酸(TBA)比色法检测细胞内丙二醛(MDA)含量,评价铅与SiO2联合染毒所致细胞的氧化应激状态;检测了细胞内抗氧化物还原型谷胱甘肽(GSH)含量以及细胞内抗氧化酶的活性,以评价铅与SiO2联合染毒对细胞抗氧化系统的影响。将实验数据进行ANOVA分析。结果表明,铅、SiO2单独染毒组各指标没有明显改变;而联合染毒能造成细胞氧化损伤,表现为细胞存活率、GSH水平、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性显著低于对照组及2个单独染毒组(P<0.05),细胞内MDA含量显著高于对照组及各单独染毒组(P<0.05)。可见,联合染毒可引起明显的细胞毒性,氧化损伤可能是铅与SiO联合染毒致肺细胞毒性损伤的作用机制之一。     

运动对2,3,7,8-四氯二苯并二噁英持续暴露大鼠肝脏氧化应激的影响

为探索运动对2,3,7,8-四氯二苯并二噁英(2,3,7,8-TCDD)持续暴露大鼠肝脏氧化应激的影响,本研究将7周龄雄性SD大鼠适应性喂养1周后,随机分为对照(NC)、运动对照(EC)、染毒1(NT1)、运动染毒1(ET1)、染毒2(NT2)、运动染毒2(ET2)、染毒3(NT3)、运动染毒3(ET3)、染毒4(NT4)及运动染毒4(ET4)共10组。染毒组(NTs、ETs)腹腔注射TCDD(溶于玉米油),对照组及各染毒组首次剂量依次为0、0.4、1.6、6.4、25.6μg·kg~(-1)(以单位体重计),之后每周给予上述剂量的21%作为维持剂量,持续染毒8周;运动组尾部负重5%游泳,每周5 d,每次30 min。实验结束取材,测定血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、肝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)活性及丙二醛(MDA)、活性氧(ROS)含量。结果显示:1)染毒可升高各染毒组大鼠血清AST活性及NT4组大鼠血清ALT活性,增加NT2、NT3组肝脏MDA含量,而降低NT1、NT2组大鼠血清ALT活性;2)运动可升高大鼠血清AST及ALT活性,增加大鼠肝组织GSH-Px活性;3)运动可升高染毒大鼠血清AST活性(T1剂量),降低染毒大鼠血清ALT活性(T1剂量),降低染毒大鼠血清AST活性(T3剂量),升高染毒大鼠血清ALT活性(T3、T4剂量),增加染毒大鼠肝组织SOD活性(T2、T3剂量)、CAT活性(T1、T2、T3剂量)及GSH-Px活性(T2、T3、T4剂量),降低染毒大鼠肝组织MDA含量(T2、T3、T4剂量)及ROS含量(T1、T3剂量)。结果表明,2,3,7,8-TCDD持续暴露8周可引起大鼠肝细胞氧化应激损伤,并产生剂量依赖效应;而有氧运动可增加2,3,7,8-TCDD持续暴露(T2、T3剂量)大鼠肝组织抗氧化酶活性,有效降低氧化应激损伤而减轻肝毒性。     

Effect of Zinc Oxide nanoparticles on cellular oxidative stress and antioxidant defense mechanisms in mouse liver

Zinc oxide nanoparticles (ZnO₂), a common ingredient of cosmetics has a huge variety of applications. Previous studies reported oxidative stress mediated toxicity of ZnO₂ nanoparticles on various mammalian cell lines. Although zinc (Zn) is an essential mineral at higher concentrations this metal is toxic. The present study focused on size determination by monitoring changes in activities of antioxidant defense mechanism in response to oxidative stress induced by ZnO₂ nanoparticles using mouse liver tissue homogenates. The study also investigated effects of oxidative stress induced DNA damage by determining formation of 8-OHdG in mouse liver homogenate. A cytotoxicity assay was also carried out in L929 cells to determine cell viability. The results of the study indicated that 50μg/ml of ZnO₂ nanoparticles induced 50% cell death. Alterations in antioxidant parameters and 8-OHdG were also noted. Data showed that there was a concentration-dependent fall in cell viability, decrease antioxidant enzyme levels and increase formation of DNA adduct (8-OHdG) when mouse liver tissue homogenate were exposed to ZnO₂ nanoparticles.     

Oxidative stress-mediated cardiac mast cell degranulation

Pulmonary mast cell degranulation is a well-characterized response to diesel exhaust exposure. A primary constituent of fossil fuel combustion is sulfur dioxide (SO₂). SO₂ was shown to induce mast cell degranulation in an immortalized cell line secondary to induction of intracellular oxidative stress; however, it is not known whether SO₂-induced oxidative stress directly triggers the activation of cardiac mast cells. Accordingly, this study sought to determine whether Na₂SO₃ induces degranulation of cardiac mast cells, and furthermore whether cardiac mast cell activation may be prevented by inhibition of oxidative stress. To this end, cardiac mast cells were isolated from epicardial surface of the heart and incubated with increasing concentrations of Na₂SO₃ (0, 0.5, or 5 mM). Antioxidant compounds targeting different mechanisms of free radical generation, including ebselen, diphenyleneiodonium (DPI), or α-tocopherol, were incubated with 5 mM of Na₂SO₃ in order to determine their efficacy in preventing mast cell degranulation. Na₂SO₃ induced a significant concentration-dependent histamine release from cardiac mast cells ranging from 8.87% to 18.86%, which was prevented by ebselen. No effect was observed with DPI and α-tocopherol under these conditions. In conclusion, these findings indicate that SO₂ is capable of producing cardiac mast cell degranulation in vitro; however, the variable effectiveness of the three antioxidants evaluated is indicative of a multifactorial mechanism mediating SO₂-induced cardiac mast cell degranulation. The particular effectiveness of ebselen in preventing mast cell degranulation may be related to its multiple mechanisms of preventing oxidative stress.     

真菌毒素引起的氧化应激及其毒理学意义

真菌毒素是一类由真菌产生的次生代谢产物,由于其在自然界污染的普遍性和广泛的毒性作用,被给予了充分关注。从机理上入手来研究真菌毒素毒性作用的起因具有重要意义。真菌毒素根据结构分类可达400种之多,它们的机理也各有不同,但是越来越多的研究表明真菌毒素与氧化应激有重大关联。真菌毒素引起的氧化应激能引起细胞毒性作用,还参与了其他靶点的毒性反应。同时真菌毒素能干扰细胞抗氧化系统的功能,降低细胞对毒素的抵抗能力。本文主要综述了真菌毒素中与氧化应激有密切联系的几种毒素的毒性作用,重点阐述了其与氧化应激之间的关系,以期对真菌毒素的毒性机理有更进一步的认识。     

Cardioprotective effects of Commiphora mukul against isoprenaline-induced cardiotoxicity: a biochemical and histopathological evaluation

Commiphora mukul commonly known as Guggul is one of the oldest and commonly consumed herb for promoting heart and vascular health. Present study was undertaken to evaluate cardioprotective potential of Commiphora mukul against isoprenaline-induced myocardial necrosis in rats. Wistar albino rats were divided into three main groups: sham (saline only), isoprenaline control (saline and isoprenaline) and Commiphora mukul treated (Commiphora mukul and isoprenaline) groups. Commiphora mukul was administered in three doses 100, 200 and 400 mg kg(-1) p.o. for 30 days. On 29th and 30th day, the animals of isoprenaline control and Commiphora mukulpretreatment groups were administered isoprenaline (85 mg kg(-1); s.c.), consecutively at an interval of 24 hr. Isoprenaline administration produced a significant (p < 0.05) decrease in myocardial antioxidants; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx), reduced glutathione (GSH), and myocyte injury marker enzymes creatine-phosphokinase-MB (CK-MB) and lactate dehydrogenase (LDH) along with enhanced lipid peroxidation; malondialdehyde (MDA) in heart. Commiphora mukul pretreatment reversed the isoprenaline-induced oxidative changes in rat myocardium by significant (p < 0.05) increase in SOD, CAT, GSHPx, GSH and reduction of MDA. In addition to improving myocardial antioxidant status, Commiphora mukul also prevented the leakage of LDH and CK-MB from heart. Further, histopathological examination showed the reduction of necrosis, edema and inflammation following Commiphora mukul pretreatment. Based on present findings, it is concluded that Commiphora mukul may be a potential preventive and therapeutic agent against the oxidative stress associated ischemic heart disease owing to antioxidant and antiperoxidative activity.     

微囊藻毒素诱导细胞氧化胁迫的研究进展(Progress in Oxidative Stress on Cell Induced by Microcystin)

微囊藻毒素对生物机体具有强烈的毒性.近几年的研究表明,微囊藻毒素能够诱导细胞产生氧化胁迫,这可能是微囊藻毒素的致毒机理的一个重要方面.在总结国内外相关研究基础上,论文从微囊藻毒素诱导细胞氧化损伤以及影响其抗氧化防御系统两个方面综述了微囊藻毒素诱导细胞氧化应激的研究进展.