The genotoxic effect of oxcarbazepine on mice blood lymphocytes

This study was conducted to assess the amount of DNA damage caused by Oxcarbazepine (OXC) through single cell gel electrophoresis (SCGE) technique/comet assay. OXC derived from dibenzazepine series is an effective second generation antiepileptic drug (AED) for both children and adults. Side effects like genotoxic effects of AEDs are of prime importance resulting from toxic metabolites, free radicals and reactive oxygen species (ROS). Forty Eight adult male Bagg’s albino mice (BALB/c) were randomly classified into eight groups, each comprising of six animals. Two of these groups were control and six were tested groups. Control groups were injected with 1% tween 80 while tested groups were injected with 10, 20, and 40?mg/kg-day OXC for seven days (acute therapy) and 28 days (subchronic therapy) in peritoneal cavity. Blood samples were collected by cardiac puncture and subjected to comet assay for the analysis of DNA damage. Per sample 100 cells were scored and classified according to comet tail length. The results showed that OXC in acute and long term therapies had significantly higher (p?相似文献   

丙烯酰胺对PC12细胞损伤及机制研究

目的探讨丙烯酰胺（AA）对PC12细胞的细胞毒性及可能机制。方法分别以0、62.5、125、250、500、1 000μmol/L AA为染毒剂量,染毒12 h后,采用MTT比色法检测丙烯酰胺对体外培养PC12细胞的增殖抑制作用,并用碱性单细胞凝胶电泳技术（single cell gel electrophoresis,SCGE）检测PC12细胞DNA的损伤作用、用MDA和T-AOC试剂盒检测细胞MDA和T-AOC改变。结果染毒12 h后,细胞生长受到明显的抑制,且染毒剂量越高,抑制作用越明显（P〈0.01）;单细胞凝胶电泳实验表明,AA对体外培养PC12细胞的DNA有明显的损伤作用,细胞上清液中MDA含量随着染毒量的上升而升高,T-AOC含量随染毒量的上升而降低。结论 AA能够显著抑制PC12细胞活性,损伤细胞DNA,并诱导细胞氧化损伤。     

白藜芦醇对过氧化损伤人牙周膜细胞DNA的保护作用

目的:建立人牙周膜细胞过氧化损伤体外模型,通过单细胞凝胶电泳技术(SCGE)观察白藜芦醇对过氧化损伤人牙周膜细胞DNA的保护作用。方法:采用H2O2建立人牙周膜细胞过氧化损伤模型,将原代培养的人牙周膜细胞分为对照组、损伤组和保护组,采用不同浓度的H2O2及白藜芦醇进行干预,应用SCGE检测细胞DNA损伤变化。结果:随H2O2浓度的增加,人牙周膜细胞DNA的损伤程度加重,尾长、尾部DNA百分含量和尾距均增加(P<0.05);白藜芦醇使H2O2损伤的人牙周膜细胞的尾长、尾部DNA百分含量和尾距均较对照组减少(P<0.05)。结论:白藜芦醇可有效减少过氧化损伤引起的细胞DNA断裂。     

不同剂量X射线对人外周血有核细胞DNA及精子DNA损伤的比较

目的:应用单细胞凝胶电泳技术检测不同剂量X射线对人离体外周血有核细胞DNA及精子DNA的损伤,评估外周血有核细胞及精子在高剂量X射线照射后DNA的损伤程度.方法:采用血常规正常的人外周血和采集精液常规正常的人精液,用能量为6MV的X射线给予0Gy,2Gy,4Gy,6Gy,8Gy,10Gy的剂量照射.照射后1h内进行单细...     

硫酸铟对小鼠成纤维细胞毒性作用的研究

[目的]了解硫酸铟对小鼠成纤维细胞（L929）的细胞毒性、DNA损伤及活性氧含量的影响。[方法]以体外培养的L929细胞为研究对象,采用四氮唑盐比色分析法（MTT法）观察不同染毒浓度（1、2、4、8mmol／L硫酸铟）在不同时间段（2、24、48h）染毒对L929细胞的毒性作用;采用单细胞凝胶电泳技术（SCGE）检测在2h作用下,不同浓度（1、2、4mmol／L硫酸铟）染毒致DNA损伤的情况及活性氧（reactive oxygen species,ROS）含量的变化。[结果]硫酸铟对L929细胞生长具有抑制作用,在各个浓度及时间段内光密度值随染毒浓度增加及染毒时间延长而降低,阴性组与染毒组差异有统计学意义（P〈0．05）。单细胞凝胶电泳结果显示,彗星拖尾率、彗尾DNA％、尾长、Olive尾矩随染毒浓度增加而增加,阴性组与染毒组之间的差异有统计学意义（P〈0．05）,且ROS含量随染毒浓度增加表现递增。[结论]本实验条件下,硫酸铟能够明显抑制L929细胞增殖,存在明显的剂量-效应关系和时间-效应关系,并在短时间内能够引起DNA单链断裂及ROS含量增多。     

Assessment of the protective effects of selected dietary anticarcinogens against DNA damage and cytogenetic effects induced by benzo[a]pyrene in C57BL/6J mice

The protective action in C57BL/6 J mice from orally administered ellagic acid (EA), benzyl isothiocyanate (BITC), an extract of epigallocatechins (Tegreen®) as well as chlorophyllin (CHL) against benzo[a]pyrene (B[a]P)-induced DNA damage and cytogenetic effects was investigated. In pilot experiment the comet assay indicated protective effects for all compounds, while such activity was confined to EA and CH with respect to B[a]P-DNA adducts and micronuclei. EA and CH were chosen for the main study where the levels of DNA adducts in liver after injection of 30 mg B[a]P/kg b.w. did not differ from those found for animals exposed to B[a]P and treated with the protective substances. In leukocytes no significant protective effect of CHL was detected while a 2-fold increase of adduct concentrations was observed after co-administration of EA. In the comet assay CHL or EA caused a 3-fold decrease of SSB, and a 2-fold decrease of FPG sites in comparison to animals treated with B[a]P. CHL or EA showed a significant protective effect against B[a]P-induced MN in polychromatic erythrocytes in bone marrow. In contrast, flow cytometry measurements in peripheral blood indicated the MN frequency after treatment with CHL or EA almost twice as high as that recorded for B[a]P alone.     

Size-dependent cytotoxicity of amorphous silica nanoparticles in human hepatoma HepG2 cells

The purpose of this study is to compare the potential cytotoxicity induced by amorphous silica particles with different sizes. The effects of one fine particle (498 nm) and three nanoparticles (68, 43, and 19 nm) on cultured human hepatoma (HepG2) cells were investigated by detecting morphological changes, cell viability, cytomembrane integrity, DNA damage, cell cycle distribution, and apoptosis after the cells were treated with 100 μg/mL of four silica particles for 24 h. The results indicated that in HepG2 cells, the cytotoxicity generated by silica particles strongly depended on the particle size, and smaller silica particle possessed higher toxic effect. In order to further elucidate the possible mechanisms of cell injuries, intracellular reactive oxygen species (ROS) was measured. Increased ROS level was also observed in a size dependent way. However, the result showed the fine particle did not promote intracellular ROS level significantly, while cell injuries were detected in this treated group. Thus, our data demonstrated that exposure to different sizes of silica particles resulted in a size dependent cytotoxicity in cultured HepG2 cells, and ROS generation should be one possible damage pathway but might not be completely responsible for the toxic effect produced by silica particles.     

r-HuEPO对放射性脑损伤的防护作用

[目的]探讨重组体人红细胞生成素(r-HuEPO)对放射性脑损伤的防护作用.[方法]随机分组动物,每组均予单次14.5Gy全脑照射,不同的组给予不同剂量的r-HuEPO,通过丙二醛(MDA)和单细胞凝胶电泳(SCGE)来观察r-HuEPO的防护作用.[结果]r-HuEPO可减少受照射后大鼠脑组织MDA含量及循环血中淋巴细胞的DNA损伤情况.[结论]在实验观察的时间范围内,高剂量的r-HuEPO对放射性脑损伤具有一定的防护作用.     

不同剂量维生素A摄入对大鼠DNA损伤的影响

目的探讨补充不同剂量维生索A(VA)对DNA氧化及烷化损伤的影响.方法将Wistar大鼠随机分为4组,分别为VA缺乏组,及补充VA11.43,42.86,142.86μgRE(视黄醇当量)/(kg·d)3个剂量组.干预时间为8周.采用单细胞凝胶电泳法(SCGE)分析比较不同组之间淋巴细胞DNA氧化损伤;用高效毛细管电泳法测定尿中O6-甲基鸟嘌呤(O6-Methyl-guanine,O6-MeG)的排出量.结果DNA损伤分析显示VA缺乏组淋巴细胞DNA自发性损伤明显高于VA补充组(P＜0.01).用H2O2诱导淋巴细胞氧化损伤时,42.86μgRE/(kg·d)组的淋巴细胞损伤最轻(P＜0.01).缺乏组大鼠尿中的O6-MeG的排出量随缺乏时间的延长明显升高(P＜0.01).42.86μgRE/(kg·d)组O6-MeG的排出量无明显改变.142.86 μgRE/(kg·d)组至第8周时,O6-MeG的排出量分别为VA缺乏组、11.43和42.86 μgRE/(kg·d)组的1.38倍(P＜0.05)、3.57倍(P＜0.01)和11.75倍(P＜0.01).结论较长时间VA缺乏可导致机体DNA自发性损伤、H2O2诱导的氧化损伤及DNA烷化损伤均明显增加;高剂量142.86 μgRE/(kg·d)VA补充对DNA损伤不但无防护作用,反而增加DNA损伤;适量摄入42.86 μgRE/(kg·d)的VA能有效地增强DNA抗氧化和烷化损伤的能力.     

N-乙酰半胱氨酸对外源性H_2O_2和内源性O_2~-引起的精子DNA损伤的保护作用

目的 :用精子单细胞凝胶电泳 ( SCGE)实验方法检测 N-乙酰半胱氨酸体外条件下对外源性 H2 O2 和内源性 O2 -引起的精子 DNA损伤的保护作用。方法 :精子分别用 0 .5mmol/ L H2 O2 和 5.0 mmol/ Lβ-NADPH处理的同时分别加入不同浓度 ( 0 .1～ 1 mmol/L )的 N-乙酰半胱氨酸 ,用单细胞凝胶电泳 ( SCGE)检测各组精子中慧星细胞百分率并比较各组平均慧星尾长的差异。结果 :精子细胞用 0 .5mmol/ L H2 O2 处理的同时加入不同浓度 ( 0 .1～ 1 mmol/ L)的 N-乙酰半胱氨酸 ,与单纯用 0 .5mmol/ L H2 O2 处理组比较 ,慧星细胞百分率明显减少 ,平均慧尾显著缩短 ;精子细胞用 5.0 mmol/ Lβ-NADPH处理的同时加入不同浓度 ( 0 .1～ 1 mmol/ L)的 N-乙酰半胱氨酸 ,与单纯用 5.0 mmol/ Lβ-NADPH处理组比较 ,平均慧尾长度显著缩短 ,但慧星细胞百分率无显著性差异。结论 :N-乙酰半胱氨酸对 0 .5mmol/ L外源性 H2 O2 引起的精子 DNA损伤有明显保护作用 ,而对 5.0 mmol/ Lβ-NADPH诱导的内源性 O2 - 引起的精子 DNA损伤的保护作用不明显。