癌变·畸变·突变
癌變·畸變·突變
암변·기변·돌변
CARCINOGENSES,TERATOGENSIS AND MUTAGENESIS
2015年
3期
202-206
,共5页
康祥锦%丁悦%杨洁%杜红姿%刘见桥%黄天华
康祥錦%丁悅%楊潔%杜紅姿%劉見橋%黃天華
강상금%정열%양길%두홍자%류견교%황천화
乙肝病毒S蛋白%氧化应激%活性氧%脂质过氧化
乙肝病毒S蛋白%氧化應激%活性氧%脂質過氧化
을간병독S단백%양화응격%활성양%지질과양화
hepatitis B virus S protein%oxidative stress%reactive oxygen species%malondialdehyde
目的:乙肝病毒(HBV)可通过血睾屏障将病毒DNA整合到男性生殖细胞的基因组中,诱发多种染色体畸变,而且还能破坏精子线粒体功能,导致精子活力受损,受精率和受精指数下降,但其机制未明。本研究主要考察乙肝病毒S蛋白(HBs)对人精子氧化应激的影响。方法:人精子与不同浓度(0、25、50、100μ g/m L ) H B s共孵育3 h后,用流式细胞术检测精子内活性氧( R O S )的变化情况,应用酶标仪检测精子细胞内丙二醛(MDA)含量和总抗氧化能力(TAC)。结果:人精子与25~100μg/mL HBs共孵育3 h后, R O S阳性精子比率、人精子细胞膜M D A水平显著高于对照组,而T A C 水平显著低于对照组( P<0.05或0.01)。M D A水平以及R O S阳性精子比率的升高与H B s呈剂量依赖关系( r=0.62, r=0.75;P均<0.01)。T A C水平的降低与H B s呈剂量依赖关系( r=-0.89;P<0.01)。结论:HBs可诱导人精子内ROS升高、TAC降低,从而产生氧化应激,使细胞膜脂质过氧化进而影响人精子的功能。
目的:乙肝病毒(HBV)可通過血睪屏障將病毒DNA整閤到男性生殖細胞的基因組中,誘髮多種染色體畸變,而且還能破壞精子線粒體功能,導緻精子活力受損,受精率和受精指數下降,但其機製未明。本研究主要攷察乙肝病毒S蛋白(HBs)對人精子氧化應激的影響。方法:人精子與不同濃度(0、25、50、100μ g/m L ) H B s共孵育3 h後,用流式細胞術檢測精子內活性氧( R O S )的變化情況,應用酶標儀檢測精子細胞內丙二醛(MDA)含量和總抗氧化能力(TAC)。結果:人精子與25~100μg/mL HBs共孵育3 h後, R O S暘性精子比率、人精子細胞膜M D A水平顯著高于對照組,而T A C 水平顯著低于對照組( P<0.05或0.01)。M D A水平以及R O S暘性精子比率的升高與H B s呈劑量依賴關繫( r=0.62, r=0.75;P均<0.01)。T A C水平的降低與H B s呈劑量依賴關繫( r=-0.89;P<0.01)。結論:HBs可誘導人精子內ROS升高、TAC降低,從而產生氧化應激,使細胞膜脂質過氧化進而影響人精子的功能。
목적:을간병독(HBV)가통과혈고병장장병독DNA정합도남성생식세포적기인조중,유발다충염색체기변,이차환능파배정자선립체공능,도치정자활력수손,수정솔화수정지수하강,단기궤제미명。본연구주요고찰을간병독S단백(HBs)대인정자양화응격적영향。방법:인정자여불동농도(0、25、50、100μ g/m L ) H B s공부육3 h후,용류식세포술검측정자내활성양( R O S )적변화정황,응용매표의검측정자세포내병이철(MDA)함량화총항양화능력(TAC)。결과:인정자여25~100μg/mL HBs공부육3 h후, R O S양성정자비솔、인정자세포막M D A수평현저고우대조조,이T A C 수평현저저우대조조( P<0.05혹0.01)。M D A수평이급R O S양성정자비솔적승고여H B s정제량의뢰관계( r=0.62, r=0.75;P균<0.01)。T A C수평적강저여H B s정제량의뢰관계( r=-0.89;P<0.01)。결론:HBs가유도인정자내ROS승고、TAC강저,종이산생양화응격,사세포막지질과양화진이영향인정자적공능。
OBJECTIVE:It has been demonstrated that HBV is able not only to pass through the blood-testis barrier and integrate into sperm genome,leading to increase of the instability of sperm chromosomes,resulting in a various types of chromosomal aberrations,but also to destroy mitochondrial functions and induce loss of mitochondrial membrane potential (MMP),causing low sperm motility and reducing fertilization rate and fertilizing index. However,the exact pathogenic mechanism of such events is largely unknown so far. The purpose of this study is to explore the relationship between hepatitis B virus S protein (HBs) andoxidative stressin human sperm cells.METHODS:After the co-incubation of sperm cells with (0,25,50,100μg/mL) HBs,the reactive oxygen species (ROS) production was assessed by flow cytometric analyses;the total antioxidant capacity (TAC) level and the Aldetect (MDA-specific) lipid peroxidation (LP) level of the human sperm were measured by microplatereader. RESULTS:After incubation with 25μg/mL of HBs for 3 h,the average rates of ROS-positive cells was significantly increased in the test groups as compared to those in the control groups,while TAC level was decreased when compared with the control.Therewas significantly higher level of MDA in the sperm cells exposed to 50μg/mL of HBs for3 h than that in the controls (P<0.05 or 0.01). HBs increased the MDA levels and the numbers of ROS-positive cells in a dose-dependent manner. HBs decreased the TAC levels in sperm cells in a dose-dependent manner. CONCLUSION:HBs exposure could lead toROS generation,lipid peroxidation,TAC reduction,resulting in loss of sperm membrane integrity and causing sperm dysfunctions.