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Lead Acetate Exposure Induced Oxidative Stress And Apoptosis In C2C12 Myoblasts

Posted on:2016-10-14Degree:MasterType:Thesis
Country:ChinaCandidate:Q J WangFull Text:PDF
GTID:2404330482977176Subject:Microbial and Biochemical Pharmacy
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Objective:Lead(Pb)is common environmental and occupational toxic heavy metal.It is toxic to many organs in human and animal,including neurological,reproductive,hematological,immunological,renal,hepatic and circulatory dysfunctions,representing a continuing threat to human health.It has been well documented that lead could be absorbed and accumulated in bone cells.While long-term exposure to lead will causes high lead levels in blood and soft tissues,and damage the muscular tissue.The aim of the present study was to determine whether lead exposure could cause apoptosis and oxidative damage in C2C12 myoblasts and explore the potential molecular mechanisms.Methods:The cell cytotoxicity was determined after treating with different concentrations of lead acetate.The cell viability was determined by the MTT assay.The release of LDH and the concentration of lead were quantified.Then the intracellular ROS and CAT were measured.Finally apoptosis induced by lead was determined,including the detection of DNA fragments,cell cycle,the expression of Bcl-2/Bax and the activity of Caspase 3.Data were expressed as mean ± S.D.and significance was tested using Student’s t-test(*p<0.05;**p<0.01).Results:1.Lead exposure decreased the cell survival,increased LDH release and the concentration of lead in the C2C12 in a dose-dependent.2.Lead exposure significantly increased ROS level and reduced the activity of CAT in the C2C12 showing a dose-dependent manner.3.The cell cycle was blocked at G2/M phase after 24 h exposure to lead.When the exposure time was extended to 48 h,an obvious apoptotic peak was observed in high-dose set with 200 μmol/L,and the expression level of pro-apoptotic protein Bax was up-regulated.In addition,the activity of Caspase-3 was increased.Conclusions:1.Lead acetate can reduce the livability of C2C12 myoblasts and damage the plasma membrane integrity with a dose-dependent manner.2.Lead acetate can injury C2C12 myoblasts by stimulating oxidative stress response,and oxidative stress response initiated by ROS may be the main pathway.3.The cell apoptosis could be induced by lead acetate,and it was possibly triggered by ROS.
Keywords/Search Tags:lead acetate, C2C12 myoblasts, oxidative stress, apoptosis
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