慢性铝暴露对大鼠精子质量的影响
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摘要
目的探讨慢性铝暴露对大鼠精子质量的影响及其与睾丸组织超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量的关系。方法取体重为180～200g雄性Wistar大鼠96只,根据饮水中AlCl_3的半数致死量(LD50),采用AlCl_3水溶液饮水暴露法使大鼠染铝,设置高剂量组[1/5LD50,256.72 mg/(kg·d)]、中剂量组[1/10LD50,128.36 mg/(kg·d)]、低剂量组[1/20LD50,64.18mg/(kg·d)]及对照组[0mg/(kg·d)],每组随机分配24只,大鼠连续16周饮水染铝。饲养结束,对大鼠附睾精子进行精子质量检测,并检测睾丸组织的SOD活性及MDA含量。结果与对照组比较,低、中、高剂量组的前向精子百分比均偏低,死精子百分比、形态异常精子百分比偏高,差异均有统计学意义(P<0.01)。低、中、高剂量组的睾丸组织SOD活性低于对照组,而MDA含量高于对照组,差异均有统计学意义(P<0.01)。Spearman相关分析显示前向运动精子百分比与铝染毒剂量、睾丸组织MDA含量呈负相关(P<0.01),与睾丸组织SOD活性呈正相关(P<0.001);死精子及形态异常精子百分比与铝染毒剂量、睾丸组织MDA含量呈正相关(P<0.001),与睾丸组织SOD活性呈负相关(P<0.001)。结论铝会降低精子质量,脂质过氧化可能是其作用机制之一。
Objective To explore the effects of chronic aluminum exposure on sperm quality in rats and its relationship with superoxide dismutase(SOD)activity and malondialdehyde(MDA)content in testis tissues.Methods Ninety-six male Wistar rats weighing 180～200 g were randomly divided into 4 groups.According to the median lethal dose(LD50)of AlCl_3 in drinking water,the rats were exposed to aluminum by drinking of AlCl_3 aqueous solution.All the rats were assigned to a high-dose group[1/5 LD50,256.72 mg/(kg·d)],the medium-dose group[1/10 LD50,128.36 mg/(kg·d)],the low-dose group[1/20 LD50,64.18 mg/(kg·d)]and the control group[0 mg/(kg·d)].Each group was randomly assigned 24 mice and the rats were fed for aluminum exposure for 16 weeks.At the end of feeding,the sperm quality of the rat epididymis sperm was tested,and the SOD activity and MDA content of the testicular tissue were examined.Results Compared with the control group,the percentage of progressive sperm in the low,middle and high dose groups was lower,and the percentages of dead sperm and abnormal sperm were higher,the differences were statistically significant(P<0.01).The SOD activity of testicular tissue in the low,medium and high dose groups was lower than that in the control group,while the MDA content was higher than that of the control group,and the differences were statistically significant(P<0.01).Spearman correlation analysis showed that the percentage of progressive sperm was negatively correlated with the dose of aluminum and the content of MDA in testicular tissue(P<0.01),and positively correlated with the activity of SOD in testicular tissue(P<0.001).The percentage of dead sperm and abnormal sperm was positively correlated with aluminum exposure dose and MDA content in testicular tissues(P<0.001),and negatively correlated with SOD activity in testicular tissue(P<0.001).Conclusion Aluminum can reduce sperm quality,and lipid peroxidation may be one of its mechanisms.
Objective To explore the effects of chronic aluminum exposure on sperm quality in rats and its relationship with superoxide dismutase(SOD)activity and malondialdehyde(MDA)content in testis tissues.Methods Ninety-six male Wistar rats weighing 180～200 g were randomly divided into 4 groups.According to the median lethal dose(LD50)of AlCl_3 in drinking water,the rats were exposed to aluminum by drinking of AlCl_3 aqueous solution.All the rats were assigned to a high-dose group[1/5 LD50,256.72 mg/(kg·d)],the medium-dose group[1/10 LD50,128.36 mg/(kg·d)],the low-dose group[1/20 LD50,64.18 mg/(kg·d)]and the control group[0 mg/(kg·d)].Each group was randomly assigned 24 mice and the rats were fed for aluminum exposure for 16 weeks.At the end of feeding,the sperm quality of the rat epididymis sperm was tested,and the SOD activity and MDA content of the testicular tissue were examined.Results Compared with the control group,the percentage of progressive sperm in the low,middle and high dose groups was lower,and the percentages of dead sperm and abnormal sperm were higher,the differences were statistically significant(P<0.01).The SOD activity of testicular tissue in the low,medium and high dose groups was lower than that in the control group,while the MDA content was higher than that of the control group,and the differences were statistically significant(P<0.01).Spearman correlation analysis showed that the percentage of progressive sperm was negatively correlated with the dose of aluminum and the content of MDA in testicular tissue(P<0.01),and positively correlated with the activity of SOD in testicular tissue(P<0.001).The percentage of dead sperm and abnormal sperm was positively correlated with aluminum exposure dose and MDA content in testicular tissues(P<0.001),and negatively correlated with SOD activity in testicular tissue(P<0.001).Conclusion Aluminum can reduce sperm quality,and lipid peroxidation may be one of its mechanisms.
引文
[1]李海,吴琪俊.铝暴露的神经毒性及其作用机制的研究进展[J].右江民族医学院学报,2016,38(6):616-618.
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[3]Klein JP,Mold M,Mery L,et al.Aluminum content of human semen:implications for semen quality[J].Reproductive Toxicology(Elmsford,N.Y.),2014,50:43-48.
[4]兰贵斌,李皇,黄承乐,等.广西某企业铝暴露工人精子线粒体PARL蛋白水平与精子活力、存活率及畸形率的相关性[J].国际检验医学杂志,2018,39(5):606-609.
[5]孙浩.亚慢性染铝对雄性大鼠生殖毒性的研究[D].哈尔滨:东北农业大学,2011.
[6]Perrard M-H,Sereni N,Schluth-Bolard C,et al.Complete Human and Rat Ex Vivo Spermatogenesis from Fresh or Frozen Testicular Tissue[J].Biology of Reproduction,2016,95(4):89-89.
[7]World Health Organization,Department of Reproductive Health and Reserch.WHO laboratory manual for the examination and processing of human semen[M].Fifth edition.Geneva:World Health Organization,2010.
[8]Vecoli C,Montano L,Andreassi MG.Environmental pollutants:genetic damage and epigenetic changes in male germ cells[J].Environmental Science and Pollution Research,2016,23(23):23339-23348.
[9]Barabasz W,Albinska D,Jaskowska M,et al.Ecotoxicology of aluminium[J].Polish Journal of Environmental Studies,2002,11(3):199-204.
[10]F9rstner U,Wittmann GTW.Metal pollution in the aquatic environment[M].Berin:Springer,1983.
[11]Martinez CS,Escobar AG,Uranga-Ocio J A,et al.Aluminum Exposure for 60days at Human Dietary Levels Impairs Spermatogenesis and Sperm Quality in Rats[J].Reproductive Toxicology,2017,73:128-141.
[12]Ford WCL.Regulation of sperm function by reactive oxygen species[J].Human Reproduction Update,2004,10(5):387-399.
[13]Baumber J,Sabeur K,Vo A,et al.Reactive oxygen species promote tyrosine phosphorylation and capacitation in equine spermatozoa[J].Theriogenology,2003,60(7):1239-1247.
[14]Sabeti P,Pourmasumi S,Rahiminia T,et al.Etiologies of sperm oxidative stress[J].International Journal of Reproductive Biomedicine,2016,14(4):231-240.
[15]Zorov DB,Juhaszova M,Sollott SJ.Mitochondrial reactive oxygen species(ROS)and ROS-induced ROS release[J].Physiological Reviews,2014,94(3):909-950.
[16]Koksal IT,Usta M,Orhan I,et al.Potential role of reactive oxygen species on testicular pathology associated with infertility[J].Asian Journal of Andrology,2003,5(2):95-99.
[17]张红,陈富裕.正常人和不育者精子膜脂类过氧化反应和精子存活率的关系[J].中华泌尿外科杂志,1997,18(6):368-370.
[2]Colomina MT,Peris-Sampedro F.Aluminum and Alzheimer's Disease[J].Advances in Neurobiology,2017,18:183-197.
[3]Klein JP,Mold M,Mery L,et al.Aluminum content of human semen:implications for semen quality[J].Reproductive Toxicology(Elmsford,N.Y.),2014,50:43-48.
[4]兰贵斌,李皇,黄承乐,等.广西某企业铝暴露工人精子线粒体PARL蛋白水平与精子活力、存活率及畸形率的相关性[J].国际检验医学杂志,2018,39(5):606-609.
[5]孙浩.亚慢性染铝对雄性大鼠生殖毒性的研究[D].哈尔滨:东北农业大学,2011.
[6]Perrard M-H,Sereni N,Schluth-Bolard C,et al.Complete Human and Rat Ex Vivo Spermatogenesis from Fresh or Frozen Testicular Tissue[J].Biology of Reproduction,2016,95(4):89-89.
[7]World Health Organization,Department of Reproductive Health and Reserch.WHO laboratory manual for the examination and processing of human semen[M].Fifth edition.Geneva:World Health Organization,2010.
[8]Vecoli C,Montano L,Andreassi MG.Environmental pollutants:genetic damage and epigenetic changes in male germ cells[J].Environmental Science and Pollution Research,2016,23(23):23339-23348.
[9]Barabasz W,Albinska D,Jaskowska M,et al.Ecotoxicology of aluminium[J].Polish Journal of Environmental Studies,2002,11(3):199-204.
[10]F9rstner U,Wittmann GTW.Metal pollution in the aquatic environment[M].Berin:Springer,1983.
[11]Martinez CS,Escobar AG,Uranga-Ocio J A,et al.Aluminum Exposure for 60days at Human Dietary Levels Impairs Spermatogenesis and Sperm Quality in Rats[J].Reproductive Toxicology,2017,73:128-141.
[12]Ford WCL.Regulation of sperm function by reactive oxygen species[J].Human Reproduction Update,2004,10(5):387-399.
[13]Baumber J,Sabeur K,Vo A,et al.Reactive oxygen species promote tyrosine phosphorylation and capacitation in equine spermatozoa[J].Theriogenology,2003,60(7):1239-1247.
[14]Sabeti P,Pourmasumi S,Rahiminia T,et al.Etiologies of sperm oxidative stress[J].International Journal of Reproductive Biomedicine,2016,14(4):231-240.
[15]Zorov DB,Juhaszova M,Sollott SJ.Mitochondrial reactive oxygen species(ROS)and ROS-induced ROS release[J].Physiological Reviews,2014,94(3):909-950.
[16]Koksal IT,Usta M,Orhan I,et al.Potential role of reactive oxygen species on testicular pathology associated with infertility[J].Asian Journal of Andrology,2003,5(2):95-99.
[17]张红,陈富裕.正常人和不育者精子膜脂类过氧化反应和精子存活率的关系[J].中华泌尿外科杂志,1997,18(6):368-370.
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