癌变·畸变·突变
癌變·畸變·突變
암변·기변·돌변
CARCINOGENSES,TERATOGENSIS AND MUTAGENESIS
2015年
3期
225-229
,共5页
徐新云%秦逍云%谭琴%柯跃斌%袁建辉%吴德生%刘威%杨晨
徐新雲%秦逍雲%譚琴%柯躍斌%袁建輝%吳德生%劉威%楊晨
서신운%진소운%담금%가약빈%원건휘%오덕생%류위%양신
邻苯二甲酸二( 2-乙基己)酯%3β-羟基类固醇脱氢酶%促性腺激素释放激素受体%卵泡刺激素受体%黄体生成素受体%生殖毒性
鄰苯二甲痠二( 2-乙基己)酯%3β-羥基類固醇脫氫酶%促性腺激素釋放激素受體%卵泡刺激素受體%黃體生成素受體%生殖毒性
린분이갑산이( 2-을기기)지%3β-간기류고순탈경매%촉성선격소석방격소수체%란포자격소수체%황체생성소수체%생식독성
di-(2-ethylhexyl) phthalate%β-hydroxysteroid dehydrogenase%gonadotropin-releasing hormone receptor%follicle-stimulating hormone receptor%luteinizing hormone receptor%reproductive toxicity
目的:探讨邻苯二甲酸二(2-乙基己)酯(DEHP)对大鼠睾丸和卵巢组织激素相关蛋白表达水平的影响。方法:将80只5周龄SD大鼠,雌雄各半,随机分为对照组(玉米油)、DEHP低剂量组(100mg/kg)、DEHP中剂量组(500mg/kg)、DEHP高剂量组(1500mg/kg),每组雌雄各10只,每周染毒5d,每天灌胃染毒1次,连续6周。末次染毒24h后处死动物,提取睾丸或卵巢组织蛋白,应用Westernblot分别检测睾丸组织中3β-羟基类固醇脱氢酶(3β-HSD)、促性腺激素释放激素受体(GnRHR)、卵泡刺激素受体(FSHR)及卵巢组织中黄体生成素受体(LHR)和GnRHR的蛋白表达水平。结果:与对照组比较,雄鼠睾丸组织在DEHP500和1500mg/kg剂量时3β-HSD蛋白表达水平均显著升高(P均<0.01);GnRHR蛋白表达水平在1500mg/kg剂量组显著下降(P均<0.01);FSHR蛋白表达水平在500和1500mg/kg组显著下降(P<0.05或P<0.01)。雌鼠卵巢组织在DEHP100mg/kg剂量组时LHR和GnRHR蛋白表达水平与对照组比较差异均无统计学意义(P>0.05),在DEHP500和1500mg/kg剂量组LHR表达水平比对照组下降25%~35%,GnRHR下降60%~80%(P<0.05或P<0.01)。结论:DEHP染毒可引起大鼠睾丸和卵巢组织激素相关蛋白表达水平的改变,干扰大鼠体内性激素的代谢,推测此作用与DEHP的生殖毒性存在密切关系。
目的:探討鄰苯二甲痠二(2-乙基己)酯(DEHP)對大鼠睪汍和卵巢組織激素相關蛋白錶達水平的影響。方法:將80隻5週齡SD大鼠,雌雄各半,隨機分為對照組(玉米油)、DEHP低劑量組(100mg/kg)、DEHP中劑量組(500mg/kg)、DEHP高劑量組(1500mg/kg),每組雌雄各10隻,每週染毒5d,每天灌胃染毒1次,連續6週。末次染毒24h後處死動物,提取睪汍或卵巢組織蛋白,應用Westernblot分彆檢測睪汍組織中3β-羥基類固醇脫氫酶(3β-HSD)、促性腺激素釋放激素受體(GnRHR)、卵泡刺激素受體(FSHR)及卵巢組織中黃體生成素受體(LHR)和GnRHR的蛋白錶達水平。結果:與對照組比較,雄鼠睪汍組織在DEHP500和1500mg/kg劑量時3β-HSD蛋白錶達水平均顯著升高(P均<0.01);GnRHR蛋白錶達水平在1500mg/kg劑量組顯著下降(P均<0.01);FSHR蛋白錶達水平在500和1500mg/kg組顯著下降(P<0.05或P<0.01)。雌鼠卵巢組織在DEHP100mg/kg劑量組時LHR和GnRHR蛋白錶達水平與對照組比較差異均無統計學意義(P>0.05),在DEHP500和1500mg/kg劑量組LHR錶達水平比對照組下降25%~35%,GnRHR下降60%~80%(P<0.05或P<0.01)。結論:DEHP染毒可引起大鼠睪汍和卵巢組織激素相關蛋白錶達水平的改變,榦擾大鼠體內性激素的代謝,推測此作用與DEHP的生殖毒性存在密切關繫。
목적:탐토린분이갑산이(2-을기기)지(DEHP)대대서고환화란소조직격소상관단백표체수평적영향。방법:장80지5주령SD대서,자웅각반,수궤분위대조조(옥미유)、DEHP저제량조(100mg/kg)、DEHP중제량조(500mg/kg)、DEHP고제량조(1500mg/kg),매조자웅각10지,매주염독5d,매천관위염독1차,련속6주。말차염독24h후처사동물,제취고환혹란소조직단백,응용Westernblot분별검측고환조직중3β-간기류고순탈경매(3β-HSD)、촉성선격소석방격소수체(GnRHR)、란포자격소수체(FSHR)급란소조직중황체생성소수체(LHR)화GnRHR적단백표체수평。결과:여대조조비교,웅서고환조직재DEHP500화1500mg/kg제량시3β-HSD단백표체수평균현저승고(P균<0.01);GnRHR단백표체수평재1500mg/kg제량조현저하강(P균<0.01);FSHR단백표체수평재500화1500mg/kg조현저하강(P<0.05혹P<0.01)。자서란소조직재DEHP100mg/kg제량조시LHR화GnRHR단백표체수평여대조조비교차이균무통계학의의(P>0.05),재DEHP500화1500mg/kg제량조LHR표체수평비대조조하강25%~35%,GnRHR하강60%~80%(P<0.05혹P<0.01)。결론:DEHP염독가인기대서고환화란소조직격소상관단백표체수평적개변,간우대서체내성격소적대사,추측차작용여DEHP적생식독성존재밀절관계。
OBJECTIVE:To explore the effects of di-(2-ethylhexyl) phthalate (DEHP) on protein expression of hormonal-related genes including 3β-hydroxysteroid dehydrogenase (3β-HSD),gonadotropin-releasing hormone receptor (GnRHR),follicle-stimulating hormone receptor (FSHR) and luteinizing hormone receptor (LHR) in rats.METHODS: A total of 80 5-week-old male and female Sprague-Dawley rats were randomly divided into four groups with 20 rats in each group. The DEHP doses were 0 mg/kg in control group (corn oil),100 mg/kg in low dose group,500 mg/kg in medium dose group and 1 500 mg/kg in high dose group. Rats were exposed to DEHP via gavage administration for consecutive six weeks,DEHP administration was once a day and five times a week. After the exposure,rats were anesthetized through ether,then sacrificed for the further studies. The protein expressions of 3β-HSD,GnRHR and FSHR in testis and ovary was analyzed by Western blot.RESULTS:Compared with control group,the expression of 3β-HSD protein was significantly increased in DEHP 500 and 1 500 mg/kg groups (P<0.01),GnRHR was decreased in DEHP 1 500 mg/kg group (P<0.01),FSHR was decreased in DEHP 500 and 1 500 mg/kg groups (P<0.05 orP<0.01, respectively). The protein expressions of LHR in DEHP 500 and 1 500 mg/kg groups were decreased by 25% to 35% when compared with control,whilst GnRHR protein expressions were decreased by 60% to 80% in DEHP 500 and 1 500 mg/kg groups ( P<0.05 orP<0.01).CONCLUSION:DEHP could cause endocrine disorder and interfere with the synthesis of sex hormones in rats,ultimately leading to male and female reproductive dysfunction.