苦参总黄酮对醋酸铅所致雄性小鼠生精障碍的影响

目的研究苦参总黄酮(flavonoids from sophora flavescens)对醋酸铅所致雄性小鼠生精障碍的作用及其机制。方法实验分为对照组、染铅组、苦参总黄酮组及人绒毛膜促性腺激素(HCG)组,采用灌胃醋酸铅(40 mg/kg)连续7 d建立雄性小鼠生精障碍模型,苦参总黄酮组灌胃苦参总黄酮600 mg/kg,HCG组腹腔注射HCG 500 IU/kg,连续30 d。观察雄性小鼠的精子密度、精子活力、精子畸形率,睾丸组织匀浆的Mg~(2+)-ATP酶、Ca~(2+)-ATP酶、超氧化物歧化酶(SOD)、山梨醇脱氢酶(SDH)活性及血清中睾酮(T)等指标,并观察睾丸组织的病理改变。结果与对照组比较,染铅组精子密度、精子活力明显降低,精子畸形率增高,睾丸组织中Mg~(2+)-ATP酶、Ca~(2+)-ATP酶、SOD及SDH活性降低、血清中T水平降低(P0.05或P0.01),染铅组睾丸组织苏木素-伊红(HE)染色可见生精上皮明显变薄,生精细胞层次和数量均减少,生精小管腔可见少量精子形成。与染铅组比较,苦参总黄酮组的精子密度、精子活力相应增高,精子畸形率降低,睾丸组织中Mg~(2+)-ATP、Ca~(2+)-ATP、SOD、SDH的活性增高、血清中T水平增高(P0.05或P0.01),HE染色显示苦参总黄酮组与染铅组比较,生精上皮增厚,生精细胞层次和数量明显增多。结论苦参总黄酮对雄性小鼠的醋酸铅所致生精障碍有一定保护作用,作用机制很可能为其通过抗氧化作用,从而影响精子发育相关的激素及能量代谢酶的水平发挥作用。     

苦杏仁苷对醋酸铅所致雄性小鼠生精障碍的影响

目的研究苦杏仁苷(amygdalin)对醋酸铅所致雄性小鼠生精障碍的影响,并探讨其作用机制。方法采用腹腔注射醋酸铅(20 mg/kg)连续7 d建立雄性小鼠生精障碍模型,造模第2天始,苦杏仁苷低、中、高剂量组分别腹腔注射苦杏仁苷(15、30和60 mg/kg),连续42 d。观察雄性小鼠的精子密度、精子畸变率变化,检测血清中睾酮(testosterone,T)的含量及睾丸组织匀浆的乳酸脱氢酶(lactic dehydrogenase,LDH)、山梨醇脱氢酶(sorbitol dehydrogenase,SDH)、Na~+-K~+-ATP酶、Mg~(2+)-ATP酶、超氧化物歧化酶(superoxide dismutase,SOD)、一氧化氮(nitric oxide,NO)、肿瘤坏死因子α(tumor necrosis factorα,TNF-α)水平的变化,并观察睾丸组织的病理改变。结果与模型组比较,苦杏仁苷各剂量组的精子密度增高、精子畸变率降低,苦杏仁苷各剂量组睾丸组织中LDH、SDH、Mg~(2+)-ATP酶的活性增高,苦杏仁苷中、高剂量组睾丸组织中Na~+-K~+-ATP酶、SOD活性增强、NO及TNF-α含量降低、血清中T含量增高,同模型组比较差异有统计学意义(P0.05或P0.01)。模型组睾丸组织生精上皮明显变薄,生精细胞层次和数量减少,多数生精小管腔见少量精子形成,而苦杏仁苷中、高剂量可改善醋酸铅所致的睾丸组织损伤。结论苦杏仁苷对醋酸铅所致小鼠生精障碍的有一定改善作用,机制可能是通过抗氧化、降低NO水平,从而能稳定细胞膜、增强精子生成中能量代谢酶活性及抑制炎症介质。     

锌和维生素A对乙醇致大鼠睾丸损伤的保护作用

目的研究锌和维生素A（VA）对长期摄入乙醇致大鼠睾丸损害的保护作用及可能机制。方法 40只健康雄性成年SD大鼠随机分为对照组、乙醇组、乙醇＋葡萄糖酸锌组、乙醇＋VA组,每组10只,4组每日分别灌胃给予乙醇0、7.5g/kg、乙醇7.5g/kg＋葡萄糖酸锌7.7mg/kg、乙醇7.5g/kg＋VA50μg/kg,连续13周。对4组大鼠的精子计数、精子活动率、精子畸形率、血清睾酮（T）、黄体生成素（LH）、卵泡刺激素（FSH）含量进行检测,光、电镜观察睾丸的形态改变。同时测定睾丸线粒体中丙二醛（MDA）的产生量,免疫组织化学法检测睾丸组织中iNOS的表达。结果与对照组相比,乙醇组大鼠精子计数减少,精子活动率下降,精子畸形率升高（P〈0.05）,血清T、LH、FSH水平明显降低（P〈0.05）;睾丸生精上皮结构破坏,支持细胞和各级生精细胞均有退化变性;睾丸生精细胞iNOS表达明显增强（P〈0.05）;睾丸线粒体丙二醛含量明显升高（P〈0.05）。与乙醇组相比,乙醇＋葡萄糖酸锌组和乙醇＋VA组精子计数、精子活动率有所上升,生精细胞退化变性程度减轻,睾丸生精细胞iNOS表达减弱（P〈0.05）,睾丸线粒体MDA减少,但血清T、LH、FSH水平仍低于对照组（P〈0.05）。结论补充锌和VA可以限制乙醇引起的睾丸过氧化损伤,保护睾丸的生精功能,但仍有生殖内分泌激素合成障碍。     

醋酸铅染毒小鼠睾丸和附睾组织病理学观察

成年小鼠经口给予醋酸铅500、100O、2000(mg·kg)/d连续28天。光镜观察发现:睾丸生精小管萎缩,生精细胞脱落、变性,层次减少、核固缩,随醋酸铅剂量增加,睾丸生精上皮病变加重;附睾管内出现大量精子细胞和精母细胞。电镜观察发现;1000mg/kg组小鼠睾丸精子细胞核变形,核染色质异常聚集;附睾精子轴丝变性浓缩,残余胞质增多,残余胞质内出现多个溶酶体,精子头核染色质成团块状,核液化,顶体破坏。     

苦参总黄酮对热应激导致的小鼠生殖功能障碍的治疗作用及机制

目的 研究苦参总黄酮对阴囊局部热应激引起雄性小鼠睾丸组织损伤的修复作用及机制。方法 使用TCMSP数据库对苦参中黄酮类化合物的靶点进行筛选,对靶点进行生信分析。使用阴囊热应激小鼠模型,使用苦参黄酮进行干预。检测各组小鼠的精子密度、精子畸变率,观察睾丸组织形态改变。q-PCR和Western blotting检测睾丸肿瘤坏死因子α（tumor necrosis factor-α,TNF-α）和白细胞介素17（interleukin 17,IL-17）的mRNA以及蛋白水平。组织匀浆检测Na⁺-K⁺-ATP酶、Mg²⁺-ATP酶、Ca²⁺-ATP酶、乳酸脱氢酶（lactate dehydrogenase,LDH）、山梨醇脱氢酶（sorbitol dehydrogenase,SDH）活性,丙二醛（malondialdehyde,MDA）、NO、TNF-α的水平及血清中睾酮含量。结果 热应激可以导致小鼠精子的密度减少、畸变的精子增加,睾丸生精上皮明显变薄,细胞层次和数量下降,ATP酶、LDH、SDH的活性显著降低,增加睾丸组织MDA、NO的含量及TNF-α和IL-17的表达。使用250,500 mg·kg^-1·d^-1苦参黄酮干预后,精子质量及睾丸组织形态损伤得到改善,血清和睾丸组织中TNF-α和IL-17的水平降低,ATP酶、SDH活性增高,睾酮水平增高。结论 苦参总黄酮的作用机制是通过抑制炎症因子TNF-α和IL-17的水平,提高抗脂质过氧化能力及抑制NO的作用,增强精子发生的能量酶的活性、提高血清睾酮水平,改善热应激导致的生殖障碍。     

铅对睾丸组织还原性谷胱甘肽和脂质过氧化作用的影响

本实验测定了铅染毒小鼠睾丸组织中还原性谷肽甘肽(GSH)和丙二醛(MDA)含量以探讨铅的睾丸毒性作用机理。小鼠连续5天醋酸铅灌胃染毒,剂量依次为250、500、1000mg/kg,在末次     

双酚A对小鼠睾丸组织氧化损伤及生殖细胞凋亡的影响

目的研究双酚A(bisphenolA,BPA)对雄性小鼠睾丸组织氧化损伤及其对生殖细胞凋亡的影响。方法将52只健康成年雄性昆明种小鼠随机分为溶剂对照组(玉米油)和低(75 mg/kg·bw)、中(150 mg/kg·bw)、高(300 mg/kg·bw)剂量组,每组13只,连续经口染毒8周。处死小鼠后,解剖取材,称量睾丸的重量并计算脏器系数;取附睾,制成精子混悬液于镜下观察精子活动率、统计精子畸形率;采用酶标仪检测睾丸组织匀浆中超氧化歧化酶(SOD)、乳酸脱氢酶(LDH)活力及丙二醛(MDA)含量;采用qPCR方法检测凋亡相关基因CytC、Caspase-3及Bcl-2 mRNA表达量。结果各染毒剂量组较对照组睾丸脏器系数升高,精子活力随剂量升高明显降低(P0.05);精子畸形数及精子畸形率均随剂量升高明显升高(P0.05);各染毒剂量组睾丸组织SOD、LDH酶活力及MDA含量均升高,差异有统计学意义(P0.05);各染毒剂量组睾丸组织中CytC及Caspase-3 mRNA表达量较对照组均升高,Bcl-2 mRNA表达量较对照组降低,差异有统计学意义(P0.05)。结论 BPA引起雄性小鼠睾丸组织的氧化损伤及生殖细胞凋亡。     

辛硫磷对大鼠生殖内分泌系统的影响

目的 研究辛硫磷对雄性大鼠生殖内分泌系统的影响.方法 将每日不同剂量辛硫磷(5.9、29.4、147.0) mg/kg分别对雄性成年SD大鼠连续灌胃染毒15 d和30 d,应用RIA法测定血清卵泡刺激素(FSH)、黄体生成素(LH)、睾酮(T)和睾丸匀浆中睾酮(T)的水平,同步测定睾丸标志酶酸性磷酸酶(ACP)、γ-谷氨酰转移酶(γ-GT)的活性,并采用精子头计数法观测每日精子生成量(Spr)的变化.结果 与对照组比较,染毒大鼠15 d时,血清LH水平5.9 mg/kg,各染毒组表现为显著升高(P<0.05);血清FSH的水平随染毒剂量增加而升高,各染毒组均明显高于对照组(P<0.01);血清T水平随染毒剂量的增加呈现为升高的趋势,在147.0 mg/kg剂量组差异有统计学意义(P<0.05).染毒至30 d时,血清中LH水平在147.0 mg/kg剂量组差异有统计学意义(P<0.05);FSH在≤29.4 mg/kg剂量组表现有统计学意义(P<0.05).ACP各染毒组有统计学意义(P<0.01).γ-GT的活性在≥29.4 mg/kg剂量组范围均有明显差异(P<0.01).Spr与染毒剂量有明显的剂量依赖关系,在≥29.4 mg/kg剂量范围Spr显著减少(P<0.01).结论 辛硫磷对雄性大鼠有明显的生殖毒性,可影响其血清及睾丸性激素水平和酶活性,导致精子生成障碍.     

乙体氯氰菊酯对雄性大鼠睾丸的损伤作用

目的　探讨乙体氯氰菊酯 (β CP)对雄性大鼠的睾丸毒性。 方法　成年Wistar雄性大鼠 ,分别以 0、2 0、40和80mg kg剂量的 β CP连续 8周灌胃染毒 ,按常规方法对染毒大鼠进行精子数、精子活动度和精子畸形检测 ,并对睾丸进行组织病理学检查。结果　 80mg kg剂量组大鼠活精率 (60 5 % )及精子活动度 (56 55 % )明显低于对照组 (分别为78 75 %和 72 2 0 % ) ,差异有显著性 (P <0 0 5) ,睾丸支持细胞和各级生精细胞发生病理改变。 2 0和 40mg kg剂量组均未见异常。结论　高剂量的 β CP对雄性大鼠睾丸有损伤作用     

哺乳期小鼠暴露双酚A对其成年后精子质量的影响

目的探讨新生雄性小鼠暴露于双酚A(Bisphenol A,BPA)对成年后睾丸和精子发育的影响及机制。方法新生雄性子鼠从出生第2天开始皮下注射BPA(剂量为0.01 mg/kg,0.1 mg/kg,5 mg/kg),持续到第21天断奶,第70天断颈椎处死,测定附睾尾精子密度、活动率,考马斯亮蓝染色进行精子形态学分析,流式细胞仪检测精子线粒体膜电位和活性氧水平。TBARS法检测睾丸过氧化脂质水平,透射电镜观察睾丸内各级生精细胞超微结构。结果 BPA组精子活力降低,畸形率显著升高,精子线粒体膜电位显著降低,中高剂量组精子数量下降,活性氧水平升高,睾丸内过氧化脂质水平显著升高。BPA组大部分生精细胞及支持细胞线粒体异常(肿胀、嵴模糊或消失、空泡化)。结论哺乳期接触BPA会通过线粒体途径影响精子发生,降低成年后精子的数量和质量。     

EFFECTS OF LEAD ON THE MALE REPRODUCTIVE SYSTEM IN MICE

The effect of environmental lead on the male reproductive system has been a major area of concern for several years. Lead toxicity to the male reproductive system of sexually mature male CF-1 mice was investigated by administering two concentrations of lead (0.25% and 0.5%) via drinking water for 6 wk. The low lead dose significantly reduced the number of sperm within the epididymis, while the high dose reduced both the sperm count and percentage of motile sperm and increased the percentage of abnormal sperm within the epididymis. There was no significant effect on testis weight; however, the high-dose treatment significantly decreased the epididymis and seminal vesicle weights as well as overall body weight gain. Plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone (T) levels were not affected by lead administration indicating that in adult male CF-1 mice, lead targets testicular spermatogenesis and sperm within the epididymis to produce reproductive toxicity rather than acting at other sites within the hypothalamic-pituitary-testicular axis.     

Effects of lead on the male reproductive system in mice

The effect of environmental lead on the male reproductive system has been a major area of concern for several years. Lead toxicity to the male reproductive system of sexually mature male CF-1 mice was investigated by administering two concentrations of lead (0.25% and 0.5%) via drinking water for 6 wk. The low lead dose significantly reduced the number of sperm within the epididymis, while the high dose reduced both the sperm count and percentage of motile sperm and increased the percentage of abnormal sperm within the epididymis. There was no significant effect on testis weight; however, the high-dose treatment significantly decreased the epididymis and seminal vesicle weights as well as overall body weight gain. Plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone (T) levels were not affected by lead administration indicating that in adult male CF-1 mice, lead targets testicular spermatogenesis and sperm within the epididymis to produce reproductive toxicity rather than acting at other sites within the hypothalamic-pituitary-testicular axis.     

Pre- and postnatal exposure to ambient levels of urban particulate matter (PM(2.5)) affects mice spermatogenesis

This work characterizes the effects of ambient levels of urban particulate matter (PM(2.5)) from the city of Sao Paulo on spermatogenesis using mice exposed during the embryo-fetal and/or postnatal phases of development. Parental generations (BALB/c mice) were exposed to air pollution in chambers with or without filtering PM(2.5) for 4 months. Animals were mated, and half of the 1-day-old offspring were moved between chambers, which yielded prenatal and postnatal groups. Remaining offspring comprised the non-exposed and pre+postnatal exposed groups. After 90 days, the animals were sacrificed for testis collection and weighing. Optical microscopy was used for the morphometric analyses of the cell counts, spermatogenic cycle, proliferation, and apoptosis. Prenatally exposed animals presented reduced body and testicular weight with an increased gonadosomatic index (GSI). Testicular volume also decreased, as well as the tubular diameter in testes of the same animals. Proliferation, apoptosis, and spermatogenic cycle analyses showed no significant differences among groups. However, the tubules at stage VII of pre- and postnatal animals presented a reduced number of elongated spermatids. Pre+postnatal group presented higher spermatid head retention at stages VIII-XII. These results show that ambient levels of PM(2.5) from Sao Paulo city affect spermatogenesis by damaging sperm production.     

血清生殖激素、精浆锌与睾丸生精障碍的关系

目的 探讨无精子症患者血清生殖激素水平、精浆锌含量与睾丸生精状态的关系。方法 对128例男性不育患者与30例正常对照者,进行了血清生殖激素（FSH,LH,T,PRL）检测、睾丸活检病理学检查、睾丸容积及精液分析,测定了40例无精子症患者和30例正常对照精浆的锌含量。结果 无精子症组的精浆锌含量降低,与正常对照组比较存在显著性差异（P<0.05）;睾丸源性无精子症血清FSH,LH升高,睾丸容积减少,睾丸容积小于15ml者,其T/LH值下降,与正常对照组间存在非常显著性差异（P<0.01）,提示睾丸功能损伤,间质细胞功能受损。结论 血清FSH含量在鉴别睾丸源发性与梗阻性无精子症中是非常重要的指标,T/LH比值是判定睾丸间质细胞损伤的指标,睾丸生精障碍程度愈严重,其FSH,LH水平愈高,而L/LH值降低愈明显,精浆Zn及血清生殖激素的检测,在男性不育无精子症诊断和在判定睾丸功能的损伤程度中具有重要作用。     

Impairment of mice spermatogenesis by sodium arsenite

In order to assess the effect of arsenic on the male reproductive impairment in mice, 7-week-old animals were exposed to 7.5 mg sodium arsenite (NaAsO(2))/kg body weight, during 35 days (one spermatogenic cycle). One group of animals was sacrificed after exposure, while another group received distilled water for an additional period of 35 days, in order to study the spermatoxic effect and the recovery of spermatogenesis. In mice sacrificed after NaAsO(2) exposure, a decrease in testis/body weight ratio and reduction of tubular diameter were observed. Both groups of NaAsO(2)-exposed animals showed remarkable histopathological changes, such as sloughing of immature germ cells. Animals sacrificed after NaAsO(2) exposure showed decreased sperm motility, increased abnormal sperm morphology and decreased sperm viability. The effects of NaAsO(2) on sperm motility recovered to normal values after one spermatogenic cycle, while increased sperm abnormality was maintained. However, at this period, a decrease in acrosome integrity was detected. Concerning oxidative stress parameters, animals sacrificed after NaAsO(2) exposure showed a decreased selenium-dependent glutathione peroxidase activity, which was not detected after the recovery. Conversely, at this period, total glutathione peroxidase activity increased in exposed animals. These results demonstrate the toxic effects of NaAsO(2) on mice spermatogenesis and show the lack of recovery after one spermatogenic cycle.     

Pre- and postnatal exposure to ambient levels of urban particulate matter (PM2.5) affects mice spermatogenesis

This work characterizes the effects of ambient levels of urban particulate matter (PM_2.5) from the city of Sao Paulo on spermatogenesis using mice exposed during the embryo–fetal and/or postnatal phases of development. Parental generations (BALB/c mice) were exposed to air pollution in chambers with or without filtering PM_2.5 for 4 months. Animals were mated, and half of the 1-day-old offspring were moved between chambers, which yielded prenatal and postnatal groups. Remaining offspring comprised the non-exposed and pre+postnatal exposed groups. After 90 days, the animals were sacrificed for testis collection and weighing. Optical microscopy was used for the morphometric analyses of the cell counts, spermatogenic cycle, proliferation, and apoptosis. Prenatally exposed animals presented reduced body and testicular weight with an increased gonadosomatic index (GSI). Testicular volume also decreased, as well as the tubular diameter in testes of the same animals. Proliferation, apoptosis, and spermatogenic cycle analyses showed no significant differences among groups. However, the tubules at stage VII of pre- and postnatal animals presented a reduced number of elongated spermatids. Pre+postnatal group presented higher spermatid head retention at stages VIII–XII. These results show that ambient levels of PM_2.5 from Sao Paulo city affect spermatogenesis by damaging sperm production.     

环烯醚萜对烟酰胺-链脲霉素诱导的2型糖尿病小鼠生精功能的影响

目的:　探讨环烯醚萜对烟酰胺-链脲霉素诱导的2型糖尿病小鼠生精功能的影响。方法: 在本实验研究中,56只雄性小鼠随机分为7组(n=8)：对照组;糖尿病小鼠组;糖尿病小鼠服用格列本脲(0.25mg/kg)治疗组;糖尿病小鼠接受环烯醚萜(20和40mg/kg)治疗组;正常小鼠接受环烯醚萜(20和40mg/kg)治疗组。糖尿病模型制作：由腹腔注射链脲霉素(65mg/kg),15分钟后注射烟碱(120mg/kg)。然后,连续喂服格列本脲和环烯醚萜28天。最后一次治疗24小时后,提取血清样本、睾丸及附睾组织,测定血激素、观察睾丸病理切片、进行精子参数评估。结果: 糖尿病小鼠体重和睾丸质量,精子浓度和活力,血清LH、FSH和T水平明显下降(p < 0.05)。接受环烯醚萜治疗组小鼠前述下降的参数得到明显提升(p < 0.05)。结论: 结果表明,针对糖尿病小鼠应用环烯醚萜可降低氧化损伤的危重程度、有效提升其生育能力, 具有确切的临床应用价值。     

Reproductive toxicity of melamine against male mice and the related mechanism

Melamine is a nitrogen-containing heterocyclic organic compound with a triazine skeleton, which has been widely applied in industrial and chemical fields. Previous toxicity studies of melamine mainly focused on renal toxicity and hepatic pathological changes, but its toxicity against the reproductive system has seldom been assessed. We investigated the effects of melamine on the reproductive system of male mice. Forty healthy male Kunming mice were randomly divided into a normal saline negative control group, a low-dose melamine group, a medium-dose melamine group and a high-dose melamine group (n?=?10). The mice were administered for five consecutive days and killed on the 35th day after first administration. In melamine administration groups, seminiferous tubules had disordered, loose arrangement, and spermatogenic cells at all levels obviously decreased. The sperm count and motility decreased significantly, and the sperm deformity rate increased significantly. Melamine induced apoptosis of testicular spermatogenic cells. To further explore the mechanism, we detected metabolism-related enzymes sorbitol dehydrogenase (SDH) and lactate dehydrogenase (LDH) as well as oxidative stress indices superoxide dismutase (SOD) and malondialdehyde (MDA). The activities of SDH, LDH and SOD in melamine treatment groups decreased significantly, and the MDA level increased obviously. The expressions of apoptosis-related proteins Bcl-2, Bax and caspase-3 were detected by immunohistochemistry. The expression of Bcl-2 significantly increased, but those of Bax and caspase-3 significantly reduced (p?相似文献   

铅对小鼠睾丸细胞DNA损伤作用研究

目的:通过建立亚慢性铅中毒动物模型探讨醋酸铅对雄性小鼠睾丸细胞DNA的损伤,为进一步了解其毒性作用机制提供科学依据。方法:将45只雄性小鼠分为0.2%、0.4%染铅组及空白对照组,每组各5只。实验组醋酸铅溶于去离子水中供小鼠自由摄取,空白对照组饮用自来水。分别于第2、4、6周分别处死动物,用单细胞凝胶电泳实验(彗星实验)检测小鼠睾丸细胞DNA损伤情况。结果:醋酸铅染毒后小鼠睾丸细胞DNA单链断裂,出现彗星状拖尾。无论是拖尾细胞的百分率,DNA迁移的长度,还是olive尾矩与空白对照组相比其差异具有极显著性(P<0.01),并且随着醋酸铅染毒浓度和时间的增加DNA的损伤越重,呈现出时间-效应关系。但0.2%与0.4%各周染毒组的拖尾细胞百分率、彗星尾长、olive尾矩的差异并无显著性(P>0.05)。结论:醋酸铅可诱导睾丸生殖细胞DNA损伤,并且其损伤作用呈现出时间依赖性。