Induction of Oxidative Stress in the Epididymis of Rats After Subchronic Exposure to Epichlorohydrin

This study investigated the effects of epichlorohydrin (ECH) on spermatogenesis and antioxidant system in rats. An increase in the incidence of clinical signs, gross pathology and histopathology findings in the epididymidis, and sperm abnormalities and a decrease in the testicular spermatid counts, epididymal sperm counts, and sperm motility were observed at 30 mg/kg/day. Oxidative stress in the epididymal tissue was detected at ≥3.3 mg/kg/day. The results show that graded doses of ECH elicit depletion of antioxidant defense system and that the adverse effects on male reproductive function in ECH-treated rats may be due to the induction of oxidative stress.     

p,p'-DDE对青春前期大鼠睾丸组织氧化应激及凋亡的影响

目的 研究p,p'-DDE对青春前期大鼠睾丸组织氧化应激及凋亡的影响.方法 将健康清洁级22日龄雄性SD大鼠25只按体重随机分为5组,分别为对照组(玉米油)、低(20 ms/kg)、中(60 mg/kg)、高(100 mg/kg)剂量P,p'-DDE染毒组和VitE干预组(100mg/kg p,p'-DDE+100mg/kg Vit E),每组5只.采用腹腔注射方式进行染毒,注射容积为10ml/kg,每隔1 d染毒1次,共10 d.染毒结束后,处死动物,取睾丸称重,并计算睾丸脏器系数;将睾丸制备组织切片和组织匀浆,分光光度计法测定大鼠睾丸组织超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量和谷胱甘肽过氧化物酶(GSH-Px)活力,采用TUNEL法检测睾丸组织的细胞凋亡情况.结果 各组动物染毒前体重及染毒期间体重变化无差异.大鼠睾丸重量及其脏器系数间比较,差异无统计学意义(P＞0.05).与对照组比较,高、中、低剂量p,p'-DDE染毒组SOD活力降低,中、高剂量p,p'-DDE染毒组MDA含量升高,高剂量p,p'-DDE染毒组GSH-Px活力下降,差异均有统计学意义(P＜0.05).与高剂量p,p'-DDE染毒组比较,Vit E干预组SOD活力升高,差异有统计学意义(P＜0.05).Vit E干预组和高剂量p,p'-DDE染毒组MDA含量和GSH-Px活力间比较,差异无统计学意义(P＞0.05).高、中、低剂量p,p'-DDE染毒组和对照组均有睾丸细胞凋亡情况发生,对照组中凋亡细胞稀少;随着p,p'-DDE染毒剂量的升高,凋亡细胞数也逐渐增多,以精原细胞和精母细胞为主,伴有支持细胞.与对照组比较,高、中、低剂量P,p'-DDE染毒组的细胞凋亡指数均升高,差异有统计学意义(P＜0.05);Vit E干预组的细胞凋亡指数低于高剂量p,p'-DDE染毒组,差异有统计学意义(P＜0.05).结论 p,p'-DDE可通过引发睾丸组织氧化应激而诱导细胞凋亡.     

上皮细胞钠通道α亚基在大鼠和人睾丸、精子中的表达及其与精子活力的关系

目的:研究上皮细胞钠离子通道α亚基(ENaC-α)在大鼠和人的睾丸、精子上的表达及其与人精子活力之间的关系。方法:用western-blot检测ENaC-α在大鼠和人睾丸、精子上的表达,同时免疫荧光检测其在大鼠睾丸的分布特点。用计算机辅助精液分析检测ENaC-α的特异阻断剂EI-PA[5-(N-ethyl-N-isopropyl)-amiloride hydrochloride]对精子活力的影响。结果:ENaC-α亚基表达于大鼠睾丸精母细胞、精子细胞,以及大鼠成熟精子的鞭毛中段;它也存在于人睾丸和成熟精子的鞭毛中段。体外精子活力实验表明,获能过程中ENaC的阻滞,可以促进人精子活力的增加,差异有显著性意义(P<0.01)。结论:ENaC-α构成的离子通道在生精细胞中表达,最终局限分布于成熟精子的鞭毛中段的质膜中。而特异阻断剂EIPA可以抑制上皮细胞钠离子通道,从而提高精子活力。     

硒对氟致大鼠睾丸和附睾损害拮抗作用的研究

目的 研究和探讨硒对氟致雄性大鼠生殖损害的拮抗作用及其机理,找出硒对氟毒性的最佳拮抗剂量.方法 给雄性大鼠饮用含氟化钠(150mg/L)及同时分别加入不同浓度亚硒酸钠(0.5,2.0和4.0mg/L)的饮水共8周,观察氟及氟硒联合对大鼠血、尿氟水平及对睾丸和附睾的影响.结果 氟暴露大鼠血液和尿液氟浓度明显升高,血清和睾丸微量元素含量异常、睾丸和附睾组织脂质过氧化物(LPO)含量增加、谷胱甘肽过氧化物酶(GSH-Px)和ATP酶活性显著降低.2.0mg/L亚硒酸钠对大鼠尿氟排泄具有显著促进作用,对氟致血清和睾丸微量元素异常改变具有一定调整作用,对氟致睾丸和附睾LPO含量升高及GSH-Px和ATP酶活性降低具有显著拮抗作用,而0.5和4.0mg/L亚硒酸钠的作用较弱.结论 2.0mg/L亚硒酸钠是本实验条件下硒拮抗氟致睾丸和附睾损害的最佳剂量.     

实验性煤矽肺大鼠氧化和抗氧化损伤的动态观察

大鼠经气管注入煤石英尘，观察肺泡巨噬细胞（ＡＭ）和支气管肺泡冲洗液（ＢＡＬＦ）中脂质过氧化产物和抗氧化物质的动态变化。结果表明，染尘后７天ＡＭ中ＭＤＡ含量增加，ＳＯＤ活性下降，以后恢复至正常，ＧＳＨＰｘ活性和ＧＳＨ含量染尘后７～３０天升高。ＢＡＬＦ中ＭＤＡ含量、ＳＯＤ活性无变化，ＧＳＨＰｘ活性、ＧＳＨ含量均低于石英组。说明煤石英尘诱发ＡＭ脂质过氧化反应发生于染尘初期，且明显弱于石英尘。说明脂质过氧化反应在煤矽肺病变形成中不起主要作用     

Induction of Oxidative Stress in the Reproductive System of Rats after Subchronic Exposure to 2,3,7,8-Tetrachlorodibenzo-P-Dioxin

No abstract available.     

锌诱导肾脏Ⅰ型金属硫蛋白改善糖尿病大鼠肾脏氧化应激

<正>锌是金属硫蛋白(metallothionein,MTs)基因表达的诱导因子[1]。MTs是富含半胱氨酸、可诱导的、多功能、小分子量金属结合蛋白,在抗氧化、维持微量元素自稳态、重金属解毒等方面有重要作用[2]。本研究以口服硫酸锌诱导糖尿病大鼠肾脏MT-1基因表达,探讨其对糖尿病肾病的保护作用。     

绿麦隆和阿特拉津联合染毒对小鼠睾丸的影响

目的 研究绿麦隆和阿特拉津单体系及联合作用对小鼠睾丸形态及结构的影响.方法 将昆明种小鼠按灌胃农药和剂量随机分为20组[1个对照组,4个绿麦隆染毒组(321.5、1250、2500、5000mg/kg),3个阿特拉津染毒组(218.75、875、1750mg/kg),12个联合染毒组],每组10只.连续25 d经口灌胃,每天1次,每次1ml.并用光学显微镜、电子显微镜对小鼠睾丸病理学变化进行观察.结果 农药单体系及联合染毒体系各剂量组对小鼠睾丸均有不同程度的损伤.与对照组比较,光学显微镜观察所见为各剂量组出现不同程度生精上皮细胞排列疏松、紊乱,生精细胞脱落,层次减少,病变严重;电子显微镜观察为各剂量组出现不同程度生精细胞线粒体呈空泡样改变,核膜肿胀、弯曲,支持细胞功能低下随染毒剂量增加,上述病理学变化有加重趋势,联合染毒组病理变化比单体系染毒组更明显.结论 绿麦隆和阿特拉津对小鼠睾丸的毒性与染毒剂量相关,联合作用体系加重了对小鼠睾丸的毒性效应.     

硫辛酸对高脂诱导肥胖大鼠氧化应激影响的实验研究

目的探讨硫辛酸（LA）对高脂诱导肥胖大鼠氧化应激水平的影响。方法 29只5~6周龄Wistar雄性大鼠,按体重随机分为2组：基础组（n=8）和高脂组（n=21）。高脂组大鼠饲养6周末尾尖采血,测定空腹血糖,按血糖水平随机分为2组：高脂组,高脂＋硫辛酸干预组（硫辛酸组）,分别用生理盐水和LA进行腹腔注射,4周后测定大鼠体重、内脏脂肪含量以及血清丙二醛（MDA）、超氧化物歧化酶（SOD）、总抗氧化能力（T-AOC）和全血谷胱甘肽过氧化物酶（GSH-Px）。结果与基础组比较,高脂组大鼠的血清MDA水平和SOD活性明显增高,T-AOC下降,差异均有统计学意义（P〈0.05）;与高脂组比较,LA组大鼠体重和内脏脂肪含量明显降低,血清T-AOC明显升高,差异有统计学意义（P〈0.05）;三组大鼠GSH-Px差异无统计学意义（P〉0.05）。结论 LA能显著降低高脂诱导肥胖大鼠的体重和内脏脂肪含量,提高肥胖大鼠的抗氧化能力。     

镉对小白鼠睾丸附睾影响的定量组织学研究

镉处理后的小白鼠睾丸,早期,间质水肿、血管扩张。给药一周后,睾丸萎缩,六周后,睾丸重量下降62%,曲细精管相对体积减小38%,而间质(间质细胞和结缔组织)相对体积增加70%左右。附睾重量也稍减轻,附睾头郎附睾管正皮相对体积减小,而管间结缔组织增加。镉对附睾的损害可用锌来预防。     

氟中毒氧化应激与细胞凋亡关系的研究

目的 研究氟、硒对大鼠肝细胞氧化应激和细胞凋亡的影响.方法 大鼠经饮水加氟化钠(150mg/L)或/和亚硒酸钠(2mg/L)10周后,检测肝细胞凋亡百分率、细胞周期构成比、活性氧(ROS)和还原型谷胱甘肽(GSH)含量以及脂质过氧化物(LPO)水平.结果 氟可使肝细胞凋亡百分率明显升高,S期细胞数增多,ROS和LPO水平升高,GSH含量下降;硒通过稳定细胞GSH含量可拮抗氟的毒性作用,使组织中ROS、LPO水平下降,GSH含量升高,凋亡百分率下降.结论 硒可部分拮抗氟化物诱导的肝细胞脂质过氧化和凋亡,氧化应激参与了介导细胞凋亡的过程.     

Camphene Attenuates Skeletal Muscle Atrophy by Regulating Oxidative Stress and Lipid Metabolism in Rats

Sarcopenia- or cachexia-related muscle atrophy is due to imbalanced energy metabolism and oxidative stress-induced muscle dysfunction. Monoterpenes play biological and pharmacological reactive oxygen species (ROS) scavenging roles. Hence, we explored the effects of camphene, a bicyclic monoterpene, on skeletal muscle atrophy in vitro and in vivo. We treated L6 myoblast cells with camphene and then examined the ROS-related oxidative stress using Mito Tracker^TM Red FM and anti-8-oxoguanine antibody staining. To investigate lipid metabolism, we performed real-time polymerase chain reactions, holotomographic microscopy, and respiratory gas analysis. Rat muscle atrophy in in vivo models was observed using ¹⁸F-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography and immunocytochemistry. Camphene reversed the aberrant cell size and muscle morphology of L6 myoblasts under starvation and in in vivo models. Camphene also attenuated E3 ubiquitin ligase muscle RING-finger protein-1, mitochondrial fission, and 8-oxoguanine nuclear expression in starved myotubes and hydrogen peroxide (H₂O₂)-treated cells. Moreover, camphene significantly regulated lipid metabolism in H₂O₂-treated cells and in vivo models. These findings suggest that camphene may potentially affect skeletal muscle atrophy by regulating oxidative stress and lipid metabolism.     

低温冷冻和孵育对人精子氧化应激水平的影响

目的：探讨低温冷冻和孵育对人精子氧化应激水平的影响。方法：60份精液，每份分成5份分别列入5组（处理前对照组、低温冷冻空白实验组、低温冷冻样本组、孵育空白实验组和孵育样本组）。以晚期氧化蛋白产物（AOPP）为蛋白氧化指标，丙二醛（MDA）为脂质过氧化指标，用分光光度法分别检测AOPP和MDA的水平。结果：低温冷冻样本组MDA水平明显高于处理前对照组和低温冷冻空白实验组（P〈0．05），但AOPP水平无明显差异（P〉0．05）。孵育样本组AOPP和MDA水平均高于处理前对照组、孵育空白实验组及低温冷冻样本组（P〈0．05）。结论：精子的低温冷冻和孵育，均存在氧化应激损伤。低温冷冻主要造成精子的脂质过氧化损伤，孵育可致精子的脂质过氧化损伤和蛋白氧化损伤。     

氧化应激在实验性糖尿病肾病中的作用

目的观察链脲佐菌素诱导的糖尿病大鼠不同时期肾组织中脂质过氧化物水平、抗氧化酶活性的动态改变,以探讨氧化应激在糖尿病肾病发生发展中的作用。方法测定糖尿病大鼠不同时期肾组织中丙二醛的含量和总超氧化物歧化酶的活性,同时观察糖尿病大鼠不同时期肾组织的组织形态学的改变。结果大鼠糖尿病1个月、3个月和6个月肾组织中丙二醛含量与对照组相比显著增高,分别为(2.16±0.57)和(1.18±0.18)nmol/mgprot,(2.03±0.39)和(1.63±0.14)nmol/mgprot,(2.09±0.26)和(1.59±0.14)nmol/mgprot,差别均有统计学意义(P<0.05或P<0.01)。糖尿病1个月肾组织总超氧化物歧化酶活性与对照组相比明显增高[(135.18±6.18)U/mgprot和(88.49±8.29)U/mgprot],差别有统计学意义(P<0.01),3个月时降至正常对照水平,6个月时显著降低(30.30±2.01)U/mgprot和(49.41±5.63)U/mgprot,差别有统计学意义(P<0.01)。组织形态学观察表明,糖尿病3个月时肾脏出现基底膜增厚、肾小球扩张等病理改变,随着病程的延长,病理改变越严重。结论糖尿病早期肾脏存在明显的氧化应激,氧化应激在糖尿病肾病的发生发展中起重要作用。     

浏阳霉素亚慢性毒性与氧化损伤的实验研究

目的　探讨浏阳霉素 (Liuyangmycin)亚慢性毒性与氧化损伤的定量敏感指标和毒作用靶器官。　 方法　将健康SD大鼠随机分成 5个组 ,每组 2 0只 ,雌雄各半。根据急性毒性试验结果 ,分别设 40、2 0 0、10 0 0mg/kg .bw三个浏阳霉素染毒组 (即低、中、高剂量组 )、空白对照组与溶剂对照组。给大鼠每天灌胃染毒 1次 ,每周 6天 ,连续 3个月 ,每天观察动物进食、饮水、活动、毛发、大小便和常见临床症状 ,动物的体重和食物消耗量每周测定 1次 ,血象指标和尿液生化指标在试验前后各测定 1次 ,试验结束时测定血液生化指标、脏器系数和血液、肝脏、肾脏组织氧化损伤等指标 ,所有受试动物实施大体解剖检查 ,其中高剂量组和对照组的主要器官组织以及其他组具有肉眼可见异常的器官组织进行病理组织学检查。　结果　浏阳霉素染毒组动物器官组织病理学、体重增长率和食物消耗量未见明显异常 ;高剂量组部分动物在染毒后期出现萎靡、毛发缺乏光泽、行为活动明显减少等现象。与空白对照组和溶剂对照组比较 ,中、高剂量组谷丙转氨酶(ALT)活性与尿液丙二醛 (MDA)含量明显增加 (P <0 .0 5 ) ,高剂量组动物肝脏脏器系数明显增大 (P <0 .0 5 ) ,肾脏组织超氧化物歧化酶 (SOD)活性水平明显降低 (P <0 .0 5 )。　结论　血清ALT活     

牛磺酸对实验性糖尿病大鼠氧化应激的预防作用

<正>近年自由基防御机能紊乱在糖尿病(DM)中的作用受到重视[1,2]。牛磺酸(taurine,Tau)是兴奋性较高组织中含量最丰富的游离氨基酸,而高糖血症可使神经、晶状体、肾小球及心肌等细胞中Tau含量显著下降[3]。本实验旨在观察预防     

Isoantigenicity of Rabbit Sperm,Testis, and Their Extracts as Demonstrated by Western Blot Enzyme Immunobinding Procedure

The isoantigenicity of rabbit germ cells and their extracts was studied by using a Western blot enzyme immunobinding procedure after systemic and local intrauterine immunization. In the deoxycholate (DOC) sperm extract, the antisperm isoantiserum (ASA) recognized proteins of 100, 96, 92, 82, 53, 47, 43, and 29 kD, and the antitestis isoantiserum (ATA) recognized proteins of 100, 96, 92, 82, 43, and 29 kD. In the lithium diiodosalicylate (LIS) sperm extract, ASA reacted with four antigen bands of 92, 30, 14, and 6 kD, and ATA reacted with proteins of 94, 92, 91, 23, 17, 7, and 6 kD. In the reduced sodium dodecyl sulfate (SDS) sperm extract, ASA recognized proteins of 95, 76, 51, 41, 33, 30, 28, 26, and 22 kD; ATA showed a reaction only with proteins of 100, 98, and 95 kD, and anti-LIS/sperm isoantiserum (ALA) recognized three proteins of 98, 81, and 65 kD.

The IgA of the immune uterine fluid (IUF) from the LIS/sperm-immunized rabbits recognized a 14-kD antigen in the DOC conceptus extract, a 51-kD antigen in the DOC testis extract, and 53-, 49-, 31-, and 28-kD proteins in the reduced SDS-sperm pellet extract. The IgA of the IUF from the NP-40/pellet-immunized rabbits showed two proteins of about 100 kD, plus ones of 56, 36, 31, 29, 19, 17, and 14 kD in the DOC conceptus extract; proteins of 92, 70, 51, 29, and 14 kD in the DOC testis extract; and of 61, 57, 53, 49, 35, 31, and 28 kD in the reduced SDS-sperm pellet extract.     

Effects of Gestational Diabetes in Cognitive Behavior,Oxidative Stress and Metabolism on the Second-Generation Off-Spring of Rats

Gestational diabetes (GD) has a negative impact on neurodevelopment, resulting in cognitive and neurological deficiencies. Oxidative stress (OS) has been reported in the brain of the first-generation offspring of GD rats. OS has been strongly associated with neurodegenerative diseases. In this work, we determined the effect of GD on the cognitive behavior, oxidative stress and metabolism of second-generation offspring. GD was induced with streptozotocin (STZ) in pregnant rats to obtain first-generation offspring (F1), next female F1 rats were mated with control males to obtain second-generation offspring (F2). Two and six-month-old F2 males and females were employed. Anxious-type behavior, spatial learning and spatial working memory were evaluated. In cerebral cortex and hippocampus, the oxidative stress and serum biochemical parameters were measured. Male F2 GD offspring presented the highest level of anxiety-type behavior, whilst females had the lowest level of anxiety-type behavior at juvenile age. In short-term memory, adult females presented deficiencies. The offspring F2 GD females presented modifications in oxidative stress biomarkers in the cerebral cortex as lipid-peroxidation, oxidized glutathione and catalase activity. We also observed metabolic disturbances, particularly in the lipid and insulin levels of male and female F2 GD offspring. Our results suggest a transgenerational effect of GD on metabolism, anxiety-like behavior, and spatial working memory.