青春期镉暴露对雄性小鼠睾丸发育及镉含量的影响

目的:探讨青春期低剂量镉暴露小鼠血清、肾脏、肝脏和睾丸中镉的蓄积情况。方法:雄性CD-1小鼠自出生后35至70 d经腹腔注射给予1 mg/kg CdCl2。阴性对照组给予等容量生理盐水。采用氘灯背景校正,选用合适的升温程序采用石墨炉原子吸收法(GFAAS)测定两组小鼠睾丸、血清、肝脏和肾脏镉含量。结果:青春期镉暴露能够明显降低小鼠睾丸重量;镉暴露组小鼠血清、肾脏、肝脏和睾丸中镉绝对量显著高于生理盐水对照组。与血清中镉的含量相比,青春期镉暴露明显增加小鼠肝脏、肾脏镉的相对量,而睾丸镉的相对含量差异却没有显著性。结论:青春期镉暴露能够影响小鼠睾丸发育,引起小鼠血清、肝脏、肾脏镉的明显增加,但睾丸中镉增加不明显,提示镉可能通过间接途径产生睾丸毒作用。     

镉对大鼠睾丸毒性作用的实验研究

目的 :观察镉对大鼠睾丸的毒性。方法 :硫酸镉染毒剂量为 6mg/kg·d ,令大白鼠连续口服 30和 60d ,观察睾丸重量的变化 ,光镜下检查对睾丸和附睾的影响。结果 :随着染镉时间的延长 ,大鼠睾丸重量明显逐渐下降 ;光镜检查 ,睾丸曲细精管有不同程度的变性 ,管内生精细胞数减少或缺如 ,精子形成少或无。结论 :染镉时间长短对睾丸的影响呈明显的剂量—反应关系。     

双酚A对雄性大鼠生殖系统的影响

目的探讨双酚A(BPA)对青春期雄性大鼠生殖系统的影响。方法30只雄性Wistar大鼠,随机分为3组,每组10只。每隔1d腹腔注射低剂量〔1mg/kg·bw〕和高剂量〔25mg/(kg·bw)〕BPA染毒8周,对照组给予等体积溶剂丙二醇。测大鼠体重、睾丸和附睾湿重并计算睾丸/体重比值、附睾/体重比值;观察睾丸、附睾组织学结构的变化;计数附睾尾精子数;应用放射免疫法测定血清性激素水平。结果与对照组比较,低剂量和高剂量BPA组大鼠的体重均下降:高剂量组大鼠死亡2只,睾丸、附睾湿重降低,睾丸/体重比值升高,精子计数减少;光镜下可见睾丸间质水肿,附睾间质血管扩张。结论双酚A可能对青春期雄性大鼠体重、生殖系统的发育及精子发生有不良影响。     

低剂量氯化镉对大鼠睾丸组织酶活性的影响

镉对雄性生殖系统的影响被认为是影响人类生育的重要因素,已受到普遍关注.有报道显示,亚慢性镉染毒可使睾丸体积变小,重量减轻,肉眼观察出现睾丸病理改变,镜检发现曲细精管呈不同程度的萎缩、变性,管内生精细胞数少或缺如,无精子形成或极少,管腔内可见坏死的细胞碎片[1,2],说明镉可以严重干扰破坏大鼠睾丸曲细精管上皮的生精过程,对大鼠的生殖功能产生影响.     

睾丸附件扭转的超声诊断

目的探讨睾丸附件扭转的超声诊断价值。方法回顾性总结近5年睾丸附件扭转22例超声声像图表现。结果睾丸附件扭转1周内声像图表现为睾丸与附睾间出现圆形、类圆形或棒状结节,较正常明显增大,回声减低,结节内部呈网状,可伴同侧睾丸及附睾肿大、阴囊壁增厚、睾丸鞘膜积液。CDFI示结节内无血流信号,同侧附睾头和睾丸血流信号较丰富。1周后声像图表现为睾丸附件体积明显缩小,回声增高,同侧附睾及睾丸体积逐渐恢复正常,鞘膜积液渐渐消失,阴囊壁接近正常。结论超声对睾丸附件扭转具有较高的诊断价值。     

高压氧对精索静脉曲张家兔生殖激素水平影响的实验研究

目的研究高压氧(HBO)对精索静脉曲张(VC)家兔生殖激素水平的影响,进一步探讨精索静脉曲张致男性不育的机制。方法采用HBO干预精索静脉曲张家兔模型,对睾丸重量、体积,精液参数及外周血浆生殖激素(FSH、LH)水平进行研究。结果与VC模型组比较,HBO干预VC模型组精液质量改善,睾丸重量增加,血浆FSH、LH水平下降(P=0.0215,P=0.0492),T水平增高(P<0·0001)。结论VC可导致睾丸间质损害,并引起生殖激素水平平衡失调,从而加重睾丸生精功能及附睾精子成熟功能的损害。主要机制为VC时睾丸缺血,缺氧及其微循环灌注障碍;HBO可有效抑制VC致睾丸间质细胞损害进程,改善睾丸间质细胞生存的微循环,维持生殖内分泌激素水平平衡。     

附睾的畸形感染和损伤

附睾是一对细长扁平的器官,依附于睾丸的后上方.其上端膨大而钝圆,称附睾头,盖于睾丸上端.其下端尖细,称附睾尾,转向后上方与输精管相接.头尾之间为附睾体,呈圆柱形.附睾的内部是一根迂回曲折盘绕其内的附睾管,附睾管上与睾丸的输出小管相接,下通输精管,所以是精子排出必经的交通要道.另一方面,附睾管又有吸收、分泌和浓缩的功能.它为精子在途经附睾管时提供营养和促进精子的发育和成熟.所以,有人把附睾称为精子的摇篮,实很确切.精子通过附睾管后获得了运动的能力,和与卵子结合的能力,最后贮存在附睾的尾部,等待性高潮射精时排出体外.     

三氯异氰尿酸对雄性大鼠生殖系统的影响

目的 观察三氯异氰尿酸(TCCA)长期暴露对SD雄性大鼠生殖系统的影响.方法 选取4～5周龄、体重41.3～55.0g雄性SD大鼠270只,按照每天0、0.71、2.29、7.59 mg/kg剂量水平经口饲养TCCA 12个月和24个月后,检查生殖系统各个脏器病理改变,采用LUCCA病理图像分析软件测量大鼠睾丸平均曲细精管直径(MSTD).结果TCCA染毒12个月,高剂量组睾丸曲细精管直径变小;染毒24个月,低、中、高剂量组睾丸、附睾重量和脏器系数与对照组相比均降低,中、高剂量组睾丸精子生成障碍、曲细精管萎缩和睾丸萎缩、附睾内无精子的发生率与对照组相比明显升高.结论 在2.29、7.59mg/kg的剂量水平时,TCCA的长期染毒能导致大鼠睾丸重量减轻、萎缩及精子生成障碍,TCCA对雄性SD大鼠睾丸具有明显的毒性作用.     

附睾精子肉芽肿14例报告

附睾精子肉芽肿１４例报告浙江省肖山市第一人民医院泌尿外科（３１１２００）任福锦附睾精子肉芽肿是指精子自睾丸精细管、附睾管或输精管溢出到周围间质引起炎症性肉芽肿，临床较少见，我院１９８０年～１９９３年１３年间收治１４例，报告如下。临床资料：年龄２５～５...     

亚慢性镉暴露对雄性大鼠生殖毒性的研究

目的　探讨亚慢性镉暴露对雄性大鼠生殖系统的毒作用。方法　 2 4只清洁级SD系雄性大鼠 ,分为对照组、低、中及高剂量染镉组。分别给予 0 ,0 1,0 2 ,0 4mgCd2 /kg体重皮下注射染毒 5周。实验结束后剖杀动物取睾丸、附睾组织待检。结果　 (1)高剂量组睾丸脏器系数高于正常对照组 (P <0 0 5 ) ;各染镉组精子数、活动率均低于对照组 (P <0 0 5 ) ,而畸形率明显上升 (P <0 0 5 ) ;(2 )中、高剂量组睾丸组织血色素水平与丙二醛 (MDA)含量显著性升高 (P <0 0 5 ) ,而金属硫蛋白 (MT)含量只有高剂量组高于对照组 (P <0 0 5 )。结论　亚慢性镉暴露对大鼠睾丸有明显的毒性作用 ,其机制与镉致睾丸脂质过氧化、睾丸MT不易被诱导或保护作用较低有关。     

Interstitial lung disease in mixed connective tissue disease

INTRODUCTION: The authors analyzed the incidence of interstitial lung disease in mixed connective tissue disease. They were seeking an answer to the following problems: the nature of the pathological course of mixed connective tissue disease complicated by and the therapy to be used in interstitial lung disease. PATIENTS AND METHODS: 179 patients were followed up during a period of 15.9 +/- 6.1 years. Interstitial lung disease was diagnosed using high resolution computed tomography. The diagnosis of interstitial lung disease was not obvious in 5 patients thus open lung biopsy was performed, which confirmed common interstitial pneumonitis. The patients were followed-up, and the data of computed tomography and respiratory function tests were detected 6 months, and then 4 years after the acute lung disease complicated by mixed connective tissue disease. RESULTS: Out of the 179 mixed connective tissue disease patients 96 (53.6%) had interstitial lung disease. The onset of interstitial lung disease was the most frequent in the 2-4 years of the disease. Four years after the first appearance of interstitial lung disease severe fibrosis was diagnosed in 24 patients (25%). A honey comb formation in the lung developed only in one patient. For the treatment of interstitial lung disease, corticosteroid treatment had to be combined with cyclophosphamide in 51 cases. In 4 patients (24%), pulmonary arterial hypertension evolved 2-4 years following interstitial lung disease. The high pulmonary arterial pressure decreased using pulsed corticosteroid treatment, cyclophosphamide, prostacyclin analogue, anticoagulants therapy and the 4 patients stay alive. The pulmonary arterial hypertension was caused by obliterative vasculopathy. CONCLUSION: Pulmonary involvement is found in more than half of the patients with mixed connective tissue disease. Early diagnosis of interstitial lung disease is possible by computed tomography. Interstitial lung disease can be treated by the combination of corticosteroids and cyclophosphamide. The authors were the first to detect the coexistence of interstitial lung disease and pulmonary arterial hypertension in mixed connective tissue disease. Subsequent respiratory alterations in these patient necessitate regular patient follow up.     

Changes in pulmonary connective tissue proteins after a single intratracheal instillation of cadmium chloride in the rat

Changes of soluble and insoluble fractions of pulmonary connective tissue proteins were studied in rats for 2-84 days following a single intratracheal instillation of cadmium chloride (10 micrograms Cd2+/lung). A transient decrease in body weight and an immediate increase in lung wet weight (200% of control value, P less than 0.01) were observed. Incorporation of [14C]proline and its conversion to [14C]hydroxyproline in vivo into different soluble and insoluble fractions of connective tissue revealed an increased metabolic turnover elicited by cadmium intoxication. A lag in the maturation of collagen into higher functional forms in the early phase of the process was demonstrated. A striking decrease in elastin was found in first 7 days (40-50%). However, this acute damage of pulmonary connective tissue was followed by a permanent increase of collagen and elastin concentration in the later phase of recovery. Histopathologic examination 14-84 days after cadmium instillation confirmed the presence of lesions in pulmonary tissue with an initial inflammation followed by reparatory changes.     

Cadmium, zinc, and copper in rabbit kidney metallothionein--relation to kidney toxicity

Twenty-two rabbits were given repeated subcutaneous injection of cadmium chloride. The cumulative cadmium dose given ranged from 13 to 214 mumole/kg body weight. Five rabbits served as controls. The treatment resulted in cadmium concentrations in kidney cortex that ranged from 0.3 to 3.2 mmole Cd/kg and a subsequent production of metallothionein. The molar ratio of cadmium, zinc, and copper in metallothionein fractions from kidneys with different concentrations of cadmium was determined. At low concentrations of cadmium in rabbit kidneys, zinc was the dominating metal bound to metallothionein (70-90%). At high concentrations of cadmium in kidneys, cadmium was the dominating metal in metallothionein. Evidence of kidney toxicity, in the form of beta2-microglobulinuria, was seen when cadmium constituted 85% of the metal ions recovered from metallothionein fractions. The remaining 15% was zinc. This indicates that at most six of the seven metal-binding sites in mammalian metallothionein are occupied by cadmium and that the remaining site is occupied by zinc. Our data provide further support for the hypothesis that chronic cadmium nephrotoxicity develops when there is a lack of metal-binding sites available for cadmium in metallothionein.     

Impact of cadmium on liver pigmentary system of the frog Rana ridibunda

The liver pigmentary system of the frog Rana ridibunda was investigated after exposure to CdCl2. There was a time-dependent alteration in the area occupied by pigment cells. Most pigment was melanin, but lipofuscin and ferritin were also detected, being similarly increased with time. There was a time-dependent increase in the dimensions of pigment cells as a result of forming a cluster of more than two pigment cells, the so-called melanomacrophage aggregates (MMC). A thin capsule of connective tissue with fibroblast-like cells surrounds some MMCs. The various possible roles of MMCs are discussed, for instance, those of scavengers of foreign substances, for lowering of metabolic activities to survive in an anoxic environment probably caused by cadmium, or as scavenger of cadmium, thus playing a protective role against this metal.     

The toxicological response of the algaAnabaena flos- aquae (cyanophyceae) to cadmium

The toxicological response of the cyanophycean algaAnabaena flos- aquae to cadmium was investigated by three integrated approaches: 1) the determination of the incipient lethal concentration of the metal, 2) study of metal incorporation and cellular compartmentalization using X-ray energy dispersive analysis, and 3) the quantification of intracellular structural changes, after metal exposure, using morphometric analysis. After 96 hr of exposure, the incipient lethal concentration was calculated to be 0.118 ± 0.04 M cadmium. At concentrations three orders of magnitude higher than the incipient lethal concentration, cadmium was incorporated into both the cellular cytoplasm and the cell's polyphosphate bodies. Cadmium also caused the polyphosphate bodies to lose Mg and Ca, resulting in ionic changes in the elemental composition of these cellular inclusions. The utilization of stereological techniques for electron microscopic morphometric analysis established that all concentrations of cadmium tested caused significant reductions in the surface area of the cell's thylakoids. Cadmium induced changes in the numbers and relative volume of the cell occupied by polyhedral bodies, polyphosphate bodies, lipid inclusions, cyanophycin granules, membrane limited crystalline, inclusions, and changes in the volume of the cell wall layers were also documented. The physiological significance of these findings are discussed in terms of the toxic action of cadmium and the cellular mechanisms for detoxification of cations once they enter the cell.     

Effects of dietary cadmium on mallard ducklings

Mallard (Anas platyrhynchos) ducklings were fed cadmium in the diet at 0, 5, 10, or 20 ppm from 1 day of age until 12 weeks of age. At 4-week intervals six males and six females from each dietary group were randomly selected, bled by jugular venipuncture, and necropsied. Significant decreases in packed cell volume (PCV) and hemoglobin (Hb) concentration and a significant increase in serum glutamic pyruvic transaminase (GPT) were found at 8 weeks of age in ducklings fed 20 ppm cadmium. Mild to severe kidney lesions were evident in ducklings fed 20 ppm cadmium for 12 weeks. No other blood chemistry measurement, hematological parameter, or tissue histopathological measurement indicated a reaction to cadmium ingestion. Body weight, liver weight, and the ratio of the femur weight to length were not affected by dietary cadmium. Femur cadmium concentration in all ducklings 12 weeks of age declined from the values detected at 4 and 8 weeks of age. Liver cadmium concentrations were significantly higher in relation to the increased dietary levels and in relation to the length of time the ducklings were fed the cadmium diets. At 12 weeks of age the cadmium concentration in liver tissue was twice that in the diet.     

Effects of dietary cadmium on mallard ducklings

Mallard (Anas platyrhynchos) ducklings were fed cadmium in the diet at 0, 5, 10, or 20 ppm from 1 day of age until 12 weeks of age. At 4-week intervals six males and six females from each dietary group were randomly selected, bled by jugular venipuncture, and necropsied. Significant decreases in packed cell volume (PCV) and hemoglobin (Hb) concentration and a significant increase in serum glutamic pyruvic transaminase (GPT) were found at 8 weeks of age in ducklings fed 20 ppm cadmium. Mild to severe kidney lesions were evident in ducklings fed 20 ppm cadmium for 12 weeks. No other blood chemistry measurement, hematological parameter, or tissue histopathological measurement indicated a reaction to cadmium ingestion. Body weight, liver weight, and the ratio of the femur weight to length were not affected by dietary cadmium. Femur cadmium concentration in all ducklings 12 weeks of age declined from the values detected at 4 and 8 weeks of age. Liver cadmium concentrations were significantly higher in relation to the increased dietary levels and in relation to the length of time the ducklings were fed the cadmium diets. At 12 weeks of age the cadmium concentration in liver tissue was twice that in the diet.     

Chronic carcinogenic and toxic effects of a single subcutaneous dose of cadmium in the male Fischer rat.

The carcinogenic effects of cadmium have not been thoroughly assessed in the commonly used Fischer (F344) rat. This study determined tumor incidence in various tissues of male F344/NCr rats after a single dose of cadmium. Cadmium (as CdCl2) was given sc in the dorsal thoracic midline at 30 mumole/kg to 70 8-week old male F344 rats while controls (n = 50) received saline. Rats were observed during the next 90 weeks. Early deaths (less than or equal to 32 weeks), due mostly to acute cadmium-induced hepatotoxicity, accounted for 37 of the cadmium-treated rats while no control rats died in the same period. A high incidence of injection site sarcomas (ISS) occurred in the cadmium-treated group (21 ISS/32 rats at risk; 66%) while only 1/50 occurred in controls (2%). In fact, ISS were the major cause of morbidity after 35 weeks in cadmium-treated rats. These tumors were mostly fibrosarcomas, although histiocytic and osteogenic sarcomas also occurred. Testicular interstitial cell tumors, which show a very high spontaneous incidence in this strain (41/49; 84%), were not markedly affected by cadmium (30/31; 97%). This is in sharp contrast to other strains, such as the Wistar, in which cadmium treatment is reported to cause as much as an eightfold increase in interstitial cell (Leydig cell) tumor incidence. The incidence of large granular lymphocyte (LGL) leukemia, which also occurred frequently in control F344 rats (12/47; 26%) was markedly decreased (2/31; 7%) by cadmium. Our recent studies indicate acute lymphonecrotic effects occur with cadmium in lymphoid tissues of rats, and this may be related to the suppression of the leukemia. These results indicate that cadmium is very effective in inducing ISS in F344 rats, as is the case with other strains thus far tested, and also markedly reduces spontaneous leukemia incidence.     

结缔组织病相关性间质性肺炎患者合并EB病毒感染炎症因子及DNA载量分析

目的探讨EB病毒感染对结缔组织病相关性间质性肺炎的影响。方法选取2017年12月-2019年12月天津市第五中心医院收治的结缔组织病相关性间质性肺炎患者190例的资料进行回顾性分析。依据患者是否发生EB病毒感染进行分析分组,感染组65例,未感染组125例。比较两组患者的临床资料、合并疾病情况及动脉血气分析结果、EB病毒检测情况、中性粒细胞百分比、治疗有效时间、转入重症监护室(ICU)比例。对比两组炎性相关指标[C-反应蛋白(CRP)、降钙素原(PCT)、白细胞计数(WBC)、白细胞介素-6(IL-6)、IL-17、IL-33]。分析两组的EB病毒DNA含量与各类炎性相关指标的相关性。结果 EB病毒感染率为34.21%(65/190)。未感染组动脉氧分压为(61.92±18.25)mmHg高于感染组,革兰阴性菌感染占比、治疗有效时间和转入ICU占比分别为45.60%(57/125)、(7.61±2.75)d、13.60%(17/125)均低(短)于感染组(P<0.05)。两组的二氧化碳分压、中性粒细胞百分比差异无统计学意义。感染组的CRP、PCT、WBC、IL-6、IL-17、IL-33分别为(53.25±5.31)mg/L、(0.78±0.10)μg/L、(14.32±0.67)×109/L、(151.58±11.25)ng/L、(116.28±12.33)ng/L、(61.56±3.65)ng/L高于未感染组(P<0.001)。EB病毒DNA含量与CRP、PCT、WBC、IL-6、IL-17、IL-33均呈正相关(P<0.05)。结论 EB病毒感染可使结缔组织病相关性肺间质性肺炎患者的病情进一步恶化,在该种类患者的治疗过程中需特别注意。     

氯化镉对小鼠免疫细胞增殖和凋亡的影响

[目的]观察镉在体内染毒条件下 ,对小鼠免疫细胞的功能和凋亡的影响。[方法]采用一次腹腔注射氯化镉0.34、1.38和5.50mg/kg后8h处死和一次腹腔注射氯化镉5.50mg/kg后4、8、12h处死动物以及连续灌胃0.3、0.6和1.2mg/(kg·d)氯化镉14d后处死动物 ,利用MTT颜色反应法观察淋巴细胞转化、用DNA凝胶电泳法和流式细胞仪法检测细胞凋亡。[结果]小鼠经一次腹腔注射CdCl25.50mg/kg后4或8h可见胸腺细胞凋亡率为24.91 %和32.45 % ,脾细胞凋亡率分别为22.64 %和16.67 % ,均高于对照组 ;注射后12h胸腺细胞凋亡仍高于对照组。同时注射氯化镉5.50mg/kg4h后 ,ConA刺激的淋巴细胞转化功能明显低于对照组 ,抑制率接近50 % ;而在注射8h后 ,除了T细胞在ConA刺激下的转化功能受到抑制外 ,未受刺激的脾细胞增殖转化功能也受到抑制 ,抑制率为47 %。连续14d灌胃给氯化镉对小鼠脾脏细胞和胸腺细胞凋亡及淋巴细胞转化均未见明显的影响。[结论]小鼠经一次腹腔注射CdCl25.50mg/kg ,在胸腺细胞和脾细胞凋亡增加 ,同时T淋巴细胞转化功能也受到抑制。连续14d灌胃0.3、0.6和1.2mg/(kg·d)氯化镉未见对小鼠脾脏淋巴细胞转化和脾脏细胞、胸腺细胞的细胞凋亡有所影响