镉对去卵巢大鼠骨密度和肾功能的影响

目的：研究镉对去卵巢大鼠骨密度的影响及其与肾脏损伤的关系。方法：将SD大鼠行人工去卵巢术，分别经饮水给不同剂量的镉染毒，24周后处死。用双能量X线骨密度仪（HOLOGIC，QDR－4000）测定股骨颈、股骨中点及腰椎的骨密度，用石墨炉原子吸收法测定血、尿及骨镉，放免法测定血清雌二醇,同时测定镉肾损伤指标尿β2－微球蛋白和尿钙。结果：大鼠去卵巢后，体内雌二醇水平低下，骨密度明显下降。镉染毒可使大鼠股骨颈的骨密度明显降低，且随镉染毒剂量增加呈下降趋势。镉染毒后，大鼠发生肾损伤，尿β2－微球蛋白和尿钙含量升高。同时股骨颈的骨密度与肾损伤指标β2－微球蛋白有显著性相关。结论：镉染毒可降低去卵巢大鼠的骨密度，对股骨颈作用尤为敏感，而且镉引起的骨损伤与镉造成的肾损伤相关。     

补肾益冲方对卵巢储备功能减退大鼠卵巢组织形态及性激素的影响

目的：研究补肾益冲方对卵巢储备功能减退（DOR）模型大鼠卵巢功能的影响。方法：选取雌性未孕SD大鼠40只,随机分为空白组、模型组、补肾益冲方组、补佳乐组。除空白组外,其余大鼠采用雷公藤多苷片混悬液灌胃制备DOR大鼠模型,造模成功后分别给予补肾益冲方及补佳乐进行相应的治疗干预。药物干预结束后,采用酶联免疫吸附试验法（ELISA）检测大鼠血清中抗苗勒管激素（AMH）、促卵泡生成素（FSH）、雌二醇（E2）、促黄体生成素（LH）的水平;HE染色观察大鼠卵巢组织的病理学形态变化。结果：与空白组比较,模型组大鼠血清FSH和LH水平升高（P<0.05）,AMH和E2水平降低（P<0.05）;卵巢中原始卵泡和生长卵泡的数量减少,闭锁卵泡增加;卵巢间质增生并纤维化。补肾益冲方干预后,DOR大鼠血清中FSH和LH激素水平降低（P<0.05）,AMH和E2激素水平升高（P<0.05）;卵巢组织形态得到改善,原始卵泡和生长卵泡增多,闭锁卵泡减少。结论：补肾益冲方对DOR大鼠卵巢组织形态、卵母细胞的数量和质量具有改善作用,能调节AMH、FSH、E2和LH从而提高DOR大鼠的卵巢储备功能...     

金雀异黄素对多囊卵巢综合征大鼠性激素水平的影响

目的 研究金雀异黄素(GEN)对多囊卵巢综合征(PCOS)大鼠性激素水平及卵巢组织3β-羟基甾脱氢酶(3β-HSD)、细胞色素P450芳香化酶(P450arom)的影响.方法 将120只大鼠随机分为对照组(n=30)、模型组(n=30)及低剂量实验组(n=30)、高剂量实验组(n=30).模型组及低、高剂量实验组大鼠均...     

不同手术方式干预对多囊卵巢综合征大鼠模型性激素水平影响研究

目的:观察多囊卵巢综合征大鼠模型在不同手术方式干预下E、T、LH、FSH、PRL、P水平变化情况,探讨不同手术方式的干预效果。方法:多囊卵巢综合征雌性SD大鼠模型40只,标记后随机均等分为4个组,并分别运用假手术、卵巢打孔术、卵巢楔形切除术及卵巢贯穿缝合术进行干预,酶联免疫吸附试验(ELISA)测定各组大鼠手术前后血清性激素水平。结果:术后第3天及术后30天:1 E:卵巢打孔术组低于假手术组和卵巢楔形切除术组、卵巢贯穿缝合术组;2 T、LH:卵巢打孔术组和卵巢楔形切除术组均低于假手术组,卵巢打孔术组低于卵巢楔形切除术组和卵巢贯穿缝合术组,卵巢楔形切除术组低于卵巢贯穿缝合术组;3 FSH:卵巢打孔术组和卵巢楔形切除术组均高于假手术组,卵巢打孔术组高于卵巢楔形切除术组,以上各组间差异均有显著性(P<0.05);4 P、PRL:各组间比较差异均无显著性。结论:卵巢局部手术干预能降低大鼠多囊卵巢模型血清中T、LH水平,卵巢打孔术对改善性激素紊乱状态更为有效。     

卵巢良性肿瘤患者腹腔镜手术治疗对血清性激素和炎性因子水平的影响

目的:评价卵巢良性肿瘤患者腹腔镜手术治疗对血清性激素和炎性因子水平的影响。方法:选取2015年10月—2016年10月期间收治的卵巢良性肿瘤患者90例资料,将其随机分为观察组和对照组(每组45例);对照组患者给予常规开腹手术治疗,观察组患者给予腹腔镜手术治疗,比较两组患者手术后的疗效,以及治疗前后黄体生成素(LH)、促卵泡激素(FSH)、雌二醇(E2)、C-反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)和白介素-6(IL-6)测得值的变化情况。结果:观察组患者术中出血量少于对照组(P<0.05),排气时间早于对照组(P<0.05);手术治疗前两组患者血清LH、FSH和E_2测得值经级间比较其差异均无统计学意义(P>0.05),治疗后两组患者血清LH、FSH和E2测得值均优于治疗前(P<0.05);观察组患者手术治疗后血清LH、FSH和E2测得值均优于对照组(P<0.05);手术治疗前两组患者CRP、TNF-α和IL-6测得值经比较其差异均无统计学意义(P>0.05),治疗后观察组患者CRP、TNF-α和IL-6测得值均低于对照组(P<0.05)。结论:采用腹腔镜手术治疗卵巢良性肿瘤患者,显著减少术中出血量、术后排气时间早,有效改善了其血清性激素水平,抑制了炎性因子的释放,促进了伤口的愈合。     

镉对雌性大鼠排卵功能的影响

选动情间期SD种雌性大鼠,分别皮下注射5和10mg/kg CdC12及生理盐水1.0ml/kg。染毒后第6天用戊巴比妥麻醉,再静脉注射0.5和2.0μg/kg LHRH。结果表明,LHRH能使垂体和血清中LH含量升高。另一试验,动情间期SD大鼠,皮下注射10mg/kg CdCl_2后第6天,注射LHRH后,血清LH和孕酮水平明显升高,能部分恢复排卵功能。实验结果提示,Cd~(2+)中止排卵过程似乎在于使垂体释放LH减少,进而使LH对卵巢黄体功能的支持减退,这可能是Cd~(2+)阻断孕酮作用的途径之一。     

性激素监测中西药治疗多囊卵巢综合征16例

目的探讨性激素监测中西药治疗多囊卵巢综合征临床疗效。方法选取2012年5月至2013年5月期间我院收治的多囊卵巢综合症患者16例,按照治疗方式的不同随机分为中药组和西药组,每组8例,观察比较两组治疗后性激素监测指标改善情况。结果两组患者卵泡刺激素（FSH）、黄体生成素（LH）、雌二醇（E2）等性激素水平均有所改善,西药组黄体生成素（LH）、雌二醇（E2）改善水平优于中药组,差异比较具有统计学意义（P〈0．05）。结论由于多囊卵巢综合症发病机制尚无确切的定论,中西药治疗方式对其均有调理作用,其中西药从短期观察来看,其疗效相对较好。     

染镉雌性大鼠垂体、卵巢对性腺激素的反应机能状况

目的 研究镉的雌性性腺素性及其机制，为镉中毒防治研究提供科学依据。方法 不同剂量的对雌性大鼠行亚慢性皮下注射染毒（每天1次，每周5d，连续6周）。染毒20d后连续观察并记录动情周期；于染毒结束时进行促性腺激素释放激素（GnRH）刺激试验，采用放免法测定FSH、LH变化；采用原子吸收光普法测定卵巢、子宫、血清镉含量；将小鼠随机分成3组，连续染镉5d，每天1次，染毒第6天进行超排卵试验。结果 （1）染毒组大鼠子宫、卵巢含量均高于低剂量和对照组（P＜0．05）且子宫与卵巢镉、血清隔含量有明显相关性；（2）高剂量组大鼠动情间期和动情周期异常经较其他剂量组明显增高（P＜0．05）；（3）注射GnRH前，各剂量组间大鼠血清中LH、FSH差异未见显著性（P＜0．05），注射GnRH后，各剂量组血清中LH、FSH水平较注射前均明显升高，差异有显著性（P＜0．05），而注射后染镉组大鼠血清中LH水平显著低于对照组（P＜0．05），FSH则否；（4）染镉小鼠超数排儿中组小鼠的儿子数差异无显著性（P＞0．05）。结论 子宫、卵巢也是镉的重要器官，镉可引起雌性大鼠动情周期明显异常，染镉大鼠垂体对超量GnRH的反应能力和代偿能力功能明显损害，面卵巢对于超量促性腺激素的反应机能基本正常，但不排除常量对反应机能下降的可能。     

镉所致大鼠性腺和附性腺的组织病理学改变

【目的】　探讨镉所致大鼠性腺和附性腺的病理学改变。【方法】　各组大鼠分别皮下注射氯化镉 0、0 5、1和 2mg/kg,每天 1次 ,每周 5d ,共 5周。【结果】　染毒大鼠的血镉和尿镉含量显著增高 ,睾丸和附睾体积缩小 ,重量减轻。染毒组睾丸曲细精管壁变薄 ,上皮排列紊乱 ,呈条索状 ,细胞层次明显减少 ;高剂量组曲细精管管腔中无精子 ;附睾上皮细胞呈低柱形 ,排列紊乱 ,管腔中有大量异常精子 ;精囊管壁和前列腺细胞壁稍变薄。【结论】　镉可使染毒大鼠性腺和附性腺重量减轻 ,导致睾丸、附睾出现明显的病理改变。     

Evaluation of the effect of cadmium on rat organs and investigation of diethyl carbamate as an oral drug in treatment of cadmium toxicity

The effect of diethyl carbamate as a chelating agent on the excretion of cadmium was evaluated in cadmium-poisoned Wistar rats following food and drink administration. The present research aimed to characterize the potential efficiency of diethyl carbamate as an oral drug chelator after cadmium administration for 60 days. This chelator significantly enhanced the urinary and biliary excretion of cadmium and restored the altered levels of iron. Diethyl carbamate was given orally to different groups of rats for a period of 1 week immediately after cadmium administration. After chelation therapy, animals were killed by exsanguination from abdominal aorta. Blood, kidneys, spleen, and heart samples were collected and prepared for determination of cadmium. Cadmium and iron concentrations in different issues were determined by graphite furnace and flame atomic absorption spectrometry (GFAAS and FAAS) methods, respectively. The chelation therapy results showed that diethyl carbamate was able to remove cadmium ions from different tissues while iron concentration returned to normal level and clinical symptoms were also reduced. In summary, we can conclude that diethyl carbamate could mobilize and promote the excretion of cadmium in rat organs and reduce the side-effects and general symptoms of toxicity. Moreover, it might be useful for preliminary testing of the efficiency of chelating agents in the human body. However, these results should be confirmed in a different experimental model before extrapolation to other systems. This testing procedure of course does not provide all the relevant answers for evaluating the efficiency of chelating agents in cadmium toxicity.     

Protective effect of sodium molybdate against the acute toxicity of cadmium chloride

Pretreatment of rats with Na₂MoO₄ (1.24 mmol/kg, once a day for 3 days, i.p.) partially protected them againts the acute toxicity of CdCl₂ (0.075 mmol/kg, once, s.c., 24 h after pretreatment with Na₂MoO₄). The survival number of rats per total number of rats in the CdCl₂-dosed group was 10/10, 8/10, 6/10, 2/10 and 0/10 on 0, 1, 2, 6 and 18 days after treatment with CdCl₂ whereas in the group where CdCl₂ is given after pretreatment with Na₂MoO₄ it is 10/10 and 6/10 on 0 and 18 days. The body weight of CdCl₂-dosed rats consistently decreased until their death while that of Na₂MoO₄- CdCl₂-dosed rats similarly decreased up to 4 days after exposure to CdCl₂ but then increased almost normally. In order to elucidate the mechanism of protective action of Na₂MoO₄ against the acute toxicity of CdCl₂, cellular components such as DNA, inorganic cations and metallothionein were measured in the liver after exposure to CdCl₂. The treatment with CdCl₂ alone reduced K content and increased Ca content but pretreatment with Na₂MoO₄ prevented such alterations in the levels of those cations caused by CdCl₂. Metallothionein content in the liver was significantly elevated in the CdCl₂-treated groups as compared to saline controls although the protein content was higher in the Na₂MoO₄-CdCl₂-dosed group than in the CdCl₂-dosed group. There was no difference in the protein content of the liver between saline controls and the Na₂MoO₄-dosed group. This suggests that Na₂MoO₄ alleviated the acute toxicity of CdCl₂ in the rat and the protective mechanism by the metal is in part related to the enhancement of liver Cd-metallothionen induction.     

The effect of cadmium on the collagen solubility of embryonic chick bone in tissue culture

The effect of cadmium (Cd) on the solubility of bone collagen was examined in cultured tibiae from 9-day chick embryos. The solubility of collagen was not significantly increased by 8.9 microM Cd, but showed a significant increase at 13.4 microM Cd. As the [3H]hydroxyproline (Hyp) formation was inhibited by Cd at 8.9 and 13.4 microM [3H]Hyp formation and collagen solubility were investigated in the presence of 200 microM Fe2+, a metal which is known to prevent the inhibitory effects of Cd on prolyl hydroxylase in vitro. Fe affected neither a decrease in [3H]Hyp formation nor an increase in collagen solubility caused by Cd. This suggests that a Cd-induced increase in collagen solubility may be due to the decrease of lysyl oxidase activity, not to the formation of underhydroxylated collagen. Zn at 48 and 134 microM depressed the Cd-induced increase in collagen solubility, but caused no increase in collagen solubility. Our present and previous results suggest that Zn can protect the disturbance of both the collagen synthesis and the collagen cross linking caused by Cd.     

Effect of low-level lifetime exposure to cadmium on calciotropic hormones in aged female rats

The effect of low-level lifetime exposure to cadmium (Cd) on calciotropic hormones and the possible association between the Cd-induced disorders in bone metabolism and these hormones were investigated on a female rat model of human environmental exposure in areas unpolluted by this metal. For this purpose, the concentrations of 25-hydroxyvitamin D (25OHD), 1,25-dihydroxyvitamin D (1,25(OH)₂D), calcitonin (CT) and parathormone (PTH) were measured in the serum of control and Cd-exposed (1 mg Cd/l in drinking water for 24 months) female rats. Calcium (Ca) and inorganic phosphorus (P_i) serum concentrations, renal tubular reabsorption of Ca (TRCa) and phosphate (TRP) and the glomerular filtration rate (GFR) were estimated as well. Moreover, 1,25(OH)₂D, metallothionein (MT) and Cd were determined in the kidney. The exposure to Cd led to a decrease in the serum concentrations of 25OHD and 1,25(OH)₂D (by 50 and 31%, respectively) and the concentration of 1,25(OH)₂D in the kidney mitochondrial fraction (by 55%). The serum concentrations of CT and PTH increased (5.2-fold and by 29%, respectively) and those of Ca and P_i were unchanged, whereas the TRCa, TRP and GFR decreased due to the exposure to Cd. The results give evidence that the low lifetime exposure to Cd disturbs the metabolism of calciotropic hormones and damages the reabsorptive and filtrative function of the kidney in aged female rats. Numerous correlations noted between calciotropic hormones and the indices of kidney function, and indices of bone turnover and bone mineral status (bone mineral content and density) of these females indicate a relationship between these hormones and the kidney functional status and bone metabolism. The results of the present study together with our previous findings on the bone status in the experimental model allow for the conclusion that the low lifetime exposure to Cd by affecting the metabolism and proper function of calciotropic hormones may contribute to the advancement of bone damage at the elderly.     

八珍益母丸对更年期雌性大鼠卵巢、子宫及激素的影响

目的探讨八珍益母丸对更年期雌性大鼠卵巢、子宫及激素的影响。方法建立更年期大鼠模型,观察口服八珍益母丸后更年期雌性大鼠卵巢、子宫指数及血清雌激素(E2)、促黄体生成激素(LH)、促卵泡激素(FSH)、孕激素(P)4项激素水平的变化。结果八珍益母丸组可显著提高子宫、血清E2和P 2项激素水平。结论八珍益母丸具有增加更年期雌性大鼠子宫指数、血清E2和P激素水平的作用。     

The effect of ozone on the expression of metallothionein in tissues of rats chronically exposed to cadmium

Our aims were to evaluate the expression of metallothionein (MT) in an experimental rat model which experienced chronic exposure to cadmium (Cd) and to measure its expression after ozone therapy (OT) or oxygen (Ox) in the same model, as compared to the control group, which was exposed to neither cadmium nor ozone.Forty male Wistar rats were divided into 5 groups: control, Cd, Cd and Ox, Cd and Oz, and Oz. During our research, Cd concentration (ASA) and MT concentration (ELISA) were determined in supernatants of the kidneys, liver and pancreas. SDS-PAGE analyses and immunohistochemical localization were used to evaluate the level of MT expression in the tissue. In rats intoxicated with Cd, the highest concentration of both Cd and MT was observed in the kidneys and liver, with a significantly lower concentration measured in the pancreas. Ozone therapy reduces the accumulation of cadmium in the liver and kidneys, resulting in a reduced expression of metallothionein in those tissues.     

硒对镉致脂质过氧化与金属硫蛋白诱导合成的影响

目的 比较亚硒酸钠(Na2SeO3)与硒代蛋氨酸(SeMet)对镉(Cd)毒性的拮抗效应，探讨脂质过氧化及金属硫蛋白(MT)的诱导合成在硒(Se)拮抗Cd毒性作用中的意义，为镉中毒的防护提供依据。方法 健康雄性Wistar大鼠36只，随机分6组。I组为正常对照组，Ⅱ组为Cd中毒组，Ⅲ组为Na2SeO3组，Ⅳ组为SeMet组，V组为Cd Na2SeO3组，Ⅶ组为Cd SeMet组。Cd按100μmol／kg体重，Se(Na2SeO3及SeMet)按10μmol／kg体重的剂量隔日1次经口灌胃，其中V组和Ⅵ组按先Se后Cd交替灌胃。Se、Cd均灌胃15次。实验时间为30d。结果 单独给Cd组大鼠肝脏和肾脏MT水平升高，而血清MT出现降低；2种Se化合物均使大鼠肾脏和肝脏MT含量轻度增高，但2个Se加cd组与单独给Cd组比较，MT水平差异不显著；染Cd大鼠仅见血清脂质过氧化产物丙二醛(MDA)含量明显升高，而2种Se化合物对其没有明显影响；无论是单独给Se组(Ⅲ、Ⅳ)，还是Se加Cd组(V、Ⅵ)，大鼠全血、肝脏及肾脏GSH-Px活力均明显增高。结论 Se能在一定程度上诱导机体合成MT，但在Se拮抗Cd毒性作用中MT的诱导合成可能不起主要作用；Se能提高机体的抗氧化能力。对拮抗Cd毒性具有一定的作用；SeMet与Na2SeO3对诱导MT的合成及提高GSH-Px的活力，其效应基本相似。