镉对正常大鼠肾成纤维细胞凋亡形态学的影响

[目的]观察氯化镉对正常大鼠肾成纤维（NRK）细胞凋亡的形态学及细胞凋亡率的影响。[方法]用20μmol／L氯化镉染毒NRK细胞24h,通过透射电镜观察细胞凋亡形态变化。分别用0、5、10、20、40、60μmol／L的氯化镉培养NRK细胞24h,用20μmol／L的氯化镉分别体外培养NRK细胞0．5、2、6、12、24h,通过流式细胞仪检测各组NRK细胞的凋亡率。[结果]氯化镉可以使NRK细胞出现凋亡征象即凋亡小体的形成,且凋亡率呈时间-效应、剂量-效应关系,剂量为0、5、10、20、40、60／amol／L的氯化镉染毒24h,凋亡率分别为3．01％、6．14％、10．0％、12．6％、23．5％和34．7％;20μmol／1氯化镉染毒NRK细胞0、0．5、2、6、12、24h,凋亡率分别为3．31％、5．96％、8．38％、8．59％、13．97％和16．16％。[结论]氯化镉可以诱导NRK细胞发生特征性的凋亡形态的变化,且氯化镉诱导NRK细胞发生凋亡存在时间-效应、剂量-效应关系。     

亚慢性镉染毒致大鼠心脏损伤探讨

目的 观察氯化镉(CdC12)亚慢性染毒对大鼠心脏组织的损伤作用.方法 96只SD大鼠随机分成镉高剂量组、中剂量组、低剂量组和生理氯化钠对照组,每组24只,雌雄各半,给予CdCl2腹腔注射,每天1次,每周5d,连续14周.测定大鼠心脏组织中镉水平和脏器系数的变化,现察其心肌组织病理学改变.结果 镉染毒雄性大鼠心脏镉水平在高剂量组、中剂量组和低剂量组分别为5.764、2.450和0.789 μg/g,分别是对照组的 115.28、49.00和15.78倍;而雌性大鼠心脏镉水平在上述3个剂量组分别为5.147、2.180和1.219μg/g,分别是对照组的102.94、43.60和24.38倍,差异均有统计学意义(P<0.01).两性大鼠心脏脏器系数均随着镉染毒水平的增加而有不同程度的升高,有明显的剂量依赖关系(P<0.01)0所有染毒大鼠心脏组织出现不同程度的形态结构改变,主要有心肌纤维排列疏松,间陈增宽,细胞核固缩、碎裂、崩解,甚至心肌坏死,这些病理学改变随着镉染毒水平的增加而更加明显.结论　亚慢性镉染毒可引起大鼠心脏组织内镉蓄积,导致染毒大鼠心肌坏死等明显的组织病理学改变.     

应用单细胞凝胶电泳研究镉对大鼠肝细胞DNA损伤的影响

目的 研究一定剂量的氯化镉对离体和在体大鼠肝细胞ＤＮＡ损伤的作用。方法 应用单细胞凝胶电泳或慧星试验。结果 在２．１８５μｍｏｌ／Ｌ、４．３７５μｍｏｌ／Ｌ、８．７５μｍｏｌ／Ｌ、１７．５０μｍｏｌ／Ｌ、３５．００μｍｏｌ／Ｌ的剂量条件下,氯化镉均可引起离体大鼠肝细胞ＤＮＡ损伤。５μｍｏｌ／ｋｇ、１０μｍｏｌ／ｋｇ、２０μｍｏｌ／ｋｇ的氯化也可引起在体大鼠肝细胞ＤＮＡ损伤。氯化镉引起的离体和在体在     

醋酸铅对大鼠亚急性毒性研究

本实验通过对30只雄性Wistar大鼠每日灌胃30mg/kg和60mg/kg,醋酸铅,历时3个月,与每日灌蒸馏水的对照组比较,发现;铅对鼠体重未产生影响。染毒组与对照组相比较;血铅和锌原卟啉明显增高,肾和肝脏的脏器系数也明显增高。     

低剂量氯化镉亚慢性染毒对大鼠精子运动功能的影响

[目的]应用计算机辅助精子分析(computer assisted sperm analysis,CASA)技术研究低剂量氯化镉(Cd-Cl2)亚慢性染毒对大鼠精子运动能力的影响. [方法]40只健康雄性SD大鼠分成4组,剂量分别为0(生理盐水)、0.1、0.2、0.4 mg/kg·bw,腹腔注射染毒,每周染毒5 d(次),共染毒8周,实验结束颈椎脱臼处死,用扩散法收集大鼠附睾尾精子制成精子悬液.1:9稀释液后甩CASA仪测定反映精子活率、精子运动能力及运动方式的各项参数. [结果]各剂量组的精子活率间差异无统计学意义(P>0.05).高剂量组的快速运动精子、中速运动精子、低速运动精子百分比与对照组比较,差异无统计学意义(P>0.05).高剂量组的VAP、VSL值与对照组比较均降低,差异有统计学意(P<0.05).高剂量组的BCF与对照组比较差异有统计学意义(P<0.05).LIN随染毒剂量增加而降低(r=-0.399,P<0.05).STR、ALH、ELON在各组间的差异无统计学意义(P>0.05). [结论]0.4 mg/kg·bw的氯化镉染毒可以引起大鼠精子运动功能的下降.     

高效氯氰菊酯动式吸入染毒对大鼠的亚急性毒性试验

目的建立农药连续动式染毒的方法,为开展农药毒理学2～4阶段试验创造必备条件。方法试验以液体农药(高效氯氰菊酯微乳剂)用2种浓度的稀释液进行雾化,在雾化过程中的3个时间段,于实验动物呼吸带水平设4个采样点,用多孔玻璃板吸收管采样气,用高效液相色谱仪测定定量,对染毒柜内的农药浓度进行测定。进而考察连续动式吸入染毒试验过程中农药的均匀性和稳定性。结果低剂量染毒组平均浓度为(99±24)mg/m3,高剂量染毒组平均浓度为(850±183)mg/m3。平均温度为(24.9±1.5)℃。平均湿度为(35.5±3.5)%。结论各个采样点平均浓度比较接近。表明染毒柜内低、高剂量毒物浓度的均匀性、稳定性比较好,达到连续动式吸入染毒标准要求。     

氯丙嗪和异搏定对镉致大鼠肾毒性的影响

目的研究氯丙嗪(CPZ)和异搏定(Ver)对镉中毒大鼠肾损伤及肾皮质蛋白激酶C改变的影响。方法大鼠按体重随机分成4组,第1组为对照组皮下注射0.9%氯化钠,第2组为单纯染镉组皮下注射7μmol/kg的氯化镉溶液,第3、4组分别是腹腔注射氯丙嗪(5mg/kg)和异搏定(4mg/kg);1h后皮下注射7μmol/kg的氯化镉,注射容量均为2mg/kg。染毒6周后,测定尿乳酸脱氢酶(LDH)、尿蛋白、尿镉、肾镉和肾皮质中的蛋白激酶C(PKC)的活性。结果单纯染镉组与对照组比较,尿LDH、尿蛋白和尿镉含量明显升高,肾镉及肾皮质细胞膜和细胞浆中PKC活性均明显升高,差异有统计学意义(P<0.01);CPZ干预组与单纯染镉组比较,细胞膜和细胞浆中PKC活性均有不同程度的下降,差异有统计学意义,尿LDH、尿蛋白和尿镉含量明显下降(P<0.05);Ver干预组细胞膜PKC活性低于单纯染镉组,且差异有统计学意义(P<0.05),尿LDH、尿蛋白和尿镉含量有下降趋势。结论氯丙嗪和异搏定均对镉中毒大鼠肾损伤及蛋白激酶C的改变有拮抗作用。     

低剂量氯化镉亚慢性染毒对大鼠精予运动功能的影响

[目的]应用计算机辅助精子分析（computer assisted sperm analysis，CASA）技术研究低剂量氯化镉（Cd-Cl2）亚慢性染毒对大鼠精子运动能力的影响。[方法]40只健康雄性SD大鼠分成4组，剂量分别为0（生理盐水）、0．1、0．2、0．4mg／kg&#183;bw，腹腔注射染毒，每周染毒5d（次），共染毒8周，实验结束颈椎脱自处死，用扩散法收集大鼠附睾尾精子制成精子悬液，1：9稀释液后用CASA仪测定反映精子活率、精子运动能力及运动方式的各项参数。[结果]各剂量组的精子活率间差异无统计学意义（P〉0．05）。高剂量组的快速运动精子、中速运动精子、低速运动精子百分比与对照组比较，差异无统计学意义（P〉0．05）。高剂量组的VAP、VSL值与对照组比较均降低，差异有统计学意（P〈0．05）。高剂量组的BCF与对照组比较差异有统计学意义（P〈0．05）。LIN随染毒剂量增加而降低（r=-0．399，P〈0．05）。STR、ALH、ELON在各组间的差异无统计学意义（P〉0．05）。[结论]0．4mg／kg&#183;bw的氯化镉染毒可以引起大鼠精子运动功能的下降。     

急性镉染毒大鼠血和尿指标与肾形态学改变的关系

目的 观察急性镉中毒大鼠尿液、血清指标与肾病理学改变的关系,以判断.肾功能损害Ζ的程度.方法 将SD健康雄性大鼠随机分成空白对照组和高、中、低3个剂量染镉组(染毒剂量分别为1.6、0.8、0.4 mg/kg,每天1次,连续染毒5 d),每组6只动物.分别测定各组血肌酐(Cr)、尿素氮(BUN)、尿β-N-乙酰葡萄糖苷酶(NAG)、肾皮质镉含量;光学显微镜、电子显微镜下观察肾组织形态学变化.结果 3个染镉组中,高剂量组血Cr及尿NAG水平较对照组升高,差异有统计学意义(P＜0.05),病理学观察相应出现肾小球萎缩,大量近曲小管上皮细胞明显肿胀,部分坏死,管腔狭窄甚至消失;尿NAG动态观察发现,中剂量组在第5天出现峰值,与对照组比较,差异有统计学意义(P＜0.05),该组可见到部分肾近曲小管上皮细胞肿胀变性,管腔萎缩.结论 急性染镉引起的肾功能生化指标变化与组织形态学变化一致,中、低剂量组的损伤为可逆的.     

镉对大鼠睾丸的影响

本文报告饮水中含镉对大鼠睾丸的慢性损害实验，并作有关酶组织化学活性检查。结果：大鼠连续饮用含ＣｄＣｌ２（氯化镉）３００ｍｇ／Ｌ水，其睾丸曲精小管内各级生精细胞损害严重。曲精小管和附睾内精子完全消失；曲精小管各级生精细胞核呈固缩状，残留甚少且难以区别。腔内可见较多多核聚体，嗜伊红团块和网状结构等坏死组织产物。糖原ＰＡＳ反应减弱；ＳＤＨ（琥珀酸脱氢酶）、Ｍｇ２＋－ＡＴＰａｓｅ（镁激活三磷酸腺苷酶）的活性明显减弱；ＬＤＨ（乳酸脱氢酶）、ＡＣＰ（酸性磷酸酶）的活性增强。提示：以含ＣｄＣｌ２３００ｍｇ／Ｌ染毒饮水已引起睾丸曲精小管上皮严重损坏。     

The potential role of combined anti-oxidants against cadmium toxicity on liver of rats

Cadmium (Cd), a widely distributed toxic trace metal, has been shown to accumulate in liver after long- and short-term exposure. Cd (2 mg/kg/day CdCl2) was intraperitoneally given to rats for eight days. Vitamin C (250 mg/kg/day) + vitamin E (250 mg/kg/day) + sodium selenate (0.25 mg/kg/day) were given to rats by oral means. The animals were treated by anti-oxidants one hour prior to treatment with Cd every day. The degenerative changes were observed in the groups given only Cd and anti-oxidants + Cd. Metallothionein (MT) immunoreactivity increased in cytoplasm of hepatocytes of the rats given Cd when compared with controls. In a number of cells with Cd and anti-oxidants treatment, immunoreactivity increase was more than in the group given Cd only and nuclear MT expression was also detected. Cell proliferation was assessed with proliferating cell nuclear antigen (PCNA) immunohistochemistry. PCNA expressions increased in all groups more than in the controls. Anti-oxidants treatment increased cell proliferation. In the animals administered with Cd, an increase in serum aspartate (AST) and alanine (ALT) aminotransferases, liver glutathione (GSH) and lipid peroxidation (LPO) levels were observed. On the other hand, in the rats treated with anti-oxidants and Cd, serum AST and ALT, liver glutathione and LPO levels decreased. As a result, these results suggest that combined anti-oxidants treatment might be useful in protection of liver against Cd toxicity.     

石棉改性后对大鼠致癌性的研究

为了探讨石棉改性后对生物体的致癌作用，采用了氯化铵（ＮＨ＿４Ｃｌ）水溶液和聚醚砜（ＰＥＳ）对川棉和茫棉两种温石棉样品进行化学和物理改性，观察其对实验大鼠胸膜内染尘产生的影响。结果表明，各石棉改性组大鼠胸膜间皮瘤诱发率均有降低，尤其是川棉化学改性组与未改性组比，差异有非常显著意义（Ｐ＜０．０１）。作者认为，化学改性使石棉中的Ｍｇ￣（２＋）等金属离子量降低，这可能是导致间皮瘤诱发率降低的一个重要原因。     

Comparative analysis of antioxidants against cadmium induced reproductive toxicity in adult male rats

Abstract

The present study was conducted to compare and evaluate the potential benefits of three different antioxidants in reversing cadmium (Cd)-induced reproductive toxicity in adult male rats. Rats (n?=?5) weighing 180?±?20?gm were divided into five groups (control, Cd, Cd?+?sulforaphane, Cd?+?vitamin E, and Cd?+?plant extract). Treated groups received CdCl₂ (0.2?mg/kg), sulforaphane (25?µg/rat), vitamin E (75?mg/kg), and plant extract (100?mg/kg) for 15 days. Blood samples and testicular tissues were obtained for estimation of testosterone, Zn, and Cd concentration and daily sperm production/efficiency of sperm production. Cadmium exposure caused a significant decrease in final body weight (p?<?0.0001). The plasma concentrations of Cd were significantly increased and Zn concentration decreased (p?<?0.0001) in the Cd group as compared to the control group. The testicular concentrations of Cd were significantly increased and Zn concentration decreased (p?<?0.0001) in the Cd group as compared to the control group. Cadmium exposure caused a significant decrease (p?<?0.0001) in plasma testosterone concentrations and daily sperm production as compared to the control group. More significant effects were observed with Cd+sulforaphane, Cd?+?vitamin E, and Cd?+?plant extract treated groups in slashing Cd-induced toxicity. Present findings suggest that Ficus religiosa and sulforaphane are more powerful antioxidants as compared to vitamin E in reversing the oxidative stress and can have a protective role against Cd induced reproductive toxicity in adult male rats. Part of the mechanism involved in this protective role seems to be associated with the antioxidant properties of these agents in reducing reproductive damage.     

镉致大鼠肾脏毒性机制研究

目的研究镉对肾脏产生的毒性作用,并初步探讨镉的肾脏毒性机制。方法低、中、高剂量染镉组大鼠分别皮下注射3,5,7μmol CdCl2/（kg·bw）6周。测定尿镉、蛋白含量和尿N-乙酰-β-D氨基葡萄糖苷酶（NAG）、碱性磷酸酶（ALP）、乳酸脱氢酶（LDH）活性,测定肝脏和肾皮质丙二醛（MDA）和谷胱甘肽（GSH）含量。结果尿蛋白含量和尿NAG、ALP、LDH活性以及肝、肾皮质MDA和GSH含量随染镉剂量增加而升高。中剂量染镉组尿蛋白含量和尿NAG、LDH活性以及肾皮质MDA、GSH含量显著高于对照组和低剂量染镉组。高剂量染镉组尿蛋白含量、ALP活性、肝和肾皮质MDA显著高于对照组和低中剂量染镉组。且尿镉、蛋白含量、尿NAG、ALP、LDH活性与肾皮质MDA含量呈显著正相关。结论镉生物学效应随染毒剂量增加而增强,CdCl2 5μmol/（kg·bw）对肾脏产生一定损伤作用,CdCl2 7μmol/（kg·bw）时肾脏损伤加重。镉的肾毒性机制与其氧化损伤作用有关。     

血管紧张素转换酶抑制剂对化学性急性呼吸窘迫综合征治疗作用的实验研究

目的　探讨血管紧张素转换酶抑制剂 (ACEI)在急性呼吸窘迫综合征 (ARDS)治疗中的具体作用。方法　将大鼠分为对照组、ARDS组和卡托普利 (Cap)组 ,后 2个组按不同取血时间再分为6个亚组 ,每组大鼠 5～ 6只。观察投用ACEI类药物Cap对油酸所致ARDS大鼠生理、生化指标及循环内皮细胞 (CEC)的影响。结果　在全身血压保持在正常水平下 ,Cap对ARDS有一定疗效。 2h时ARDS大鼠肺动脉压从 (2 3 5 0± 5 79)mmHg(1mmHg =0 133kPa)降到接近正常的 (14 4 3± 1 5 1)mmHg;反映肺毛细血管内皮损伤情况的CEC数量从 (6 88± 1 90 ) / 0 9μl减少到 (4 2 5± 0 2 0 ) /0 9μl;动脉血氧分压从 (35 0 8± 4 5 9)mmHg上升到 (70 4 8± 9 5 4 )mmHg ,同时肺湿干重等指标已接近正常 ;说明即使投用大剂量油酸亦仅能引起轻度肺损伤。结论　ACEI能降低肺动脉高压 ,阻抑ARDS的病情进展并对肺血管内皮细胞有一定保护作用     

Acute and subacute toxicity study of inhaled methyl isocyanate in Charles Foster rats

Charles Foster male and female rats were exposed only once to 3.52 and 35.32 ppm doses of methyl isocyanate in separate experiments for 10 min each in an acute toxicity study, while in subacute toxicity experiments, they were exposed to 0.212, 0.265, and 0.349 ppm doses for 30 min daily, for 6 days, by inhalation. Clinical signs, mortality, body and organ weights, and changes in hematology and clinical pathology were routinely monitored to determine the principal organ sites damaged on exposure to the gas. During exposure, animals were observed to have congestion in eyes, lachrymation, nasal secretion and dyspnea, progressively increasing ataxia, and immobility. Uncoordinated movements were also observed, indicating effects on the nervous system. Upon microscopic examination of the viscera, pathological findings confined to bronchial tree, lung parenchyma, liver, and kidneys were observed.     

Influence of protein deficiency on cadmium toxicity in rats

The effects of a low protein diet on the body uptake and retention of cadmium, levels of essential trace elements, and cadmium-induced biochemical alterations in liver and kidneys of the rat were investigated. Low dietary protein disturbs cadmium induced alterations in carbohydrate metabolism, essential trace elements metabolism and offsets the hepatic and renal process of cadmium detoxification. Protein malnutrition enhances the susceptibility to cadmium intoxication.     

Influence of copper and iron on subacute cadmium intoxication in protein-malnourished rats

Male albino rats maintained on low-protein (9%) diets were dosed intraperitoneally with 0.75 mg Cd/kg, as cadmium chloride, for 20 days. Groups of these animals were provided with diets supplemented with 40 ppm Cu, 400 ppm Fe or a combination of both during the exposure period. Hepatic and renal distribution of Cd, Zn, Cu, and Fe along with activity of acid and alkaline phosphatases and ribonuclease and glutathione content were studied. Uptake of Cd both in liver and in kidney was significant and was accompanied by increased Zn and depletion of Fe concentration. The Cu level remained unaltered. Dietary supplementation of Cu or Fe interacted effectively and influenced the metal distribution. Acid and alkaline phosphatases in both liver and kidney were inhibited by Cd exposure. However, Cu and/or Fe supplements could to a varying degree offset the Cd-induced inhibition. Cadmium exposure did not, however, elicit any effect on hepatic and renal ribonuclease activity of low-protein-fed animals. The glutathione concentration registered profound increase on Cd exposure, possibly to act as a defence mechanism.