二硫化碳对血管内皮舒张因子的影响及其机制探讨

报道了亚慢性ＣＳ２接触对大鼠血管内皮衍生舒张因子／一氧化氮的影响及其机制探讨。用３２０，１６０ｍｇ／ｋｇＣＳ２染毒后血清ＮＯ水平下降，ＬＰＯ明显增高，与对照比较Ｐ＜０．０１，心肌一氧化氮合成酶活力无明显变化。分析显示：ＮＯ下降、与ＬＰＯ增高与ＣＳ２剂量密切相关。多元回归分析，Ｆ＝５时，ＬＰＯ是进入方程的唯一因素（ｒ＝－０．６６６５，Ｐ＜０．０１）；在ＣＳ２染毒同时给抗氧化剂后，血清ＬＰＯ水平下降，ＮＯ增高，Ｐ＜０．０１。提示：ＣＳ２可因致脂质过氧化作用而加快ＮＯ的氧化分解，导致ＮＯ下降，这在ＣＳ２心血管毒性机制中可能具有重要意义。     

过氧化氢亚急性吸入毒性研究

本研究应用Ｈ２Ｏ２蒸气（５．４，３２．１ｍｇ／ｍ３）进行大鼠亚急性吸入染毒。大鼠吸入Ｈ２Ｏ２蒸气后，发现血清ＡＫＰ和ＡＣＰ活性增高，全血ＣＡＴ及肺组织ＳＤＨ活性降低。同时还发现肺组织ＧＳＨ含量明显降低，ＭＤＡ含量显著升高。Ｈ２Ｏ２对呼吸系统不仅有刺激作用还可诱发对肺脏的氧化性损伤。     

三硝基甲苯对大鼠肾脏某些抗氧化酶活性的影响

本研究观察了三硝基甲苯（ＴＮＴ）不同剂量染毒和阳性对照安妥明处理对大鼠肾组织匀浆过氧化氢酶（ＣＡＴ）、谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）、超氧化物歧化酶（ＳＯＤ）活性及肾组织蛋白含量的影响。结果表明,ＴＮＴ染毒组、阳性对照组大鼠肾匀浆ＣＡＴ与ＧＳＨ－ＰＸ活性显著高于对照组（Ｐ＜０．０５）,而肾蛋白含量显著降低（Ｐ＜０．０５）,表明ＴＮＴ染毒和安妥明处理均可诱导肾组织过氧化氢生成。推测ＴＮＴ可能具有诱发肾脏过氧化物小体增生作用     

基因重组促红细胞生成素导致高血压的机制研究

目的：探讨基因重组促红细胞生成素（ｒ－ＨｕＥＰＯ）在治疗慢性肾衰（ＣＲＦ）贫血中导致高血压的机制及防治对策。方法：对ｒ－ＨｕＥＰＯ治疗中出现高血压的ＣＲＦ血液透析贫血患者１５例及对照组１５例，应用分光光度法及放免法观察治疗前后血浆一氧化氮代谢产物（ＮＯ２－／ＮＯ３－）及内皮素－１（ＥＴ－１）的变化。同时用大鼠进行对照试验。结果：１．ＣＲＦ贫血患者及贫血鼠用ｒ－ＨｕＥＰＯ１６周后，红细胞压积（Ｈｃｔ）升高、血压升高，ＥＴ－１增加（Ｐ＜０．０１），血浆ＮＯ２－／ＮＯ３－下降（Ｐ＜０．０５），而对照组用药前后无明显变化（Ｐ＞０．０５）。２．在用药１６周后，ＲＴＰＣＲ测得实验组大鼠肾皮质及髓质ｉＮＯＳｍＲＮＡ比对照组明显减少（Ｐ＜０．０５）。结论：研究表明ｒ－ＨｕＥＰＯ导致高血压与ｉＮＯＳｍＲＮＡ减少，合成的ＮＯ减少及ＥＴ－１增加有着重要的关系     

甲状腺功能状态对普萘洛尔药物动力学的影响

本文通过建立具有亚临床病例特点的实验性甲亢和甲低模型，以及通过参照文献的方法建立应用荧光分光光度计测定血浆中普萘洛尔（ｐｒｏｐｒａｎｏｌｏｌ）的方法，研究了甲状腺功能状态对普萘洛尔药物动力学的影响。结果如下：对照组，甲亢组和甲低组大鼠ｉｐ普萘洛尔４ｍｇ／ｋｇ，求得其主要药物动力学参数：Ｔ１／２β（ｈ）分别为４．５４±０．６５，３．５８±０．３５（Ｐ＜０．０５）和６．４±０．８（Ｐ＜０．０５）；Ｋ１０（ｈ－１）分别为０．９９±０．０２，１．２３±０．０９（Ｐ＜０．０１）和０．６６±０．０８（Ｐ＜０．０１）；ＡＵＣ〔ｎｇ／（ｍｌ·ｈ）〕分别为６５４．２±９０．４，４４８．２±６６．８（Ｐ＜０．０１）和１０３４．６±１３２．３（Ｐ＜０．０１）；ＣＬ〔ｍｇ／（ｋｇ·ｈ）／（ｎｇ·ｍｌ）〕分别为０．００６２２±０．０００９６，０．００９１±０．００１６（Ｐ＜０．０１）和０．００３９２±０．０００５８（Ｐ＜０．０１）；Ｃｍａｘ（ｎｇ／ｍｌ）分别为５０１．４６±４０．１３，４０８．３３±５７．６５（Ｐ＜０．０１）和６０７．８±２７．２（Ｐ＜０．０１）。     

复方丹参对急性汞中毒家兔血浆、肾组织脂质过氧化物的清除作用

目的：观察复方丹参注射液对急性汞中毒家兔血浆、肾组织脂质过氧化物（ＬＰＯ）的清除作用。方法：家兔３０只，分３组，汞中毒组和治疗组皮下注射ＨｇＣｌ２１．７ｍＬ／ｋｇ（每ｍＬ含ＨｇＣｌ２１０ｍｇ）。治疗组在注汞后３０ｍｉｎ及１０ｈ分别给予复方丹参注射液２ｍＬ／ｋｇ，ｉｖ。正常对照组及汞中毒组给予等剂量生理盐水。各组在中毒前、中毒后分别测定血浆、肾组织ＬＰＯ及血尿素氮（ＢＵＮ）。结果：急性汞中毒组血浆、肾组织ＬＰＯ及ＢＵＮ明显升高（Ｐ＜０．０１）。治疗组均明显下降（Ｐ＜０．０１）。结论：复方丹参注射液对汞中毒家兔血浆及肾组织ＬＰＯ有清除作用。     

小儿肺部疾患时超氧化物歧化酶及丙二酶的改变

我科自１９９３年７月－１９９４年１月的住院病人中，选择肺部疾患患儿５２例（包括肺炎３２例，喘息性支气管炎１１例，支气管哮喘９例），测定红细胞超氧化物歧化酶（ＳＯＤ）活性和血浆丙二醛（ＭＤＡ）的含量。结果表明在患病极期ＳＯＤ活性校对照组明显下降（Ｐ＜０．０１）；ＭＤＡ的含量较对照组明显升高（Ｐ＜０．０１）。在３２例肺炎患儿中ＳＯＤ活性与对照组比较有所下降（０．０１＜Ｐ＜０．０５）；ＭＤＡ含量较对照组比较明显升高（Ｐ＜０．０１）。说明氧自由基（ＯＦＲ）与小儿肺部疾患有密切关系，并参与了该病的病理过程。     

Menadione reduced doxorubicin resistance in Ehrlich ascites carcinoma cells in vitro

目的：研究维生素Ｋ３（Ｍｅｎ）降低ＥＡＣ／Ｄｏｘ细胞对阿霉素（Ｄｏｘ）的抗药性．方法：测定谷胱甘肽（ＧＳＨ），细胞膜流动性及谷胱甘肽Ｓ转移酶（ＧＳＴ）活性．细胞存活力以甲基四唑蓝法测定．结果：ＥＡＣ／Ｄｏｘ细胞ＧＳＨ，ＧＳＴ及膜流动性均较ＥＡＣ细胞增加（Ｐ＜００１）．Ｄｏｘ对ＥＡＣ／Ｄｏｘ细胞ＩＣ５０为２２３（１５８－２８８）ｍｇ·Ｌ－１．Ｍｅｎ５或１０ｍｇ·Ｌ－１可降低ＥＡＣ／Ｄｏｘ细胞ＧＳＨ（Ｐ＜００１），１ｍｇ·Ｌ－１对ＧＳＨ无影响（Ｐ＞００５），但可降低细胞膜流动性（Ｐ＜００５）．Ｍｅｎ１，５或１０ｍｇ·Ｌ－１可使ＤｏｘＩＣ５０降低到９．６（７８－１１３），６０（２８－９２），或５３（３９－６７）ｍｇ·Ｌ－１（Ｐ＜００１）．结论：Ｍｅｎ在体外降低ＥＡＣ／Ｄｏｘ细胞对Ｄｏｘ抗药性与对ＧＳＨ的耗竭有关．     

脂必妥对大鼠高脂血症模型血脂水平的影响

目的：研究脂必妥的降脂疗效。方法：通过对大鼠腹腔注射脂酶抑制剂——１０％泰洛沙泊溶液（３ｍＬ／ｋｇ）后７ｍｉｎ，分别用脂必妥２．５９，１．２９，０．６５ｇ／ｋｇ，及洛伐他汀１０ｍｇ／ｋｇ灌胃给药。结果：脂必妥２．５９ｇ／ｋｇ组及洛伐他汀组（１０ｍｇ／ｋｇ）的胆固醇（ＴＣ）值分别降低３３％（Ｐ＜０．０１）及３１％（Ｐ＜０．０１），组间比较Ｐ＞０．０５；低密度脂蛋白胆固醇（ＬＤＬ－ｃｈ）值分别降低５０％（Ｐ＜０．０１）及４４％（Ｐ＜０．０１）；脂必妥１．２９ｇ／ｋｇ组亦能降低ＴＣ及ＬＤＬ－ｃｈ值１８％（Ｐ＜０．０５）及２６％（Ｐ＜０．０５）；小剂量０．６５ｇ／ｋｇ的脂必妥仅能降低ＴＣ１４％（Ｐ＜０．０５）；各组对三酰甘油（ＴＧ）值均无显著降低作用（Ｐ＞０．０５）。结论：脂必妥有显著降低血脂过多大鼠ＴＣ及ＬＤＬ－ｃｈ值的作用。     

多塞平对大鼠急性脑缺血再灌注损伤的保护作用

目的：观察多塞平对大鼠急性脑缺血再灌注引起损伤的保护作用。方法：６０只大鼠，分为多塞平大、中、小剂量（１５，１０，５ｍｇ／ｋｇ）组，尼莫地平阳性对照组、空白对照组和假手术对照组。用阻断四血管方法造成大鼠急性脑缺血再灌注损伤，原子吸收分光光度计测定脑组织Ｃａ２＋，Ｎａ＋，Ｋ＋的含量。结果：与空白对照组比较，尼莫地平阳性对照组和多塞平大、中剂量组脑组织Ｃａ２＋，Ｎａ＋，Ｈ２Ｏ含量显著降低（Ｐ＜０．０５或Ｐ＜０．０１）；多塞平小剂量组脑组织Ｃａ２＋含量显著降低（Ｐ＜０．０５），其余含量变化均不显著（Ｐ＞０．０５）。结论：多塞平能显著降低因缺血引起的脑组织Ｃａ２＋，Ｎａ＋，Ｈ２Ｏ含量增高，表现出钙拮抗作用     

The possible role of the ethanol-inducible isozyme of cytochrome P450 in the metabolism and distribution of carbon disulfide

Acute treatment with ethanol and other alcohols has been shown to potentiate the hepatotoxicity of certain xenobiotics, in part via induction of the mixed-function oxidase (MFO) system. Carbon disulfide (CS2)-induced hepatotoxicity and inhibition of the MFO system have been shown to be a consequence of MFO metabolism. In the present study, the ability of several different alcohols to induce the hepatic MFO metabolism of CS2 and the effects of this induction on CS2 distribution and hepatotoxicity were examined in rats. Eighteen hours after alcohol administration (1/2 LD50 dose, po), CS2 microsomal MFO metabolism was significantly enhanced, in order of descending potency, by isopropanol, methanol, and ethanol pretreatments, but not by isobutanol pretreatment. The degree of enhancement of CS2 metabolism by different alcohols paralleled the enhancement of nitroanisole O-demethylation and aniline hydroxylation, MFO activities associated with the ethanol-inducible isozyme of cytochrome P450. CS2 (1 mg/kg, ip, 3 hr) inhibited only the cytochrome P450-mediated activities enhanced by alcohol pretreatment. These results suggest that CS2 metabolism is catalyzed by the ethanol-inducible isozyme. Alcohol-induced rats had significantly more 14CS2-derived radioactivity in the liver than control and isobutanol-pretreated rats 3 hr after dosing (1 mg/kg, ip). However, only methanol pretreatment resulted in an increased retention of 14CS2-derived radioactivity in plasma, brain, and kidney. Unlike other alcohol pretreatments, methanol decreased the total 14C expired during the 3-hr period after CS2 dosing and caused a significant (twofold) increase in plasma glutamic-pyruvic transaminase, measured 24 hr after CS2 exposure (625 mg/kg). These data indicate that alcohol induction of MFO-dependent CS2 metabolism per se is not sufficient to result in CS2-induced hepatic damage although it does lead to loss of specific cytochrome P450 function.     

MESENTERIC VASCULAR ANGIOTENSIN-CONVERTING ENZYME IS INCREASED IN EXPERIMENTAL DIABETES MELLITUS

1. Diabetes mellitus was induced by streptozotocin in male Wistar rats, and angiotensin-converting enzyme measured in plasma and mesenteric vessels 3 weeks later. 2. Diabetes was associated with increased mesenteric wet weight/bodyweight ratio (control 0.2 s.e.m. 0.02 mg/g, n = 21, vs diabetes 1.0 s.e.m. 0.3 mg/g, n = 27, P less than 0.01, ANOVA). 3. Plasma angiotensin-converting enzyme activity was increased in diabetic rats (98 s.e.m. 3 nmol HL/mL per min) compared with controls (64 s.e.m. 6 nmol HL/mL per min, P less than 0.01, ANOVA). 4. Mesenteric vessel angiotensin-converting enzyme was increased in diabetes mellitus estimated by radioligand binding site density (fmol/mg protein; 1407 s.e.m. 166 fmol/mg protein) compared with controls (890 s.e.m. 56 fmol/mg protein, P less than 0.05, ANOVA) and by enzyme kinetic assay (diabetes, 15.5 s.e.m. 1.5 nmol HL/mg protein per min, controls, 8.3 s.e.m. 0.7 nmol HL/mg protein per min, P less than 0.01, ANOVA). The equilibrium dissociation constant of ligand-angiotensin-converting enzyme interaction was unchanged. 5. Increased vascular angiotensin-converting enzyme concentration may contribute to vascular hypertrophy and diabetic vasculopathy by increased local synthesis of angiotensin II.     

中分子质量岩藻聚糖硫酸酯的抗血栓活性及作用机制

目的观察中分子质量岩藻聚糖硫酸酯(MMWF)的抗血栓作用并探讨其作用机制。方法 50只大鼠随机分为正常对照组、模型组、阿司匹林组、MMWF0.25 mg·kg~(-1)组和0.1mg·kg~(-1)组,采用下腔静脉血栓模型,考察血栓湿重和血栓抑制率。酶联免疫吸附测试法(ELISA)测定动物血浆抗凝血酶-Ⅲ(AT-Ⅲ)、蛋白质C(PC)、纤溶酶原(PLG)、组织型纤溶酶原激活物(t-PA)和纤溶酶原激活物抑制物-1(PAI-1)指标。另外50只大鼠按前述分组,通过大鼠血瘀模型考察血液流变学改变。结果在静脉血栓模型中,与正常对照组比较,模型组的AT-Ⅲ和PC活性、t-PA含量及t-PA/PAI-1比值均显著降低,PAI-1和PLG含量显著增加(均P<0.01)。与模型组和阿司匹林组比较,MMWF 0.25 mg·kg~(-1)组和0.1 mg·kg~(-1)组血栓湿重均显著减轻(均P<0.01),AT-Ⅲ和PC无显著改变(P>0.05),t-PA含量和t-PA/PAI-1比值显著升高,PAI-1和PLG含量显著降低(均P<0.01)。在血瘀模型中,与正常对照组比较,模型组的全血黏度、血浆黏度、血细胞比容、红细胞沉降率及红细胞沉降率方程K值等血液流变学指标均有明显升高(均P<0.01)。与模型组比较,MMWF 0.25 mg·kg~(-1)和0.1 mg·kg~(-1)组上述指标均显著改善(P<0.05或P<0.01)。结论 MMWF具有明显的抗血栓作用,其机制可能与增加纤溶作用和改善血液流变学性质有关。     

长期服用生大黄、熟大黄对大鼠肝肾功能影响的比较

目的:观察生、熟大黄对SD大鼠肝、肾功能的作用,明确生、熟大黄的毒性作用差异。方法:生、熟大黄总提物10 g·kg^-1给予大鼠灌胃95 d,相当于临床用量的100倍,观察对大鼠行为活动、肝肾功能、电解质影响,并对大鼠脏器进行系统观察和组织病理学检查。结果:与正常对照组比较,生大黄组、熟大黄组的BUN、Cys-c、Crea、β2-MG显著性升高、Na⁺显著降低(P<0.01);与生大黄组相比,熟大黄组的BUN、Cys-c、Crea、β2-MG均显著性下降、Na⁺显著升高(P<0.01~0.05);生大黄组大鼠肾脏有色素沉积、肿胀变性,熟大黄组大鼠色素沉积。结论:长期服用生、熟大黄对大鼠的肾功能有一定的损伤,熟大黄可减轻生大黄的肾损伤作用。     

Cardiotoxicity in rats induced by methidathion and ameliorating effect of vitamins E and C

We have examined the effect of subchronic methidathion (MD) administration on heart damage, and have evaluated possible ameliorating effects of a combination of vitamins E and C against MD toxicity. The experimental groups were: control group, rats treated with 5 mg/kg MD and rats treated with 5 mg/kg body weight MD plus vitamin E and vitamin C (MD+Vit). The groups were given MD by gavage 5 days a week for four weeks at a dose level of 5 mg/kg/day (MD and MD+Vit) by using corn oil as the vehicle. Vitamin E and vitamin C were injected at doses of 50 mg/kg i.m. and 20 mg/kg i.p., respectively, after the treatment with MD in the MD+ Vit group. The levels of malondialdehyde (MDA) were determined in the heart tissue, and the levels of cardiac troponin I (TnI) in serum. An autoanalyser was used to determine the serum activities of cholinesterase (ChE). Histopathological examination was carried out in the heart tissue. MDA significantly increased in the MD group as compared to controls (P <0.01). When MD was given concurrently with vitamins E and C, the increase in MDA was significantly less (P <0.01). ChE activity significantly decreased in the MD group as compared to controls (P <0.01). When MD was given concurrently with vitamins E and C, the decrease in ChE activity was significantly higher (P <0.05). The serum TnI levels significantly increased in the MD group as compared to controls (P <0.01). When MD was given concurrently with vitamins E and C, the increase in the serum TnI was significantly less (P <0.01). MD caused the diffuse loss of striation and myocytolysis of the cardiomyocytes, whereas the combination of vitamins E and C caused a significant decrease in these effects of MD. In conclusion, subchronic MD administration caused heart damage and, in addition, treatment with a combination of vitamins E and C after the administration of MD reduced heart damage caused by MD.     

脑瘤消胶囊对环己亚硝脲减毒作用的实验研究

目的观察脑瘤消胶囊对环己亚硝脲（CCNU）所致S180肉瘤小鼠骨髓造血功能与肝肾功能损害的预防治疗作用。方法在建立S180肉瘤小鼠模型的基础上,设荷瘤空白对照组（以生理盐水灌胃）、环己亚硝脲组（以40mg／kg的CCNU灌胃）及CCNU＋小剂量NLX组、CCNU＋中剂量NLX组、CCNU＋大剂量NLX组5％平消胶囊混悬液和40mg／kg的CCNU灌胃）;检测外周血象与肝肾功能、骨髓粒细胞、红细胞数,测定脾脏指教和（分别以2．5％、5％、10％的脑瘤消胶囊混悬液和40mg／kg的CCNU灌胃）和平消胶囊＋CCNU组（以胸腺指数。结果脑瘤消胶囊在500、1000、2000mg／kg剂量并联合CCNU时,与CCNU单用组比较,可对抗环己亚硝脲引起的荷瘤S180小鼠外周血白细胞和网织红细胞减少（P〈0．01）,可使荷瘤S180小鼠骨髓柱细胞比值上升和骨髓红细胞比值回落（P〈0．01）,可减轻CCNU引起的小鼠肝功能损害（P〈0．05）,对肾功能无明显影响（P〉0．05）;可升高荷瘤S180小鼠胸腺和脾脏指数（P〈0．01）。结论脑瘤消胶囊可对抗细胞毒药物环己亚硝脲所引起的骨髓遣血功能和肝功能损害及免疫抑制作用。     

尿石汤配方颗粒改善肾草酸钙结石大鼠肾功能效果及其机制

目的:探讨尿石汤配方颗粒改善肾草酸钙结石(CaXO)大鼠肾功能效果及其机制.方法:建立草酸钙肾结石大鼠模型,检测大鼠造模前后体质量变化,肾脏质量、脏器系数变化,排尿量、尿液pH、尿液Ca2+、尿液结晶数量及类型,观察肾结石模型在大鼠机体上的宏观变化.采用He染色和Von-Kossa'S染色,观察尿石汤配方颗粒对肾结石模...     

慢性氟中毒大鼠肾脏自由基含量与形态学变化

目的研究慢性氟中毒大鼠肾脏自由基含量与形态学变化的关系。方法wistar大鼠随机分为三组。正常对照组,未作任何处理;染氟组,自由饮用含氟化钠132．6mg／L的含氟水;抗氧化中药一染氟组,自由饮用含氟化钠132．6mg／L的含氟水,同时每日经腹腔内注射抗氧化中药丹参绞股蓝复方3．125毫克／公斤／天,实验6个月时检查动物。用电子自旋共振的方法检测肾组织内自由基的含量,并观察肾脏的形态学变化。结果与正常对照组动物相比,染氟组自由基明显升高,电镜下见肾小管上皮细胞有巨大线粒体及髓鞘样结构形成,内质网扩张,粗面内质网上核糖体脱落,细胞浆内游离核糖体增加,胞核内异染色质有向核膜下聚集的趋势;光镜下呈颗粒性变,偶见坏死。抗氧化中药一染氟组肾组织中自由基含量不增高,光镜及电镜下均未见明显病变。结论慢性氟中毒时肾脏病变与自由基含量增多有密切关系。     

Effect of treatment with mercury chloride and lead acetate during the second stage of rapid postnatal brain growth on δ-aminolevulinic acid dehydratase (ALA-D) activity in brain, liver, kidney and blood of suckling rats

The sensitivity of developing rodents to toxic metals differs considerably from that of adults. In the present study, we investigated the in vivo and in vitro effects of inorganic mercury and lead on δ-aminolevulinic acid dehydratase (ALA-D) from brain, liver, kidney and blood of young rats. Eight day-old rats were injected with one or five doses of lead acetate (0, 3.5, or 7.0 mg/kg) or HgCl₂ (0, 2.5, or 5.0 mg/kg). In vitro, the IC₅₀ for mercury inhibition of cerebral, renal and hepatic ALA-D was in the 124 to 160 μM range, while values for lead acetate was in the 7 to 12 μM range. The IC₅₀ of blood enzyme for lead (0.8 μM) and mercury (6.5 μM) was significantly lower than that observed for the other tissues. A single dose of lead did not affect the enzyme activity, but a single dose of HgCl₂ (5 mg/kg) caused a significant inhibition of ALA-D from kidney (40%, P < 0.01) and liver (25%, P < 0.05). Five doses of lead acetate (3.5 or 7 mg/kg) caused an inhibition of about 25 and 40%, respectively (P < 0.01), of hepatic ALA-D, and an increase of 1.4-fold (P < 0.05) and 2.6-fold (P < 0.01) of blood enzyme, respectively. Treatment with five doses of HgCl₂ (5 mg/kg) caused an inhibition of about 25, 60, 50, and 80% of ALA-D from brain, blood, liver and kidney, respectively (all P < 0.05). Five doses of 2.5 mg/kg HgCl₂ caused an inhibition of ALA-D from liver (40%, P < 0.01) and kidney (45%, P < 0.01). These results demonstrate that ALA-D from young rat tissues show different sensitivities to mercury and lead. The enzyme was more affected by mercury than by lead in vivo, while in vitro lead was more potent that mercury as an ALA-D inhibitor.     

甲基肼及氯化汞对大鼠的急性肾损伤

大鼠ip甲基肼(MMH)25mg/kg及60mg/kg;sc HgCl_2 0.5 mg/kg及5mg/kg后不同时间测定尿中酶活性及蛋白质含量和组分的变化。结果表明MMH两种剂量对尿中NAG、LDH及ALP均无明显影响,但尿蛋白排泄明显增加及SDS-PAGE图谱明显改变。血液学检查表明血管内无溶血。HgCl_2 0.5mg/kg对尿中NAG,LDH及ALP无明显影响,5mg/kg时尿中这三种酶活性均明显升高。两种剂量均引起尿蛋白排泄增加,SDS-PAGE图谱明显改变。