硒对大鼠血清蛋白、血脂的亚慢毒性作用研究

硒对大鼠血清蛋白、血脂的亚慢性作用研究结果表明，大鼠在长期高硒摄入的条件下，其血清蛋白、血脂等项生化指标，与对照组相比，均有不同程度的降低，且随摄入硒的剂量增大，降低得越多。说明高硒对肝脏具有一定的毒性作用。

拉米夫定治疗病毒性肝炎乙型慢加亚急性肝衰竭临床观察

目的了解病毒性肝炎乙型慢加亚急性肝衰竭患者使用拉米夫定抗病毒治疗疗效、对预后的影响及不良反应。方法对65例病毒性肝炎乙型慢加亚急性肝衰竭患者,随机分为治疗组(31例)和对照组(34例),治疗组在综合治疗基础上加用拉米夫定抗病毒治疗。结果治疗组HBVDNA转阴率78.7%,对照组12.5%,治疗组好转率89.4%,对照组76.7%,死亡率治疗组10.5%,对照组23.26%。治疗组对照组治疗后比较,差异有显著性(P<0.05)。结论综合治疗基础上加用拉米夫定抗病毒,能有效抑制病毒复制,提高好转率,降低死亡率,且近期无明显不良反应。

之江菌素的毒性实验

之江菌素对ＩＣＲ小鼠灌胃，ＬＤ５０为１１５３．８ｍｇ／ｋｇ，属低毒物质。致畸致突变试验阴性。亚慢毒性试验表明，大鼠饲喂含之江菌素４００ｐｐｍ的饲料连续２８ｄ，对生长发育、饲料利用率、血液及生化指标。

丙炔菊酯的毒性研究

目的 了解丙炔菊酯的急性与亚慢性毒性、刺激性、突变性和致敏性。方法 按国家标准GB15 6 70 -1995《农药登记毒理学试验方法》进行大鼠急性经口、经皮与吸入毒性试验 ,小鼠急性皮下、腹腔注射试验 ,皮肤致敏试验 ,Ames试验和亚慢性经口试验。结果 大鼠急性经口LD50 :雌性为 5 0 1mg/kg ,雄性为 92 6mg/kg ;经皮LD50 :雌性为 2 6 10mg/kg ,雄性大于 2 15 0mg/kg ;急性吸入LC50 为 471 5mg/m3;小鼠急性皮下注射LD50 :雌性为 2 710mg/kg ,雄性为 2 370mg/kg ;急性腹腔注射LD50 :雌、雄鼠均为 316mg/kg ;眼、皮肤刺激为轻度刺激性 ;Ames试验为阴性 ;皮肤致敏率为 6 7% ;亚慢性经口毒性试验最大无作用剂量为每天 2 340mg/kg。结论 丙炔菊酯的急性经口、经皮毒性为低毒级 ,急性吸入毒性为中毒级 ;为弱致敏物 。

氟化钇、铽、镱和镨的卫生标准

俄罗斯“工人健康保护和预防医学科学中心”的对氟化钇、铽、镱和镥的化合物进行了毒性实验研究,提出了工作场所空气中上述稀土氟化物的最大一次允许浓度和工作班平均允许浓度的卫生标准。作者选用雌性和雄性非良种小白鼠和大白鼠,通过腹腔内和胃内注入染毒,进行了急性和亚慢毒性实验研究。对家兔进行了皮肤及粘膜的刺激性实验研究。 急性毒性实验:腹腔内一次注入氟化镱和氟化铽的致死剂量达到10g/kg。

Autoantibodies and hepatitis C virus genotypes in chronic hepatitis C patients in Estonia

AIM: To determine the prevalence of several autoantibodies in chronic hepatitis C patients, and to find out whether the pattern of autoantibodies was associated with hepatitis C virus (HCV) genotypes. METHODS: Sera from 90 consecutive patients with chronic hepatitis C were investigated on the presence of anti-nuclear (ANA), anti-mitochondrial (AMA), anti-smooth muscle (SMA), anti-liver-kidney microsomal type 1 (LKMA1), anti-parietal cell (PCA), anti-thyroid microsomal (TMA), and anti-reticulin (ARA) autoantibodies. The autoantibodies were identified by indirect immunofluorescence. HCV genotypes were determined by a restriction fragment length polymorphism analysis of the amplified 5' noncoding genome region. RESULTS: Forty-six (51.1%) patients were positive for at least one autoantibody. Various antibodies were presented as follows: ANA in 13 (14.4%) patients, SMA in 39 (43.3%), TMA in 2 (2.2%), and ARA in 1 (1.1%) patients. In 9 cases, sera were positive for two autoantibodies (ANA and SMA). AMA, PCA and LKMAI were not detected in the observed sera. HCV genotypes were distributed as follows: 1b in 66 (73.3%) patients, 3a in 18 (20.0%), and 2a in 6 (6.7%) patients. CONCLUSION: A high prevalence of ANA and SMA can be found in chronic hepatitis C patients. Autoantibodies are present at low titre (1:10) in most of the cases. Distribution of the autoantibodies show no differences in the sex groups and between patients infected with different HCV genotypes.

The expression of Bcl-2 and Bax produced by sub-chronic intoxication with the cyanotoxin Microcystin-LR

Objective:We explored the role and molecular mechanism of Microcystin-LR(MC-LR) in hepatocarcinogenesis.Methods:The two-stage-medium-term theory was applied to the establishment of the animal model.The promoting effect of MC-LR on liver tumor was evaluated with the Albert γ-GT methods.During the tumor-promoting course,the effects of MC-LR on the regulation and expression of the Bcl-2 and Bax genes were studied with immunohistochemical technique and RT-PCR.Results:MCLR could enhance the positive reaction of Albert γ-GT(GGT),a preneoplasm marker.The positive reaction rate of GGT in diethylnitrosamine(DEN) + MC group was significantly higher than that in the DEN control group.The protein and RNA expression of Bcl-2 was significantly increased by MC-LR,and that the protein expression of Bax was decreased simultaneously.Conclusion:These results indicate that the MC-LR can inhabit apoptosis through the Bcl-2 and Bax genes.Therefore,we conclude that the expression change of Bcl-2 and Bax genes possibly plays an important role in the promotion of liver tumor by MC-LR.

朱砂及含朱砂制剂的肝肾毒性研究

目的探讨朱砂、含朱砂制剂(柏子养心片)及甲基汞对大鼠的体内外毒性,为其临床安全用药提供科学依据。方法(1)对比甲基汞、朱砂及柏子养心片体外对人肝HL-7702细胞和人肾近曲小管上皮HK2细胞的毒性,计算半数抑制浓度(IC_(50))。(2)SD大鼠随机分为对照组,朱砂组0.1 g/kg,柏子养心片0.2、0.4、0.8 g/kg组,甲基汞组0.001 g/kg,每天ig 1次,连续给药90 d后,取血及肝、肾组织;试剂盒法检测血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、肌酐(CREA)、尿素氮(BUN)水平,测汞仪固体直接进样法检测肝、肾组织中汞蓄积量,并对大鼠肝脏和肾脏做组织病理学检查。结果体外试验表明,朱砂、柏子养心片及甲基汞对HL-7702细胞的IC_(50)分别为7.852、6.035、0.009 5 g/L;对HK2细胞的IC_(50)分别为6.297、4.484、0.008 9 g/L。亚慢性毒性试验表明,甲基汞组大鼠肝、肾组织中汞蓄积量及血清中ALT、AST、CREA、BUN值均显著高于对照组,而朱砂及柏子养心片(高、中、低剂量)组与对照组比较均没有显著性差异;甲基汞组大鼠肝脏呈现肝细胞变性,肾脏可见明显肾小管损伤,而朱砂及柏子养心片(高、中、低剂量)组与对照比较没有明显差异。结论朱砂及柏子养心片的体内外毒性均显著低于甲基汞,在目前药典规定的临床用量下使用安全性较好。

A combined dynamic inhalation device designed for moxa-smoking toxicity testing

OBJECTIVE： To design a combined dynamic inhalation device for testing the toxicity induced by moxa smoking. METHODS： The new apparatus （Patent No. 201120101911.5） includes air renewal and recycling systems, a gas generating device, a gas control unit, and a device to measure and control tem- perature and humidity. Sprague-dawley rats were tested for acute and sub-chronic toxicity after exposure to moxa-burning smoke.METHODS： The new apparatus （Patent No. 201120101911.5） includes air renewal and recycling systems, a gas generating device, a gas control unit, and a device to measure and control tem- perature and humidity. Sprague-dawley rats were tested for acute and sub-chronic toxicity after exposure to moxa-burning smoke.RESULTS： We found an LQ0 of 1.2× 10^4 mg/m^3 in the acute toxicity assays. In sub-chronic toxicity tests the organ coefficients studied showed no sig-nificant differences within rats groups of the same gender after treatment with moxa smoke or a month of recovery. However, mean gray degree of lung 70 heat shock protein （HSP70） was significantly elevated in the high dose group in comparison with the low dose group （P 〈 0.05）, mean gray degree, mean optical density, gross area of HSP70 in other organs and caspase-9 parameters showed no significant differences between groups.CONCLUSION： These results suggest that moxa smoke had no overt toxicity in rats. This work pro- vides evidence and reference for the design of dy- namic inhalation exposure systems.

Effects of subchronic oral toxic metal exposure on the intestinal microbiota of mice

Oral exposure to toxic metals such as cadmium （Cd）, lead （Pb）, copper （Cu） and aluminum （AI） can induce various adverse health effects in humans and animals. However, the effects of these metals on the gut microbiota have received limited attention. The present study demonstrated that long-term toxic metal exposure altered the intestinal microbiota of mice in a metal-specific and time-dependent manner. Subchronic oral Cu exposure for eight weeks caused a profound decline in gut microbial diversity in mice, whereas no significant changes were observed in groups treated with other metals. Cd exposure signif- icantly increased the relative abundances of organisms from the genera Alistipes and Odoribacter and caused marked decreases in Mollicutes and unclassified Ruminococcaceae. Pb exposure significantly decreased the abundances of eight genera： unclassified and uncultured Ruminococcaceae, unclassified Lachnospiraceae, Ruminiclostridium_9, Rikenellaceae_RCg_gut group, Oscillibacter, Anaerotruncus and Lachnoclostridium. Cu exposure affected abundances of the genera Alistipes, Bacteroides, Ruminococcaceae_UCG-014, AUobaculum, Mollicutes_RF9_norank, Rikenellaceae_RCg gut_group, Ruminococcaceae_unclassified and Turicibacter. A1 exposure increased the abundance of Odoribacter and decreased that of Anaerotruncus. Exposure to any metal for eight weeks significantly decreased the abun- dance of Akkermansia. These results provide a new understanding regarding the role of toxic metals in the pathogenesis of intestinal and systemic disorders in the host within the gut microbiota framework.