羧乙基锗倍半氧化物在黄曲霉毒素B1致大鼠肝癌过程中的抗氧化作用研究

目的与方法：本文采用ＡＦＢ１致大鼠肝癌体内短期实验模型，测定血清与肝组织的ＳＯＤ活力，进一步研究摄入Ｇｅ－１３２的剂量、时间与抗氧化作用的关系。结果：发现Ｇｅ－１３２具有抵抗ＡＦＢ１降低ＳＯＤ活力的作用，Ｇｅ－１３２的摄入时间、剂量可影响ＳＯＤ活力大小。结论：Ｇｅ－１３２的抗氧化作用与抑癌作用有关，并具有一定的防癌作用。     

有机锗Ge—132对肝脏缺血再灌注损伤的保护作用

目的：研究有机锗Ｇｅ－１３２对肝脏缺血再灌注损伤过程的影响。方法：将４０只Ｗｉｓｔａｒ大鼠平均分成４个组：模拟手术组,对照组（缺血再灌注损伤模型组）,丹参预处理组及有机锗Ｇｅ－１３２溶液、丹参注射液。测定各实验组大鼠肝组织内ＭＤＡ含量,ＳＯＤ、ＧＳＨ－ＰＸ活性,Ｎａ＾＋、Ｋ＾＋－ＡＴＰ酶,Ｃａ＾２＋－ＡＴＰ酶活力。各实验组大鼠肝组织行病理检查。结果：发现预处理组大鼠肝组织内ＳＯＤ,ＧＳＨ－ＰＸ活性     

大、小鼠摄入AFB_1和羧乙基锗倍半氧化物体内超氧化物歧化酶变化研究

本实验通过观察摄入ＡＦＢ１及Ｇｅ－１３２后Ｗｉｓｔａｒ大鼠和昆明小鼠体内ＳＯＤ活力的变化，进一步了解ＡＦＢ１代谢途径和Ｇｅ－１３２与自由基的关系。实验表明，摄入ＡＦＢ１的ＳＯＤ活力受到抑制，而摄入Ｇｅ－１３２后ＳＯＤ活力得到提高，且一次性摄入ＡＦＢ１后ＳＯＤ活力最终得到恢复，其中大鼠对ＡＦＢ１敏感性相对较大。     

有机锗(Ge-132)对大鼠肝细胞色素P_(450)、EROD活性抑制作用的研究

利用雄性ＳＤ大鼠每日经口给予有机锗（Ｇｅ－１３２）１００、２５０、５００ｍｇ／ｋｇ连续二十五ｄ，发现高剂量组的肝细胞色素Ｐ４５０受到明显抑制（Ｐ＜０．０５）。对Ｐ４４８的标志酶乙氧基异吩口恶唑脱乙氧基酶（ＥＲＯＤ）的抑制也近５０％；动物以Ｇｅ－１３２５００ｍｇ／ｋｇ／ｄ预先处理２０ｄ，再分别给予苯巴比妥钠盐（ＰＢ）、３－甲基胆蒽（３－ＭＣ），发现Ｇｅ－１３２对ＰＢ诱导Ｐ４５０的抑制不明显，而对３－ＭＣ诱导ＥＲＯＤ的抑制仍达３３％。     

有机锗（Ge—132）对大量肝细胞色素P450,EROD活性抑制作用的研究

利用雄性ＳＤ大鼠每日经口给予有机锗（Ｇｅ－１３２）１００、２５０、５００ｍｇ／ｋｇ连续二十五ｄ，发现高剂量组的肝细胞色素Ｐ４５０受到明显抑制（Ｐ〈０．０５）。对Ｐ４４８的标志酶乙氧基异吩恶唑脱乙氧基酶（ＥＲＯＤ）的抑制也近５０％；动物以Ｇｅ－１３２５００ｍｇ／ｋｇ／ｄ预先处理２０ｄ，再分别给予苯巴比妥钠盐（ＰＢ）、３－甲基胆蒽（３－ＭＣ），发现Ｇｅ－１３２对ＰＢ诱导Ｐ４５０的抑制不明显，而对３－Ｍ     

STUDY ON EXPRESS OF a-HCG AND a-HCGmRNA IN PANCREATIC ENDOCRINE TUMORS

ＳＴＵＤＹＯＮＥＸＰＲＥＳＳＯＦａＨＣＧＡＮＤａＨＣＧｍＲＮＡＩＮＰＡＮＣＲＥＡＴＩＣＥＮＤＯＣＲＩＮＥＴＵＭＯＲＳＹｕＪｉｙａｏ虞积耀ＣｅｓａｒｅＢｏｒｄｉＧｅｎｅｒａｌＨｏｓｐｉｔａｌｏｆｔｈｅＮａｖｙ，Ｂｅｉｊｉｎｇ１０００３７Ｃｈｉｎａ...     

EXPRESSION OF P53 AND C-MYC IN MOUSE LUNG CANCER INDUCED BY COAL BURNING

ＥＸＰＲＥＳＳＩＯＮＯＦＰ５３ＡＮＤＣ－ＭＹＣＩＮＭＯＵＳＥＬＵＮＧＣＡＮＣＥＲＩＮＤＵＣＥＤＢＹＣＯＡＬＢＵＲＮＩＮＧＬｉｎＣｈｕｎｙａｎ林春艳，ＤａｉＸｕｄｏｎｇ戴旭东，ＳｕｎＸｉｗｅｎ孙喜文，ＬｉＦｅｎｇｈｕａ李风华，ＳｈｉＹｕｂｏ石于波（Ｃａ...     

硒酸酯多糖对癌症患者血清MDA含量及CuZn—SOD活性的影响

了解硒酸酯多糖对肿瘤患者丛内ＭＤＡ及ＣｕＺｎ－ＳＯＤ活性的影响。方法；对６０例肿瘤病人随机分成３组：不服硒组，服硒４００μｈ／ｄ组及服８００μｇ／ｄ组并与１５名正常人对照比较。结果：癌症患者血清ＭＤＡ明显高于正常人，血清Ｓｅ及ＣｕＺＮ－ＳＯＤ活性明显低于正常人，服硒酸酯多糖者化疗后血清Ｓｅ较不服者明显升高，ＣｕＺｎ－ＳＯＤ也明显升高，ＭＤＡ含量显著下降；     

QUALITATIVE STUDY OF SIALOMUCINS CHANGES DURING N－METHYL－N－NITROSOUREA－INDUCED C OLONIC CARCINOGENESIS IN MICE

ＱＵＡＬＩＴＡＴＩＶＥＳＴＵＤＹＯＦＳＩＡＬＯＭＵＣＩＮＳＣＨＡＮＧＥＳＤＵＲＩＮＧＮ－ＭＥＴＨＹＬ－Ｎ－ＮＩＴＲＯＳＯＵＲＥＡ－ＩＮＤＵＣＥＤＣＯＬＯＮＩＣＣＡＲＣＩＮＯＧＥＮＥＳＩＳＩＮＭＩＣＥＷａｎｇＱｉａｎｇ王强；ＷａｎｇＹｕａｎｈｅ王元和；...     

羧乙基锗倍半氧化物（Ge－l32）的抗诱变作用研究

本研究用果蝇伴性隐性致死（ＳＬＲＬ）实验，鼠伤寒沙门氏菌回复突变实验（Ａｍｅｓ）实验，小鼠骨髓细胞微核（ＭＮ）实验分别检测了Ｇｅ－１３２的抗诱变作用，结果表明：Ｇｅ－１３２在低浓度一定范围内（０．１％，０．０１％）对甲基磺酸乙酯诱发果蝇ＳＩＲＬ突变具有较弱的抗诱变作用Ｇｅ－１３２对２－氢基芴诱发的ＴＡ９８．ＴＡ１００回变无抗诱变作用，对环磷酰胺诱发小鼠髓细胞微核效应呈现剂量反应关系的抗诱变作用，但由于Ｇｅ－１３２处理组微核率仍远远离于阴性对照组，故认为抗诱变作用有限，并认为除在特殊适应症人群中可适量应用Ｇｅ－１３２外，健康人群中不提倡使用。     

Antitumor activity of Ge-132, a new organogermanium compound, in mice is expressed through the functions of macrophages and T lymphocytes

The antitumor activity of Ge-132 against a variety of allogeneic and syngeneic murine ascites tumors was first evaluated. The antitumor effects of Ge-132 were observed when mice inoculated with Ehrlich carcinoma (allogeneic) or RL male 1 leukemia (syngeneic) cells were treated orally. However, Ge-132 had no activity on a T-cell lymphoma (EL 4, syngeneic) or a methylcholanthrene-induced fibrosarcoma (Meth-A, syngeneic). The antitumor effect of Ge-132 in mice was related to the dose administered as well as the administration schedule. The antitumor activity of Ge-132 was next studied in mice pretreated with some blockers against immunocompetent cells. The antitumor efficacy of Ge-132 was not observed when tumor-bearing mice were treated with trypan blue and carrageenan or monoclonal anti-Thy 1.2 antibody. However, when natural killer cells were eliminated from mice bearing RL male 1 or Ehrlich ascites tumors by treatment with anti-asialo GM 1 antiserum, the antitumor efficacy of the compound was unchanged. These results suggest that Ge-132 is effective against certain ascites tumors regardless of whether the tumor is syngeneic or allogeneic. Further, its effect might be expressed through host defense mechanisms, including macrophages and/or T lymphocytes.     

Antitumor mechanisms of carboxyethyl-germanium sesquioxide (Ge-132) in mice bearing Ehrlich ascites tumors

The administration of IFN-containing sera (Ge-sera) obtained from Ge-132-treated mice (Ge-mice) or the passive transfer of macrophages (M phi) to mice bearing ascites tumors resulted in the inhibition of tumor growth. The cooperative role of Ge-sera and Ge-M phi in the display of Ge-132-antitumor activity was studied. When mice were pretreated with antimouse IFN gamma antiserum, no IFN-inducing or antitumor activities of the compound were detected. Cytotoxic activities were detected in peritoneal M phi of mice treated with Ge-sera, and passive transfer of these M phi to tumor-bearing mice resulted in the inhibition of tumor growth. When tumor-bearing mice were pretreated with substances toxic to M phi, no antitumor activity of Ge-sera was observed. However, Ge-132 antitumor activity was observed in mice depleted of T-cells, even though the antitumor effects of the compound itself were not demonstrable in T-cell-depleted mice. Therefore, a part of the antitumor activity of Ge-132 appears to be expressed as follows: Ge-132 stimulates T-cells to produce circulating lymphokine(s) which are inactivated by anti-IFN gamma treatment; activated M phi are generated from resting M phi by these lymphokine(s); the transplanted tumors are inhibited by these M phi.     

Importance of T-cells and macrophages in the antitumor activity of carboxyethylgermanium sesquioxide (Ge-132)

The purpose of this study was to investigate the effective mechanisms of Ge-132, an organogermanium compound with immunomodulatory activity, on experimental murine ascites tumors. The antitumor effects of Ge-132 were observed when mice inoculated with Ehrlich carcinoma (allogeneic) or RL male 1 leukemia (syngeneic) cells were treated orally. However, Ge-132 had no activity on EL-4 lymphoma (syngeneic) or Meth A fibrosarcoma (syngeneic). The antitumor activity of Ge-132 was not observed when tumor-bearing mice were treated with trypan blue, carrageenan, or monoclonal anti-Thy 1.2 antibody. However, when natural killer (NK) cells were eliminated from mice bearing RL male 1 or Ehrlich ascites tumors by treatment with anti-asialo GM1 antiserum, the antitumor activity of the compound was unchanged. This suggests that Ge-132 was effective against certain ascites tumors regardless of whether the tumor was syngeneic or allogeneic. Furthermore, its effect might be expressed through host defense mechanisms, including macrophages and/or T-cells.     

Effect of combination immunochemotherapy with an organogermanium compound, Ge-132, and antitumor agents on C57BL/6 mice bearing Lewis lung carcinoma (3LL)

The antitumor effect of combination immunochemotherapy with Ge-132 and antitumor agent was studied using C57BL/6 mice bearing Lewis lung carcinoma (3LL). Ge-132 was administered orally at a daily dose of 100 mg/kg. Antitumor agents were administered intraperitoneally once a week. Initially, the effect of combination immunochemotherapy with Ge-132 and 5-fluorouracil (5-FU) was studied on 3LL local tumor growth, pulmonary metastases, survival, delayed type hypersensitivity (DTH) and body weight in tumor-bearing mice, and the following results were obtained: Inhibition of tumor growth in the combined group; Enhanced anti-metastatic effect; Prolonged survival time, and; Recovery of loss of both DTH and body weight as a result of combination therapy. These antitumor effects were also obtained by adoptive transfer of Ge-132-stimulated splenocytes in 5-FU-treated mice bearing 3LL. These results therefore suggest that the effects of Ge-132 were expressed through modification of immunocytes. Furthermore, Ge-132 enhanced the antitumor activity of bleomycin as well as that of 5-FU. These facts suggested that Ge-132 is useful for antitumor combination immunochemotherapy.     

羧乙基锗倍半氧化物对实验诱发小鼠前胃癌变率的影响

 用羧乙基锗倍半氧化物（Ge-132）处理NSEE诱发的小鼠前胃鳞状上皮增生、癌变，结果发现实验组的癌变率显着低于对照组（P<0.05）,抑癌率为42.9%,实验组核仁组成区相关嗜银蛋白（Ag-NOR）数目及不规则型颗粒的比例显着低子对照组（P<0.05）,而实验组之癌周淋巴细胞浸润反应程度较对照组显着增强（P<0,05）.以上结果表明Ge-132可显着降低NSEE诱发小鼠前胃癌的癌变率，并可影响Ag-NOR在小鼠前胃鳞状上皮细胞中的表达，Ge-132的以上作用可能与其提高小鼠局部细胞免疫力有关。     

羧乙基锗倍半氧化物对实验诱发小鼠前胃癌变过程中的免疫作用

Ｎ—亚硝基肌氨酸乙酯（ＮＳＥＥ）诱发昆明小鼠前胃癌变，再以羧乙基锗倍半氧化物（Ｇｅ－１３２）治疗结果发现实验组中癌细胞的浸润深度显著浅于对照组（Ｐ＜０．０５）；实验组核仁组成区相关嗜银蛋白（ＡｇＮＯＲ）计数及细小、不规则颗粒所占比例均低于对照组（Ｐ＜０．０５）；实验组癌周淋巴细胞浸润反应则较对照组显著（Ｐ＜０．０５）。提示Ｇｅ－１３２对ＮＳＥＥ诱发的小鼠前胃癌有一定的治疗作用；并从免疫形态学证实介导宿主免疫反应可能是Ｇｅ－１３２发挥抗癌作用的机制之一。本研究为Ｇｅ－１３２用于临床提供理论依据。     

Ability of sera from mice treated with Ge-132, an organo-germanium compound, to inhibit experimental murine ascites tumors

Serum specimens from mice treated orally with Ge-132 (100 mg/kg) exhibited antitumor activity against Ehrlich (allogeneic) and RL 1 (syngeneic) ascites tumors in BALB/c mice. Sera obtained from mice 24 hours after Ge-132 administration displayed the highest antitumor effect and the antitumor activity was dose-dependent. Sera prepared from mice 12, 36 or 48 hours after Ge-132 treatment had no protective effect. Circulating interferon (IFN) was induced at 24 hours after administration. The antiviral activity of serum from Ge-132-treated mice was inactivated by treatment with trypsin, low pH, and anti-IFN-gamma antiserum. The inactivated preparations of serum IFN induced by Ge-132 did not show antitumor activity when administered to mice bearing Ehrlich ascites tumors. These results suggest that the antitumor activity in the sera of Ge-132-treated mice may have been expressed through IFN-gamma which was induced by Ge-132.     

Ability of sera from mice treated with Ge-132, an organic germanium compound, to inhibit experimental murine ascites tumours

Sera from C57Bl/6 mice treated orally with Ge-132 exhibited antitumour activity against Ehrlich (allogeneic) and RL male 1 (syngeneic) ascites tumours in BALB/c mice. Sera obtained from mice 24 h after Ge-132 administration displayed the greatest antitumour effect and this was dose dependent. Sera prepared from mice 12, 36, or 48 h after Ge-132 treatment had no protective effect. Circulating interferon (IFN) was induced at 24 h after administration of Ge-132 but was not detected in the sera at 12, 36, or 48 h after administration. The antiviral activity of sera from Ge-132-treated mice was inactivated by treatments with trypsin, low pH, and anti-IFN gamma antiserum. The inactivated preparations of serum IFN induced by Ge-132 did not exhibit antitumour activity when administered to tumour-bearing mice. These results suggest that antitumour activity in the sera of Ge-132-treated mice may be expressed through activities of Ge-132-induced lymphokine(s), such as IFN gamma.     

Cooperation of lymphokine(s) and macrophages in expression of antitumor activity of carboxyethylgermanium sesquioxide (Ge-132)

The administration of IFN containing sera (Ge-sera) obtained from Ge-132-treated mice (Ge-mice) or the passive transfer of macrophages (M phi) to mice bearing ascites tumors resulted in the inhibition of tumor growth. The cooperative role of Ge-sera and Ge-M phi in the display of Ge-132-antitumor activity was studied. When mice were pretreated with antimouse IFN gamma antiserum, no IFN-inducing and antitumor activities of the compound were detected. Cytotoxic activities were detected on peritoneal M phi of mice treated with Ge-sera, and passive transfer of these M phi to tumor-bearing mice resulted in the inhibition of tumor growth. When tumor-bearing mice were pretreated with substances toxic to M phi, there was no antitumor activity of Ge-sera observed. However, there was antitumor activity of Ge-sera in mice depleted of T-cells, even though the antitumor effects of the compound itself were not demonstrable in T-cell depleted mice. Therefore, a part of the antitumor activity of Ge-132 may appear to be expressed as follows: (1) Ge-132 stimulated T-cells to produce circulating lymphokine(s) which were inactivated by anti-IFN gamma treatment; (2) activated M phi were generated from resting M phi by such lymphokine(s); (3) the transplanted tumors were inhibited by these M phi.