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     

PROMOTION OF IN VITRO GROWTH OF HUMAN MEDULLOBLASTOMA CELLS BY EXOGENEOUS IL－6

ＰＲＯＭＯＴＩＯＮＯＦＩＮＶＩＴＲＯＧＲＯＷＴＨＯＦＨＵＭＡＮＭＥＤＵＬＬＯＢＬＡＳＴＯＭＡＣＥＬＬＳＢＹＥＸＯＧＥＮＥＯＵＳＩＬ－６ＬｉｕＪｉａｉ刘佳；ＬｉＨｏｎｇ李宏；ＨａｍｏｕＭａｒｉｅ－Ｆｒａｎｃｅ；ＮｉｃｏｌａｓｄｅＴｒｉｂｏｌｅｔ（１Ｄｉ...     

羧乙基锗倍半氧化物抗移植瘤实验

将移植了ＨｅｐＡ鼠肝癌的ＮＩＨ鼠随机分为四组，一组作对照组，另三组分别给予Ｇｅ－１３２、ＣＹ、Ｇｅ－１３２＋ＣＹ治疗。２周后处死，测定血清中ＳＯＤ活性，对瘤体进行病理切片检查。结果表明：治疗组肿瘤重量较轻，ＳＯＤ活性较高（Ｐ＜０．０５）。Ｇｅ－１３２组的癌组织中白细胞浸润程度较高，细胞免疫力较强。对鼠肝癌的抑制率，Ｇｅ－１３２与ＣＹ合用有相加作用。     

刺五加抗癌作用的实验研究

目的：为进一步探讨刺五加对实验性肝癌发的干预作用及可能机理。方法：４３只雄性大鼠被随机分成３组（１）正常对照组：喂普通饲料（２）３－ＭｅＤＡＢ组：喂含０．０６％３－ＭｅＤＡＢ饲料１０周（３）刺五加组,除致癌剂外另加入刺五加,历时２０周。实验过程中所有动物均自由进食及饮水。结果：刺五加组较３－ＭｅＤＡＢ组：Ｆ（１）外周血液及肝组织中ＰＡＩ－１含量明显减少。（２）肝细胞周期时相Ｇ０／Ｇ１比率增加,Ｓ期     

半乳糖基修饰的反义硫代寡核苷酸对肝癌多药耐药细胞株MDR_1基因过度表达的抑制作用

设计合成三种互补ＭＤＲ１ｍＲＮＡ的反义硫代寡核苷酸（ＡＳＯＤＮ），分别互补ＭＤＲ１ｍＲＮＡ序列起始区、含ＡＵＧ起始密码子区及针对Ｌｏｏｐ形成位点区的序列，作用于阿霉素（ＤＯＸ）诱导的肝癌多药耐药细胞株ＢＥＬ－７４０２／ＤＯＸ。经流式细胞分析及ＲＴ－ＰＣＲ的方法检测，发现三种ＡＳＯＤＮ均能不同程度地降低ＢＥＬ－７４０２／ＤＯＸ细胞膜表面Ｐ－ＧＰ含量；同时ＭＤＲ１ｍＲＮＡ的表达也有轻度降低，其中尤以互补ＭＤＲ１ｍＲ－ＮＡＬｏｏｐ形成位点的ＡＳＯＤＮ抑制作用最强。以导向配体Ｇａｌ１０－ＰＬＬ修饰此ＡＳＯＤＮ后，作用于ＢＥＬ－７４０２／ＤＯＸ细胞，发现与相同剂量未修饰ＡＳＯＤＮ比较，Ｐ－ＧＰ含量由７６．８％降至１９．８％；对ＡＤＭ的ＩＣ５０由１．２８μｇ／ｍｌ降至０．４２μｇ／ｍｌ。实验说明，半乳糖基修饰的互补ＭＤＲ１ｍＲＮＡＬｏｏｐ形成位点的ＡＳＯＤＮ能够明显降低肝癌多药耐药细胞膜表面Ｐ－ＧＰ的含量，并较大程度地逆转多药耐药细胞ＢＥＬ－７４０２／ＤＯＸ对化疗药物的耐受性。     

THE LATE RESPONSE OF PIG SKIN TO FRACTIONATED DOSES OF 35 MeV P→Be FAST NEUTRON IRRADIATION

ＴＨＥＬＡＴＥＲＥＳＰＯＮＳＥＯＦＰＩＧＳＫＩＮＴＯＦＲＡＣＴＩＯＮＡＴＥＤＤＯＳＥＳＯＦ３５ＭｅＶＰ→ＢｅＦＡＳＴＮＥＵＴＲＯＮＩＲＲＡＤＩＡＴＩＯＮＷａｎｇＪｕｎｊｉｅ；王俊杰；ＤｉＷｅｉ；狄薇；ＬｉＹａｇａｎｇ；李亚钢（Ｄｅｐａｒｔｍｅｎｔｏｆ...     

ANTITUMOR EFFECTS OF HUMAN IL-15 GENE MODIFIED LUNG CANCER CELL LINE

ＡＮＴＩＴＵＭＯＲＥＦＦＥＣＴＳＯＦＨＵＭＡＮＩＬ－１５ＧＥＮＥＭＯＤＩＦＩＥＤＬＵＮＧＣＡＮＣＥＲＣＥＬＬＬＩＮＥＳｈｅｎＹｏｎｇｑｕａｎ１沈永泉ＣｕｉＬｉａｎｘｉａｎ２崔莲仙ＨｅＷｅｉ１何维ＸｕｅＬｉ１薛莉ＢａＤｅｎｉａｎ１巴德年１Ｉｎｓｔ...     

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％。     

THE BLOCKING EFFECTS OF GLYCYRRHIZE URALENSIS AND CHELIDONIUM MAJUS ON MUTAGENESIS INDUCED BY AFLATOXIN B1

ＴＨＥＢＬＯＣＫＩＮＧＥＦＦＥＣＴＳＯＦＧＬＹＣＹＲＲＨＩＺＥＵＲＡＬＥＮＳＩＳＡＮＤＣＨＥＬＩＤＯＮＩＵＭＭＡＪＵＳＯＮＭＵＴＡＧＥＮＥＳＩＳＩＮＤＵＣＥＤＢＹＡＦＬＡＴＯＸＩＮＢ１ＳｈｉＧｕｉｚｎｉ；史桂芝；ＪｉＸｉｎｈｕａ；纪新华；ＬｉａｎｇＹ...     

大、小鼠摄入AFB1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。     

三种有机锗（G－132，Ge－162，Ge－164）对小鼠骨髓嗜多染红细胞微核率的影响

本文以三种有机锗（Ｇｅ－１３２，Ｇｅ－１６２．Ｇｅ－１６４）对小鼠进行灌胃处理，以测定对环磷酰胺（ＣＰ）诱发的骨髓嗜多染红细胞微核率的抑制作用，结果表明，三种有机锗均能降低微核率，与阳性对照组比较有显著性差异（Ｐ＜０．０５）．而三种有机锗之间抑制微核率的效能无差异（Ｐ＜０．０５）。提示，三种有机锗均可拮抗ＣＰ的致突变作用。     

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.     

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.     

Suppression of tumor growth by peritoneal macrophages isolated from mice treated with carboxyethylgermanium sesquioxide (Ge-132)

In a murine model it has been shown that the antitumor activity of carboxyethylgermanium sesquioxide (Ge-132) can be depleted by administration of macrophage (M phi) blockers. In the present study, the role that M phi play in the antitumor activity of the compound was investigated. Oral administration of Ge-132 in mice was demonstrated to be effective in activating M phi (Ge-132-cytotoxic M phi), and the cytotoxic activity of these M phi appeared in the peritoneal cavity of mice 48 hours after the oral administration of the compound. Co-cultivation of RL male-1 leukemia or Ehrlich carcinoma cells with Ge-132-cytotoxic M phi in vitro resulted in marked suppression of the growth of tumor cells. The transfer of peritoneal exudate cells (PEC), or purified M phi fractions of PEC from Ge-132-treated mice to mice bearing Ehrlich or RL male-1 ascites tumors resulted in significant protection. However, when the cytotoxic M phi were depleted by carbonyl-iron treatment in vitro, no antitumor effect was demonstrated in mice bearing Ehrlich or RL male-1 ascites tumors. Macrophage fractions obtained from PEC of Ge-132-treated mice exhibited an inhibitory effect against certain tumors both in vivo and in vitro suggesting that the antitumor effect of Ge-132 observed in vivo resulted from the activation of M phi.     

两种不同剂量Ge—132对二甲肼诱发大鼠大肠癌的作用

在以二甲肼(DMH)诱发大鼠大肠癌的同时,给大鼠灌胃Ge-132 100mg/kg体重或300mg/kg体重共27周。Ge-132 100mg/kg体重组大鼠的平均癌灶数和平均癌灶体积,均显著少于对组照和Ge-132 300mg/kg体重组(P均<0.01)。Ge-132 300mg/kg体重组与对照组差异无显著意义(P>0.05)。肠镜检查显示,Ge-132 100mg/kg体重组致癌物所致结肠粘膜的炎症、萎缩和不典型增生明显轻于对照组(P<0.05),癌肿发生的潜伏期比对照组长3周。Ge-132 300mg/kg体重组与对组照差异无显著意义(P>0.05)。结果表明,Ge-132对化学诱癌的预防作用具有剂量依赖性。