羧乙基锗倍半氧化物对抗化学诱导大鼠肝癌的作用

用黄曲霉素(320μg/kg/天×2周),N-2-乙酰氨基芴(0.02％混入饲料中喂饲2周)以及部分肝切除等联合处理可在8周内诱导SD大鼠出现肝癌癌前病变。若在诱癌过程中同时饲以Ge-B2(300μg/kg/天,每周 4天)共8周,或诱癌处理前,先按上述Ge-132用量喂饲两周,再在诱癌处理过程饲以上述量Ge-132,直至实验终结,共10周。加锗组见动物健康状况明显改善:体重净增重与阴性对照相近,比之未加锗组显见增高;肝癌前期病变程度减轻;肝癌标志酶GST-P与r-GT表达减弱。提示锗对于化学诱导肝癌有明显对抗作用。     

海狗油脂肪乳对大鼠的一般生殖毒性研究

背景与目的:观察海狗油脂肪乳对大鼠配子成熟、交配行为、生育力和早期胚胎发育方面的毒性作用. 材料与方法:160只Wistar大鼠随机分为海狗油脂肪乳不同剂量组(250、500和1 000 mg/kg)和溶剂对照组,共4组.雄性大鼠在交配前连续腹腔注射海狗油脂肪乳35 d,雌性大鼠在交配前连续腹腔注射给予海狗油脂肪乳18 d,相同剂量组内大鼠按雄:雌=1:1同笼交配,连续10 d.在确定雌鼠受精后处死同笼的雄鼠,解剖检查睾丸和附睾等生殖器官及精子的活力.雌鼠交配期间继续给药至妊娠第14 d处死,解剖检查卵巢、子宫和胚胎的情况. 结果:给药期间各剂量组大鼠除体重增长缓慢(体重增重平均最大差值达到50 g,与对照组比较,差异显著,P<0.05)外,精神、行为、活动及被毛正常;雄性大鼠生殖器官发育良好,性功能正常,精子数量多、成熟.畸形率低.妊娠大鼠500 mg/kg和1 000 mg/kg组的活胎数减少(窝平均最大差值2.0个),胎仔平均体重降低(每只平均最大差值0.03 g)以及1 000mg/kg剂量组的交配率为65%(13/20),与对照组比较差异有统计学意义(P<0.05).妊娠率、黄体数、着床数、吸收胎数、死胎数、受精卵着床前后丢失率和胎仔体表畸形数等与对照组比较无显著差异(P>0.05).结论:海狗油脂肪乳可影响成年大鼠体重增长,引起妊娠大鼠早期胚胎和胎仔的生长发育障碍,但对大鼠其他生殖功能无明显损害作用.     

塞莱昔布对化学诱导大鼠乳腺肿瘤病理分级影响的研究

目的:评价预防性应用选择性环氧化酶-2(COX-2)抑制剂塞莱昔布对化学诱导大鼠乳腺肿瘤及正常乳腺组织病理分级的影响。方法:雌性SD大鼠予二甲基苯并蒽(DMBA)1次性灌胃诱发乳腺肿瘤过程中,给予不同剂量塞莱昔布,观察肿瘤发生率、数量和体积,并与正常对照组进行病理学分析。结果:与对照组相比,塞莱昔布100和150 mg/kg两剂量组大鼠乳腺肿瘤发生率和肿瘤数量均显著低于模型对照组,但各组间肿瘤平均体积差异无统计学意义,P>0.05。塞莱昔布显著降低大鼠乳腺肿瘤的组织病理分级(100 mg/kg,P=0.021;150 mg/kg,P=0.036),显著降低DMBA导致的乳腺小叶和腺泡的病变程度(100 mg/kg,P=0.004)。结论:预防性应用塞莱昔布具有降低乳腺肿瘤的病理分级,保护正常乳腺组织的作用,其临床应用价值值得进一步探索。     

香加皮三萜类化合物对实验性大鼠食管癌的阻断作用及机制

目的探讨中药香加皮提取物三萜类化合物（TCCP）对甲基苄基亚硝胺（NMBA）诱导F344大鼠食管癌前病变形成的阻断作用及其机制。方法健康雄性F344大鼠90只,随机分为模型组、TCCP干预组、大豆油对照组和正常对照组。模型组大鼠皮下注射0.5 mg/kg NMBA,TCCP干预组大鼠同时给予0.5 mg/kg NMBA皮下注射及香加皮三萜类化合物20 mg/kg肌肉注每周给药3次,连续5周;大豆油对照组大鼠肌注大豆油1 ml/kg,正常对照组大鼠常规饲养。分别在给药后第9、15和25周,麻醉后解剖大鼠,HE染色后光镜下观察食管上皮组织病理学变化;用Western blot法检测GSK-3β和β-catenin蛋白表达水平;用RT-PCR法检测c-myc mRNA表达水平。结果(1)正常对照组及大豆油对照组在整个实验过程中未发现食管异常变化,模型组大鼠随诱癌时间延长食管病变逐渐加重。TCCP干预可缓解食管上皮的病变。(2)正常大鼠食管上皮中有少量β-catenin蛋白表达,模型组大鼠食管上皮β-catenin蛋白表达显著增强（P<0.05）;正常大鼠食管上皮GSK-3β的蛋白表达丰富,随着诱癌时间延长表达水平逐渐降低;与模型组相比,在诱癌9、15和25周时TCCP干预组大鼠食管上皮组织中β-catenin蛋白表达水平均显著下降（P<0.05）;而GSK3β蛋白表达显著升高（P<0.05）。(3)与正常对照组相比,各时间点模型组大鼠食管上皮c-myc mRNA表达水平均显著升高。与模型组相比,在诱癌9、15周时TCCP干预组大鼠食管上皮组织中c-myc mRNA表达水平均显著下降,而诱癌25周时差异无统计学意义（P>0.05）。结论TCCP可能通过促进Wnt信号分子GSK-3β的表达,抑制β-catenin蛋白的表达,进而下调下游靶基因c-myc的转录,干扰细胞周期转化,逆转细胞的分化,可能是其抑制食管癌变细胞生长机制之一。     

2, 4-二氯苯氧乙酸对子代大鼠发育及脑组织的氧化损伤作用

目的:研究大鼠孕期和哺乳期暴露2,4-二氯苯氧乙酸(2,4-D)对子代发育及脑组织脂质过氧化的损伤作用。方法:Wistar大鼠于受孕后第2天开始经口灌胃染毒2,4-D(0、25、50和100 mg/kg)直至仔鼠出生后第21天,每天1次,连续42 d。期间检测仔鼠生理及早期神经行为发育指标。断乳1周后处死仔鼠检测脑组织丙二醛(MDA)、还原型谷胱甘肽(GSH)的含量及谷胱甘肽过氧化物酶(GSH-Px)的活力。结果:与对照组相比,100 mg/kg剂量组仔鼠体质量从出生后14 d开始降低,50 mg/kg剂量组仔鼠体质量从出生后21 d开始降低,差异均有统计学意义(P<0.05),而其他各生理发育指标差异均无统计学意义(P>0.05)。神经行为测试中100 mg/kg剂量组仔鼠断崖回避、空中翻正及听觉惊愕的阳性发生率均明显低于对照组(P<0.05),出现神经行为发育迟缓。50和100 mg/kg剂量组仔鼠脑组织中MDA含量升高,100 mg/kg剂量组仔鼠脑组织GSH含量及GSH-Px的活性下降,与对照组相比差异均有统计学意义(P均<0.05)。结论:大鼠孕期和哺乳期暴露2,4-D致子代神经发育迟缓可能与2,4-D引起脑组织脂质过氧化损伤有关。     

硒干预对DEHP暴露下SD大鼠血细胞参数的作用

目的：探讨不同剂量邻苯二甲酸二（2-乙基）己酯（DEHP）染毒后硒对大鼠外周血血细胞参数的影响。方法：将77只健康清洁级雄性SD大鼠,随机分为7组,即对照组、3个不同浓度（300、600、900 mg/kg）DEHP染毒组、1 mg/kg Se+不同剂量（300、600和900 mg/kg）DEHP染毒干预组,连续饲喂90 d,试验期间观察大鼠中毒状况（精神亢奋、被毛蓬松、局部脱毛现象）,试验期末称取大鼠体质量并取全血测定各类血细胞参数的变化。结果：与对照组比较,900 mg/kg DEHP染毒大鼠体质量明显下降（P < 0.05）,600和900 mg/kg DEHP染毒组大鼠出现中毒体征比例分别为63.63%（7/11）和100%（11/11）,均较对照组0（0/11）显著升高（P均 < 0.05）。与相同剂量DEHP染毒组比较,1 mg/kg Se干预后大鼠体质量均明显增加,差异均有统计学意义（P均 < 0.05）;300、600 mg/kg DEHP染毒组大鼠中毒体征明显降低（P均 < 0.05）。白细胞参数中,与对照组比较,600和900 mg/kg DEHP染毒组大鼠白细胞数（WBC）明显降低、单核细胞（MONO）显著升高,差异均有统计学意义（P均 < 0.05）。与相同剂量DEHP染毒组比较,1 mg/kg Se+600 mg/kg DEHP干预组白细胞数（WBC）明显升高、单核细胞（MONO）显著降低（P < 0.05）。红细胞参数中,与对照组比较,DEHP染毒后大鼠平均血红蛋白量（MCH）、血红蛋白含量分布宽度（HDW）均明显升高;600、900 mg/kg DEHP染毒组大鼠红细胞数（RBC）、红细胞压积（HCT）明显降低（P < 0.05）。与相同剂量DEHP染毒组比较,1 mg/kg Se干预后大鼠红细胞参数未见显著差异。血小板参数中,未发现DEHP染毒与Se干预对SD大鼠血小板各参数产生显著影响。结论：300~900 mg/kg DEHP染毒可对大鼠某些红细胞和白细胞参数产生影响,硒的干预在300~600 mg/kg DEHP染毒条件下可保护某些血细胞功能。     

海狗油脂肪乳对大鼠致畸毒性研究

背景与目的:探讨海狗油脂肪乳对大鼠致畸毒性作用。材料与方法:孕鼠设3个海狗油脂肪乳剂量组(800、400和200mg/kg)、环磷酰胺(CP)阳性对照组和溶剂对照组。在受孕大鼠妊娠的第6～15d连续尾静脉注射受试物10d,阳性对照组大鼠妊娠第10d一次性腹腔注射CP。结果:与溶剂对照组比较,海狗油脂肪乳200mg/kg剂量组的孕鼠体重增长缓慢(P<0.01);400mg/kg剂量组出现胎仔身长和体重减轻的胚胎毒性(P<0.05);800mg/kg剂量组出现吸收胎数增多(P<0.05)。各剂量组胎仔的黄体数、着床数、活胎数、死胎数、胎仔尾长和胎仔性别等与溶剂对照组间的差异无统计学意义(P>0.05)。海狗油脂肪乳各剂量组未见明显的骨骼畸形和内脏器官畸形。结论:海狗油脂肪乳剂量在200mg/kg时,对大鼠具有一定的母体毒性;海狗油脂肪乳在剂量400mg/kg时有胚胎毒性;在剂量800mg/kg时,未见大鼠胎仔骨骼和内脏器官的致畸毒性。     

大豆异黄酮和DEHP对雌性大鼠体内雌激素水平的影响

目的:探讨大豆异黄酮和邻苯二甲酸二(2-乙基己)酯(DEHP)对雌性大鼠体内雌激素的影响。方法:32只雌性SD大鼠按体质量随机分为4组,即大豆异黄酮(86 mg/kg)组、DEHP(68 mg/kg)组、大豆异黄酮(86 mg/kg)+DEHP(68 mg/kg)组和对照组(基础饲料),每组8只。受试物均混匀在大鼠饲料中,记录大鼠每周体质量及摄食量,喂养4周后处死,取各脏器称取质量。高效液相色谱法测定大鼠血清中DEHP含量,放射免疫法检测大鼠血清中雌二醇(E2)和睾酮(T)的水平。采用免疫组化检测大鼠子宫内膜ERα的表达量。结果:与对照组相比,各组雌鼠体质量增长无明显差异(P均>0.05);DEHP能明显增加雌性大鼠肝脏和脾脏系数(P<0.05); DEHP组和大豆异黄酮+DEHP组大鼠血清中DEHP的水平显著高于对照组(P<0.05),且二者联合作用组低于DEHP单独作用组(P<0.05)。各处理组对大鼠血清睾酮水平无显著影响,而大豆异黄酮+DEHP组和DEHP组大鼠血清中E2浓度低于对照组,差异有统计学意义(P<0.05)。免疫组化结果显示,大豆异黄酮、DEHP及二者联合作用组的大鼠子宫内膜ERα的表达与对照组相比差异均无统计学意义(P>0.05)。结论:DEHP能够显著增加雌性大鼠肝和脾的脏体比值且能显著降低血清中E2水平,大豆异黄酮可以一定程度上降低大鼠血清中DEHP的残留。     

CCT亚基γ基因在AFB_1诱发大鼠肝癌过程中表达的变化

目的探讨AFB1诱发肝癌过程中CCT亚基γ基因蛋白的表达及其意义。方法 45只Wistar大鼠随机分为AFB1组和对照组,AFB1组以200μg/kg体重腹腔注射AFB1,第13周、第33周和第53周对大鼠进行肝活检,第73周处死全部动物并取肝组织。用免疫组化法检测AFB1诱发肝癌过程中不同时期CCT亚基γ基因蛋白的表达情况。结果在第73周AFB1组CCT亚基γ基因蛋白表达水平显著高于对照组(P<0.05)。同一组不同时段比较,随着诱癌的进行,CCT亚基γ基因蛋白表达上调,第73周AFB1组CCT亚基γ基因蛋白的表达水平不仅明显高于第13周,而且亦高于第33周(P<0.01)。其余各组和同组不同时段之间CCT亚基γ基因蛋白的表达差异无统计学意义(P>0.05)。AFB1组中发生肝癌的动物肝组织CCT亚基γ基因蛋白表达率为100%(10/10),显著高于同期对照组CCT亚基γ基因蛋白的表达率30%(3/10)(P<0.05)。结论 AFB1诱癌过程中CCT亚基γ基因蛋白表达上调,CCT亚基γ基因蛋白有可能参与了肝细胞癌的发生和发展。     

分化型甲状腺癌术后首次不同剂量131I清除残留甲状腺组织的临床观察

目的 探讨分化型甲状腺癌术后首次不同剂量131 I清除残留甲状腺组织(清甲)的临床效果.方法 将84例分化型甲状腺癌患者随机分为观察组(131I清甲剂量>100 mCi)和对照组(131I清甲剂量≤100 mCi)各42例.观察组空腹一次性口服131 I 100~120 mCi,对照组空腹一次性口服131 I 30~40 mCi.清甲半年后行131 I甲状腺显像检查,对两组清甲成功率进行评价,并检测促甲状腺激素(TSH)、甲状旁腺素(PTH)和甲状腺球蛋白(TG)水平,以及两组不良反应发生情况.结果 观察组乳头状癌与滤泡状癌清甲成功率与对照组比较,差异无统计学意义(P>0.05).同组内乳头状癌与滤泡状癌清甲成功率比较,差异无统计学意义(P>0.05).清甲前血清TSH浓度≥30 mIU/mL与血清TSH浓度﹤30 mIU/mL比较,差异具有统计学意义(P<0.05).清甲前血清Tg值﹤30 ng/mL与血清Tg值≥30 ng/mL比较,差异具有统计学意义(P<0.05).清甲6个月后,观察组TSH和PTH水平均显著高于对照组,Tg水平显著低于对照组,差异具有统计学意义(P<0.05).对照组胃肠道反应及泪腺功能紊乱发生率均低于观察组,差异具有统计学意义(P<0.05).对照组唾液腺功能紊乱及颈部疼痛发生率与观察组比较,差异无统计学意义(P>0.05).结论 分化型甲状腺癌术后首次应用131 I与剂量无太大关系,且低剂量的不良反应少于高剂量,低剂量131 I方案值得推广.     

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.     

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。     

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.     

Antitumor effect in mice of an organic germanium compound (Ge-132) when different administration methods are used

The antitumor effect of an organic germanium compound, carboxyethylgermanium sesquioxide (Ge-132), was examined in mice using two systems: one, the ascitic form of Ehrlich carcinoma in DDI mice, and the other, the solid form of Meth-A fibrosarcoma in BALB/c mice. In the mice with Ehrlich ascitic tumors, a remarkable prolongation in life span was observed after intraperitoneal (i.p.) or per oral (p.o.) administration of Ge-132 (300 mg/kg), but not after intravenous (i.v.) injection of the same compound. Following i.p. or p.o. administration, cytotoxic macrophages (M?) were induced in the peritoneal cavity after 48 h. although this was not the case after i.v. injections. When the in vivo effect of these in vitro active M? was examined after adoptive transfer to mice bearing Ehrlich ascitic tumor cells, a significant antitumor effect was noted. In the mice bearing solid Meth-A tumors, i.v. injections of Ge-132 (100 mg/kg) were found to inhibit tumor growth remarkably, although i.p. and p.o. administrations did not have the same result. This inhibitory effect of Ge-132 by i.v. administration was explained by the continued augmentation of NK activity in peripheral blood, which was followed by the induction of specific killer cells appearing in the spleen. When the mice which had recovered from Meth-A tumor growth, following i.v. injections of Ge-132, were challenged with the same tumor on day 30, all mice were able to tolerate the challenge, but not a challenge of RL male 1 tumor cells. These observations may indicate that the differing antitumor effects of Ge-132 produced when different administration methods are used can be explained by the variation in effector cells induced by such different administration routes.     

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％。     

Prevention of mouse lung tumors by targretin

Targretin has indicated chemotherapeutic activity against nonsmall-cell lung cancer and chemoprevention in rat mammary gland. Therefore, targretin was evaluated for the prevention of 4-(methylnitrosoamino)-1-(3-pyridyl)-1-butanol (NNK) and vinyl carbamate-induced lung tumors in female strain A mice. Three experiments were performed: (i) a dose-response study with vinyl carbamate-induced tumors; (ii) a limited treatment study also with vinyl carbamate and (iii) prevention of NNK-induced tumors. In the dose-response study, 0, 10, 30, 100 and 300 mg/kg targretin were administered after vinyl carbamate. Dose levels of 30 mg/kg and greater significantly decreased tumor multiplicity by >19%. However, the efficacy of 30 and 300 mg/kg was not significantly different demonstrating a shallow dose-response relationship. In the limited treatment study, 200 mg/kg targretin was administered to the mice from 4-13, 4-19, 4-25 and 23-25 weeks after vinyl carbamate. Administering targretin from weeks 4-19 and 4-25 decreased the multiplicity of tumors from 35.3 +/- 1.43 to 29.1 +/- 1.51 and 25.0 +/- 0.93, respectively, and along with administering it from weeks 23-25 decreased tumor size. In the third study, when targretin (100 and 300 mg/kg) was administered for 3 weeks after NNK followed by a 20 weeks holding period, tumor multiplicity was reduced from 10.6 +/- 1.13 to 6.38 +/- 0.75 and 4.60 +/- 0.70, respectively. Hence, targretin demonstrated both preventive and therapeutic activity with respect to mouse lung tumors supporting its further development as a preventive and therapeutic agent for lung cancer.     

Induction of interferon and activation of NK cells and macrophages in mice by oral administration of Ge-132, an organic germanium compound

After oral administration of an organic germanium compound, Ge-132 (300 mg/kg), a significant level of interferon (IFN) activity was detected in the sera of mice at 20 hr and it reached a maximum of 320 U/ml at 24 hr. This IFN activity was lost after heat- or acid-treatment, suggesting that the induced IFN is of gamma nature. The molecular weight of this IFN was estimated to be 19,000 daltons by gel filtration. After the oral administration of Ge-132, NK activity of spleen cells had increased at 24 hr and cytotoxic macrophages were induced in the peritoneal cavity at 48 hr. In mice, receiving intraperitoneal (i.p.) injections of trypan blue or carrageenan 2 days before oral administration of Ge-132, neither induction of IFN nor augmentation of NK activity followed. X ray irradiation of mice also rendered the mice incapable of producing IFN, all suggesting that both macrophages and lymphocytes are required for this IFN induction. After i.p. administration of induced IFN, both NK and cytotoxic macrophage activities appeared at 48 hr with as little as 20 U/ml titered IFN. These facts may indicate that the augmentation of NK and activation of macrophages in mice after oral administration of Ge-132 is mediated by induced IFN.     

Effects of 3-aminobenzamide on induction of multiorgan carcinogenesis by N-nitrosobis(2-hydroxypropyl)amine in hamsters

The effects of an inhibitor of poly(ADP-ribose)polymerase, 3-aminobenzamide (ABA), on N-nitrosobis(2-hydroxypropyl)amine (BHP)-induced pancreas, liver, gallbladder and lung carcinogenesis in Syrian golden hamsters were investigated. Animals were given either BHP alone, by subcutaneous injection at a dose of 500 mg/kg body weight, or in combination with an intraperitoneal injection of ABA 30 min after the BHP at a dose of 300 or 600 mg/kg body weight once a week for 5 weeks, and then killed 35 weeks after the commencement of the experiment. ABA exerted inhibitory effects on pancreas and lung carcinogenesis induced by BHP, with mean numbers of lesions (including hyperplasias and carcinomas) being significantly decreased compared with the BHP-alone group values, while no significant effect was observed on liver or gallbladder carcinogenesis. These results suggest that the effects of ABA on carcinogenesis depend on the target organ as well as the chemical carcinogen examined.     

The effect of an oral administration of Lactobacillus casei strain shirota on azoxymethane-induced colonic aberrant crypt foci and colon cancer in the rat

The preventive effect of oral administration of viable Lactobacillus casei strain Shirota (LcS) on azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) and colon cancers in the rat was investigated. The study consisted of two experiments; in a short-term experiment (Exp-I), the inhibitory effect of 8- and 12-week treatments with LcS. Forty rats each received weekly a subcutaneous injection of AOM at a dose of 15 mg/kg of body weight for 5 weeks. Eight and twelve weeks after the start of the carcinogen treatment, each subgroup of rats were sacrificed, and the colon and the mesenteric lymph nodes (MLN) were removed. The number of ACFs and the surface marker of lymphocytes derived from the MLN were investigated. The large ACF (those comprising four or more aberrant crypts per focus) had significantly decreased in the rats which had consumed the LcS diet. And oral administration of viable LcS significantly recovered CD8 positive lymphocytes to the levels in the control group. In a long-term experiment (Exp-II), 30 rats each received weekly a subcutaneous injection of AOM at a dose of 7. 4 mg/kg of body weight for 10 weeks. Twenty-five weeks after the start of the carcinogen treatment, each subgroup of rats were sacrificed, and the colon were removed. The number and incidence of colon cancers were investigated. The number of rats with colon cancers and the number of colon cancers per rat, were significantly decreased in the rats which had consumed the LcS diet. LcS inhibited chemically-induced colon carcinogenesis in the rat. CD8 positive T lymphocytes may play a key role in the preventive effect against colon carcinogenesis.     

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。