低剂量甲基汞在小鼠体内分布及其对细胞周期进程的影响

连续９０天饮用含甲基汞浓度为１／１０００ＬＤ５０、１／１００ＬＤ５０、１／５０ＬＤ５０和１／１０ＬＤ５０的自来水的雄性昆明小鼠，各脏器中总汞含量均高于对照组（Ｐ＜０．０５～０．００５），并且随着染毒剂量增加，脏器中总汞含量也随之增高。同时采用ＦＡＣＳｃａｎ流式细胞仪和“ＣｅｌｌＦＩＴ”软件分析脾细胞周期进程，发现除１／１０００ＬＤ５０剂量组外，其余各剂量组从Ｇｏ／Ｇ１时相进入Ｓ时相的脾细胞百分数均明显高于对照组（Ｐ＜０．０５），与染毒剂量呈明显正相关。表明连续经口摄入低剂量甲基汞小鼠脾细胞周期进程加快，细胞ＤＮＡ复制增强。     

氯化甲基汞对小鼠卵巢细胞周期的影响

为探讨氯化甲基汞对雌性动物生殖系统的影响，采用氯化甲基汞给雌性昆明种小鼠急性染毒，剂量为１／２００ ＬＤ５０，１／２０ ＬＤ５０和１／２ ＬＤ５０，染毒后采用ＦＡＣ－Ｓｃａｎ流式细胞仪技术分析了氯化甲基汞对卵巢细胞周期的影响。结果表明：１／２０ ＬＤ５０组和１／２ ＬＤ５０组中处于Ｇ０／Ｇ１期时相的细胞百分数高于对照组（Ｐ〈０．０５），而１／２－ ＬＤ５０组和１／２ ＬＤ５０组的Ｓ期时相的细胞的百     

甲基汞对卵巢细胞酶及其线粒体的影响

用氯甲基汞（以１／２００ＬＤ５０、１／２０ＬＤ５０和１／２ＬＤ５０即０．１９２５ｍｇ／ｋｇ、１．９２５ｍｇ／ｋｇ和１９．２５ｍｇ／ｋｇ体重的剂量）给昆明种雌性小鼠经口染毒，然后测定卵巢细胞中的ＬＤＨ、Ｇ－６－ＰＤ和ＳＤＨ活性，同时做卵巢细胞线粒体的电镜观察。结果表明：各剂量组的ＬＤＨ、Ｇ－６－ＰＤ活性明显低于对照组（Ｐ＜０．０５）。１／２ＬＤ５０和１／２０ＬＤ５０组的ＳＤＨ活性也明显低于对照组（Ｐ＜０．０５）。从电镜看到线粒体膜较完整，但在１／２ＬＤ５０和１／２０ＬＤ５０组中的线粒体嵴数目减少，甚至完全消失，基质呈空泡状改变。总之，酶活性改变，能量代谢的异常和线粒体的损伤可能是氯化甲基汞造成卵巢细胞功能改变的重要原因。     

氯化甲基汞对卵巢细胞酶及其线粒体的影响

用氯化甲基汞（以１／２００ＬＤ５０、１／２０ＬＤ５０和１／２ＬＤ５０即０．１９２５ｍｇ／ｋｇ、１．９２５ｍｇ／ｋｇ和１９．２５ｍｇ／ｋｇ体重的剂量）给昆明种雌性小鼠经口染毒，然后测定卵巢细胞中的ＬＤＨ、Ｇ－６－ＰＤ和ＳＤＨ活性，同时做卵巢细胞线粒体的电镜观察。结果表明：各剂量组的ＬＤＨ、Ｇ－６－ＰＤ活性明显低于对照组（Ｐ＜０．０５）。１／２ＬＤ５０和１／２０ＬＤ５０组的ＳＨＤ活性也明显低于对照组（Ｐ＜０．０５）。从电镜看到线粒体膜较完整，但在１／２ＬＤ５０和１／２０ＬＤ５０组中的线粒体嵴数目减少，甚至完全消失，基质呈空泡状改变。总之，酶活性改变，能量代谢的异常和线粒体的损伤可能是氯化甲基汞造成卵巢细胞功能改变的重要原因。     

低剂量甲基汞对小鼠胸腺和脾细胞周期进程的影响（摘要）

低剂量甲基汞对小鼠胸腺和脾细胞周期进程的影响（摘要）李修义，刘洪宇，张迎春，李艳华，牟颖，林秀武采用ＦＡＣＳｃａｎ流式细胞仪（ＦＣＭ）技术，分析了低剂量甲基汞连续饮用，对小鼠胸腺和脾细胞周期进程的影响。一、材料与方法１．动物染毒及分组：采用本枚实验动...     

氯化甲基汞对雄性小鼠的生殖毒作用

以１／５０００ＬＤ５０、１／１０００ＬＤ５０和１／１００ＬＤ５０的氯化甲基汞剂量分别给雄性小白鼠经口染毒７５天后，测定睾丸组织中的ＬＰＯ和ＬＤＨ－ｘ。结果表明，实验组的ＬＰＯ高于对照组；１／１０００ＬＤ５０和１／１００ＬＤ５０组的ＬＤＨ－Ｘ均低于对照组和１／５０００ＬＤ５０组；睾丸脏器系数各组间无差别。同时探讨了甲基汞造成雄性动物生殖能力下降的可能机制。     

扩张型心肌病恶性室性心律失常的心率变异性分析

本文对２９例扩张型心肌病（ＤＣＭ）分两组─发生室颤或室速（ＶＦ／ＶＴ）组和未发生室颤或室速组进行短程（３００个心动周期）心率变异性（ＨＲＶ）分析。时域法的参数为平均心率标准差（ＨＲＳＤ），连续３００个心动周期平均正常ＲＲ间期标准差（ＳＤＡＮＮ）相邻ＲＲ间期差的均方根（ｒＭＳＳＤ）相邻ＲＲ间期差异≥５０ｍｓ的百分数（ＰＮＮ５０）；频域法的参数为极低频（ＶＬＦ）、低频（ＬＦ）、高频（ＨＦ）成分，总功率（ＴＰ）及ＬＦ／ＨＦ比值。结果ＤＣＭ中发生ＶＦ／ＶＴ的ＨＲＳＤ、ＳＤＡＮＮ、ｒＭＳＳＤ、ＰＮＮ＿（５０）、ＶＬＦ、ＬＦ、ＨＦ、ＴＰ均明显低于未发生ＶＦ／ＶＴ（组Ｐ＜０．０５），ＬＦ／ＨＦ比值前组高于后组（Ｐ＜０．０５）。可见：ＨＲＶ在ＤＣＭ中发生ＶＦ／ＶＴ明显下降。提示：ＨＲＶ是ＤＣＭ恶性室性心律失常的重要预测手段。     

脱氧雪腐镰刀菌烯醇、黄曲霉毒素G_1对体外培养人外周血淋巴细胞凋亡影响的研究

以细胞培养、流式细胞仪ＤＮＡ含量分析及ＤＮＡ琼脂糖凝胶电泳方法研究了我国食管癌高发区磁县居民粮食中优势污染霉菌毒素脱氧雪腐镰刀菌烯醇（ＤＯＮ）和黄曲霉毒素Ｇ１（ＡＦＧ１）对人淋巴细胞凋亡的影响。流式细胞术（ＦＣＭ）检测结果显示,ＤＯＮ、ＡＦＧ１处理组淋巴细胞出现了典型的亚二倍体凋亡细胞峰,凋亡百分率与毒素作用时间（ＤＯＮ：２～７２小时;ＡＦＧ１：２～２４小时）及剂量（ＤＯＮ：５０～２０００μｇ／Ｌ;ＡＦＧ１：３．１２～２０００μｇ／Ｌ）呈正相关关系。ＤＮＡ琼脂糖凝胶电泳结果表明,ＤＯＮ（１０００μｇ／Ｌ）、ＡＦＧ１（１０００μｇ／Ｌ）处理２４小时淋巴细胞出现特征性的ＤＮＡ＂Ｌａｄｄｅｒ＂条带。因此表明,ＤＯＮ、ＡＦＧ１可诱导和促进体外培养的人外周血淋巴细胞发生凋亡。     

硒、维生素E对血脂及脂质过氧化作用的影响

成年雄性Ｗｉｓｔａｒ大鼠随机分为５组：正常对照组；高脂（ＨＦＤ）对照组；ＨＦＤ＋Ｓｅ（０．５ｍｇ／ｋｇ）组；ＨＦＤ＋ＶＥ（０．６ｇ／ｋｇ）组；ＨＦＤ＋Ｓｅ（０．５ｍｇ／ｋｇ）＋ＶＥ（０．６ｇ／ｋｇ）组。观察１２周。结果表明：ＨＦＤ＋Ｓｅ组、ＨＦＤ＋ＶＥ组及ＨＦＤ＋Ｓｅ＋ＶＥ组血清总胆固醇（ＴＣ）、甘油三酯（ＴＧ）及低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）水平皆明显低于ＨＦＤ组，而血清高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）水平明显高于ＨＦＤ组；ＨＦＤ＋Ｓｅ组、ＨＦＤ＋ＶＥ组及ＨＦＤ＋Ｓｅ＋ＶＥ组三组血清脂质过氧化物（ＬＰＯ）水平皆明显低于ＨＦＤ组，而血浆超氧化物歧化酶（ＳＯＤ）活力明显高于ＨＦＤ组；补Ｓｅ组（ＨＦＤ＋Ｓｅ组及ＨＦＤ＋Ｓｅ＋ＶＥ组）血浆谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活力明显高于ＨＦＤ组，而ＨＦＤ＋ＶＥ组血浆ＧＳＨ－Ｐｘ活力与ＨＦＤ组无显著性差异；肝脏病理检查结果，ＨＦＤ＋Ｓｅ组、ＨＦＤ＋ＶＥ组及ＨＦＤ＋Ｓｅ＋ＶＥ组肝脏脂变明显轻于ＨＦＤ组；其中ＨＦＤ＋Ｓｅ＋ＶＥ组效果最显著。结果提示，Ｓｅ和／或ＶＥ有调节血脂代谢、阻止脂肪肝形成及提高机体抗氧化能力的作用，对高脂血症有一定的预防作用。     

对苯二甲酸亚慢性肾毒效应的动态观察

为研究对苯二甲酸（ＴＰＡ）亚慢性毒性并为制定其卫生标准提供依据,以５０００、５００、５０ｍｇ／ｋｇ３个剂量ＴＰＡ对ＳＤ大鼠连续染毒９０天,动态观察大鼠血清酶（ＡＳＴ、ＧＰＴ、ＡＬＢ、ＡＬＰ、ＮＡＧ、ＧＧＴ）和尿酶（ＡＳＴ、ＡＬＰ、ＮＡＧ、ＧＧＴ、α１－ＭＧ）等参数的变化。结果表明：３０天时,５０００ｍｇ／ｋｇ剂量组尿α１－ＭＧ、ＮＡＧ有一过性升高（Ｐ〈０．０５）,５００、５０ｍｇ／ｋｇ剂量组ＡＬＰ     

甲基汞对小鼠睾丸生殖细胞凋亡作用

目的研究甲基汞对小鼠睾丸生殖细胞凋亡及其作用机制。方法采用原位末端标记（TUNEL）和免疫组织化学方法研究甲基汞对小鼠睾丸生殖凋亡及其凋亡基因的表达。结果甲基汞可使雄性小鼠睾丸生殖细胞的凋亡率增加，随着甲基汞染毒剂量的增加，1150LD50、1／10LD50组凋亡率与阴性对照组比较差异有统计学意义（P〈0．0S）。1／10LD50剂量染毒组低于1150LD50组，差异无统计学意义（P〉0．05）。Fas、Fas—L、半胱氨酸天冬氨酸特异性蛋白酶-3（caspase-3）表达增强，11100LD50组阳性表达率最高，与阴性对照组比较差异有统计学意义（P〈0．05），随着染毒剂量的增加。各染毒组的阳性表达率有所下降。结论甲基汞可以诱导雄性小鼠生殖细胞的凋亡。     

DHPO生殖毒性的毒理学评价

目的研究1，2-二甲基-3-羟基-4-吡啶酮（DHPO）的急性毒性及不同剂量、不同时间的生殖毒性。方法以昆明种近交小鼠为实验对象．首先进行半数致死量（LD50）实验，然后对DHPO低（1／8LD50）、中（1／4LD50）、高（1／2LD50）剂量组染毒小鼠进行精子畸变率观察。结果DHPO染毒小鼠经口LD50为562．34mg／kg.精子畸变实验显示，1／8LD50组、1／4LD50组与阴性对照组比较，在第14．28，35，42，70d观察，差异均无统计学意义（P〉0．05）；1／2LD50组与阴性对照组比较，在第14，28，35d观察．差异均有统计学意义（P〈0．05），而在第42，70d观察，差异无统计学意义（P〉O．05）。结论DHPO的低（1／8LD50）、中（1／4LD50）剂量未显示有生殖毒性，高剂量（1／2LD50）具有一定生殖毒性。但可在42d后恢复。     

大豆异黄酮对电离辐射小鼠胸腺细胞周期、凋亡与增殖的影响

目的:研究大豆异黄酮(SI)对辐射小鼠免疫器官胸腺的影响。方法:90只雄性昆明小鼠,随机分为正常组、对照组和补充0.5%大豆异黄酮组,喂养2w后,4.0Gyγ-射线照射,于照射后12、24h和1w、2w杀死部分小鼠取胸腺,测定小鼠胸腺指数、胸腺细胞周期、细胞增殖指数及细胞凋亡率等指标。结果:辐射使小鼠胸腺明显萎缩,胸腺细胞凋亡率和G0-G1期细胞百分比明显增加(P<0.01),细胞G2-M期和S期的百分比及胸腺细胞增殖指数明显降低(P<0.05);补充SI,可使上述指标更接近正常组水平,使胸腺萎缩和胸腺细胞G0-G1期百分比比对照组明显减少(P<0.05),胸腺细胞的G2-M期百分比较对照组明显增加(P<0.05)。结论:膳食中补充0.5%大豆异黄酮可对免疫系统的胸腺起到辐射防护的作用。     

Iron deficiency alters the progression of mitogen-treated murine splenic lymphocytes through the cell cycle.

The influence of iron deficiency on the progression of mitogen-treated splenic lymphocytes through the cell cycle was studied in 16 control, 16 pair-fed, 15 iron-deficient (ID) and 16 ID mice that were repleted for up to 3 d (R3). The test and control diets differed only in iron concentrations (0.09 vs. 0.9 mmol/kg). When mice were killed (68 d of feeding), the hemoglobin concentration and liver iron stores of ID and R3 mice were <50% those of control mice (P < 0.05). Iron deficiency did not reduce the percentage of CD3(+) cells, but decreased CD3(+) cells/mg spleen (P < 0.05). In concanavalin A-treated and nonactivated cultures, there were no significant differences among groups in the percentages of cells in resting phase of the cell cycle (G0) to cell cycle initiation phase (G1), DNA synthesis phase (S) and exit from the S phase (G2) to mitosis phase (M) phases. In anti-CD3 and anti-CD3/anti-CD28-treated cultures, higher percentages of lymphocytes from ID and R3 mice than those from control and pair-fed mice were in the G0--G1 phase (P < 0.05). Conversely, lower percentages of activated cells from ID and R mice than those from control and pair-fed mice were in S and G2--M phases (P < 0.05). Incubation of lymphocytes with mitogens decreased the percentages of cells in G0--G1 phase from 90% to 80% in control and pair-fed but not in ID and R3 mice (P < 0.05). In activated cells, indices of iron status negatively correlated with the percentages of cells in G0--G1 (r = -0.306 to -0.597) but positively with those in S (r = 0.166--0.511) and G2--M phases (r = 0.265-0.59; P < 0.05). Data suggest that altered cell cycle progression likely contributes to impaired lymphocyte proliferation usually associated with iron deficiency.     

氯化镉对小鼠免疫细胞增殖和凋亡的影响

[目的]观察镉在体内染毒条件下 ,对小鼠免疫细胞的功能和凋亡的影响。[方法]采用一次腹腔注射氯化镉0.34、1.38和5.50mg/kg后8h处死和一次腹腔注射氯化镉5.50mg/kg后4、8、12h处死动物以及连续灌胃0.3、0.6和1.2mg/(kg·d)氯化镉14d后处死动物 ,利用MTT颜色反应法观察淋巴细胞转化、用DNA凝胶电泳法和流式细胞仪法检测细胞凋亡。[结果]小鼠经一次腹腔注射CdCl25.50mg/kg后4或8h可见胸腺细胞凋亡率为24.91 %和32.45 % ,脾细胞凋亡率分别为22.64 %和16.67 % ,均高于对照组 ;注射后12h胸腺细胞凋亡仍高于对照组。同时注射氯化镉5.50mg/kg4h后 ,ConA刺激的淋巴细胞转化功能明显低于对照组 ,抑制率接近50 % ;而在注射8h后 ,除了T细胞在ConA刺激下的转化功能受到抑制外 ,未受刺激的脾细胞增殖转化功能也受到抑制 ,抑制率为47 %。连续14d灌胃给氯化镉对小鼠脾脏细胞和胸腺细胞凋亡及淋巴细胞转化均未见明显的影响。[结论]小鼠经一次腹腔注射CdCl25.50mg/kg ,在胸腺细胞和脾细胞凋亡增加 ,同时T淋巴细胞转化功能也受到抑制。连续14d灌胃0.3、0.6和1.2mg/(kg·d)氯化镉未见对小鼠脾脏淋巴细胞转化和脾脏细胞、胸腺细胞的细胞凋亡有所影响     

Reduced thymocyte proliferation but not increased apoptosis as a possible cause of thymus atrophy in iron-deficient mice

Iron deficiency induces thymus atrophy in laboratory animals and very likely in humans by unknown mechanisms. The atrophy is associated with impaired cell-mediated immunity. In this study, we tested the hypothesis that thymus atrophy is a result of increased apoptosis and reduced thymocyte proliferation. Thymocytes were obtained from twenty-seven control, twenty-seven pairfed, twenty-seven iron-deficient (ID) mice; twelve and fourteen ID mice that received the control diet (0.9 mmol/kg versus 0.09 mmol/kg for the ID diet) for 1 d (repletion, R1) and 3 d (R3), respectively. Cell cycle analysis and apoptosis were studied by flow cytometry using propidium iodide staining and terminal deoxyuridine nick end labeling of DNA breaks assay respectively. When mice were killed, haemoglobin, haematocrit, and liver iron stores of ID, R1, and R3 mice were 25-40 % of those of control and pairfed mice Absolute and relative thymus weights and thymocyte numbers were 19 to 68 % lower in ID, R1, and R3 than in control and pairfed groups We found no significant difference among groups in the percentage of cells undergoing apoptosis. A higher percentage of thymocytes from ID and R1 mice than those of control, pairfed, and R3 mice were in the resting phase of the normal cell cycle Conversely, a lower percentage of thymocytes from ID and R1 mice than those from control, pairfed, and R3 mice were in the DNA synthesis phase and late phase of DNA synthesis and onset of mitosis (G2-M) Indicators of iron status positively correlated (r 0.3 to 0.56) with the percentage of thymocytes in the G2-M phase Results suggest that reduced cell proliferation but not increased apoptosis is the cause of thymus atrophy associated with iron deficiency.     

急性氧乐果中毒大鼠血清酶的变化及维生素C保护作用

目的探讨急性氧乐果中毒大鼠血清丙二醛(MDA)、超氧化物岐化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的动态变化及维生素C的保护作用.方法 72只Wistar大鼠皮下注射不同浓度(0.1、0.5LD50)的氧乐果制备急性有机磷中毒(AOPP)模型,并给予维生素C 200mg/kg治疗,动态检测各组大鼠血清MDA、SOD、GSH-Px含量.结果 0.1LD50和0.5LD50组MDA含量明显高于对照组(P＜0.05),SOD和GSH-Px含量明显低于对照组(P＜0.05):而0.5LD50组MDA含量明显高于0.1LD50组(P＜0.05),SOD和GSH-Px含量明显低于0.1LD50组(P＜0.05);而给予VitC治疗后,MDA含量明显降低,SOD和GSH-Px含量明显升高.结论急性有机磷中毒时氧自由基参与了组织细胞的损伤,VitC治疗有一定的保护作用.     

不同强度微波辐射对小鼠胸腺的影响

目的　探讨不同强度微波辐射对小鼠胸腺细胞的影响。方法　取幼年小鼠 ,分别在微波频率 2 4 5 0MHz,功率密度 1、5、15mW cm2 条件下 ,每天辐射 1h ,连续全身辐射 30d后 ,断颈取出胸腺。测定小鼠胸腺指数 ,观察胸腺组织学变化 ,流式细胞术分析胸腺T细胞亚群、胸腺细胞凋亡率、胸腺细胞周期进程的变化情况。结果　 5、15mW cm2 辐射组体重分别为 (2 8.10± 1.4 6 )、(2 7.5 0± 2 .5 2 )g,与对照组 [(31.95± 2 .5 1)g]相比 ,差异均有显著性 (P <0 .0 5 ) ;病理观察发现 ,中、高强度辐射组小鼠胸腺实质细胞可见深染核碎块 ,有些细胞核偏向一侧 ,胸腺小体略显增多 ;中、高强度辐射组胸腺细胞亚群CD8标记率 (2 9.14 %± 1.6 8%、2 9.18%± 0 .81% )比对照组 (2 6 .95 %± 1.2 7% )明显增高 ,差异有显著性 (P <0 .0 5 ) ;中、高强度微波辐射导致胸腺细胞周期进程中G2 M期细胞百分比 (12 .2 4 %±1.82 %、11.19%± 1.36 % )较对照组 (14 .5 8%± 0 .6 4 % )降低 ,且差异有显著性 (P <0 .0 1) ;3个辐射组胸腺细胞凋亡率分别为 7.18%± 0 .99%、10 .0 6 %± 1.5 8%、9.4 5 %± 0 .92 % ,与对照组 (4 .2 5 %±1.6 3% )相比 ,均有明显增加 ,差异有显著性 (P <0 .0 1) ,但 5、15mW cm2 两组间差异无显著性 (P >0     

褪黑素对小鼠淋巴细胞电离辐射损伤的防护作用

目的 探讨褪黑素(MLT)对小鼠淋巴细胞电离辐射损伤的防护作用及其机制。方法 采用流式细胞术和荧光分光光度法在离体和整体条件下分别检测小鼠淋巴细胞凋亡小体百分率和DNA裂解率。在此基础上,腹腔注射MLT,观察2 Gy X射线全身照射后24 h小鼠胸腺、脾脏淋巴细胞数量及胸腺细胞³H-TdR掺入率和Con A、LPS诱导的脾T、B淋巴细胞转化率的变化。结果 离体研究中,小鼠胸腺和脾脏淋巴细胞体外接受0.5~6.0 Gy照射后,凋亡小体百分率、DNA裂解率均呈剂量依赖性增加,而照射前预先加入2 mmol/L MLT,细胞凋亡小体百分率、DNA裂解率与单纯照射组比较均显著降低。整体研究中,2Gy全身照射前腹腔注射MLT,小鼠胸腺和脾脏淋巴细胞凋亡小体百分率和DNA裂解率显著低于单纯照射组,接近或低于假照水平,MLT剂量在0.1~2.5 mg/kg范围内均有作用,但无明显剂量依赖性。小鼠胸腺、脾脏淋巴细胞数量、胸腺细胞³H-TdR掺入率及有丝分裂原诱导的脾脏T、B淋巴细胞转化率在2 Gy全身照射后均显著低于假照组(P <0.001)。0.5~10 mg/kgMLT预先腹腔注射,胸腺、脾脏淋巴细胞数显著高于0 mg/kg体重组(单纯照射),其中0.5 mg/kg体重组增高最显著;胸腺细胞³H-TdR掺入率显著增高(P <0.01或P <0.001),以0.5 mg/kg体重组增高最显著;Con A诱导的T细胞转化率显著增高,也以0.5 mg/kg体重组为著;LPS诱导的B细胞转化率增高,以10mg/kg体重组最显著。结论 MLT在体内和体外均可减轻电离辐射诱导的小鼠淋巴细胞损伤,对免疫功能具有保护作用。     

Genistein inhibits growth of estrogen-independent human breast cancer cells in culture but not in athymic mice

The studies presented were conducted to assess the effect of the soy isoflavone genistein on proliferation of estrogen-independent human breast cancer cells (MDA-MB-231) in vitro and in vivo. Genistein (20 mcmol/L) inhibited cell proliferation in vitro by approximately 50%. Cell cycle progression was blocked in G(2)/M with 40 and 80 mcmol/L genistein. To evaluate the effect of dietary genistein on tumor growth in vivo, genistein was fed to female athymic mice inoculated with MDA-MB-231 cells. After solid tumor masses had formed, mice were fed genistein at a dose (750 mcg/g AIN-93G diet), shown to produce a total plasma genistein concentration of approximately 1 mcmol/L. This dose of genistein did not significantly (P > 0.05) alter tumor growth. Studies were then conducted to assess the effect of dietary genistein on initial tumor development and growth. Genistein (750 mcg/g AIN-93G diet), fed 3 d before cells were inoculated into mice, did not significantly (P > 0.05) inhibit tumor formation or growth. The plasma concentration of genistein in mice fed this dose of dietary genistein (750 mcg/g AIN-93G diet) does not appear sufficient to inhibit tumor formation or growth. Dietary genistein at 750 mcg/g AIN-93G diet does not inhibit tumor formation or growth. Additional studies were conducted to determine the effect of dietary dosages ranging from 0 to 6000 mcg/g AIN-93G diet on plasma genistein concentration. Plasma genistein concentration increased in a dose-dependent manner up to 7 mcmol/L at 6000 mcg/g AIN-93G diet. These data suggest that although genistein inhibits cancer cell growth in vitro, it is unlikely that the plasma concentration required to inhibit cancer cell growth in vivo can be achieved from a dietary dosage of genistein.