盐亭食管癌高发区饮食对人食管癌细胞增殖的影响

目的采用血清生理学方法,观察盐亭食管癌高发区饮食喂饲大鼠血清对人食管癌细胞Eca-109生长增殖的影响。方法将24只雄性SD大鼠分为3组,分别喂饲大鼠常规饲料、健康成人饮食及盐亭饮食7天,每天定时记录采食量及体重。用MTT法探讨用大鼠血清培养人食管癌细胞的适宜条件;分别以人正常肝上皮细胞HL7702及10%灭活小牛血清作为对照,采用细胞生长曲线、细胞群体倍增时间、3H-TDR掺入实验研究盐亭饮食喂饲大鼠血清对人食管癌细胞生长增殖的影响。结果喂饲健康成人饮食与常规饲料的大鼠其采食量及体重无差异;用5%未灭活大鼠血清取代10%灭活小牛血清适合人食管癌细胞培养;盐亭食管癌高发区饮食喂饲大鼠血清可明显促进人食管癌细胞生长,却不利于人正常肝上皮细胞生长,且与其他3个组均有统计学差异(P<0.05)。结论盐亭食管癌高发区饮食具有促进人食管癌细胞Eca-109生长增殖的作用。     

枸杞多糖对人食管癌细胞Eca-109的抑制作用及凋亡的研究

目的研究枸杞多糖(LBP)诱导人食管癌细胞Eca-109的凋亡作用及其作用机制。方法体外培养的人食管癌细胞Eca-109,细胞经不同剂量LBP处理后,采用MTT法测定细胞的增殖情况,流式细胞仪分析LBP对Eca-109细胞周期和凋亡的影响,用RT-PCR技术检测Eca-109细胞Survivin mRNA的表达。结果 LBP可明显抑制人食管癌细胞Eca-109的生长,并能诱导Eca-109细胞凋亡,凋亡率(%)分别为6.20±0.62、12.80±0.47和18.10±0.70,与对照组(0.78±0.91)%比较,差异有统计学意义(P0.01);各剂量药物处理组的肿瘤细胞SurVivin mRNA表达水平均明显降低(P0.01)。结论 LBP可抑制Eca-109细胞增殖,诱导细胞凋亡,该作用可能与下调细胞Survivin表达有关。     

Serum lipid levels correlate with solid tumor weight in hepatoma-bearing rats fed dietary fish oil

The effects of dietary fish oil (FO) on serum lipid levels and tumor proliferation were studied in Donryu rats subcutaneously implanted with the ascites hepatoma cell line AH109A. Solid tumor weight was significantly less and serum total cholesterol (T-Ch) level significantly lower in the groups fed the FO diet both before and after AH109A implantation than in the groups fed the corn oil diet. There were no significant effects in the serum lipid levels and tumor proliferation in the groups fed the FO diet only before or after the hepatoma implantation. The serum triacylglyceride, phospholipid, nonesterified fatty acid, T-Ch, and very-low-density lipoprotein+low-density lipoprotein-Ch levels showed significant positive correlations with the solid tumor weight. These results suggest that dietary FO ingestion after hepatoma implantation suppresses tumor proliferation and reduces serum lipid levels along with suppressing tumor proliferation.     

The role of dietary fatty acids in predicting myocardial structure in fat-fed rats

Background

The purpose of this study was to identify the affect on the proliferation Eca-109 cells treated with oxidized low-density lipoprotein (ox-LDL) combined with adriamycin (ADM).

Methods

Eca-109 cell were cultured in the presence of oxLDL/ADM, and cell proliferation tested by MTT and cell apoptosis was monitored by the proportion of apoptosis and cell cycle by flow cytomester. We simultaneously evaluated the level of associated- apoptosis Bcl-2, Bax, and Caspase-3 gene mRNA and protein.

Results

OxLDL were cytotoxic and activate apoptosis. OxLDL combined with ADM significant enhanced the proportion rate of apoptosis on a time and dose dependency. The expressions of the inhibiting apoptosis Bcl-2 gene mRNA and protein were down regulated, whereas, the expressions of the promoting apoptosis Bax, and Caspase-3 genes mRNA and protein were up regulation.

Conclusion

These results suggested that oxLDL have cytotoxicity and activate apoptosis on the Eca-109 cells. OxLDL combined with ADM have a synergistic effect on the apoptosis induced Eca-109 cells. Furthermore, oxLDL may contribute to the improvement of clinical chemotherapy of cancer need to make further investigation.     

硒和锌对人食管癌细胞株Eca109生长增殖影响的血清生理学研究

目的观察不同剂量硒、锌灌胃大鼠血清对人食管癌细胞株Eca109生长增殖的影响。方法将SD大鼠随机分为7组(基础饲料组、低硒组、高硒组、低锌组、高锌组、低硒低锌组、高硒高锌组),每组8只。喂养30天后取大鼠血清培养人食管癌细胞株Eca109和人正常肝上皮细胞株HL7702。用AAS法分别测定各组大鼠血清硒、锌;采用MTT法、3H-TDR掺入实验研究不同浓度硒、锌灌胃大鼠血清对两株细胞生长增殖的影响。结果 (1)基础饲料组血清硒、锌水平最低,高锌组血清锌最高;高硒高锌灌胃组大鼠血清硒水平最高,低硒低锌灌胃组血清硒水平次之,均明显高于基础饲料组;而此两组大鼠血清锌与基础饲料喂饲组大鼠血清锌水平差异无统计学意义(P>0.05);(2)与小牛血清对照组相比,只有高硒高锌灌胃组大鼠血清从第72h起抑制癌细胞生长(P<0.05),其余各组均促进食管癌细胞的生长;且该组大鼠血清也抑制肝细胞生长(P<0.05);(3)高硒高锌灌胃组大鼠血清明显抑制食管癌细胞DNA合成(P<0.05),其余各组与对照组作用相近,但该组对肝细胞DNA合成的抑制作用也最强。结论硒、锌在吸收、代谢等方面可能存在相互抑制作用;血清硒、锌含量较低会促进人食管癌细胞的增殖,而增加硒、锌的摄入可提高血清硒、锌的含量且可能抑制癌细胞的增殖。     

高脂膳食对人肺腺癌细胞SPCA1增殖活性影响的血清生理学研究

目的探讨用血清生理学方法直接在细胞水平上研究高脂膳食对人肺腺癌细胞系SPCA1增殖活性的影响。方法在探讨合适的血清生理学实验条件后,将20只SD雌性大鼠按体重随机分为高脂组和对照组,对照组自由进食普通饲料,高脂组自由进食高脂饲料(猪油∶普通饲料=1∶9),喂养7周后取血分离血清,用大鼠血清代替细胞培养液中小牛血清培养人肺腺癌细胞系SPCA1,用MTT比色法、3HTdR掺入法、流式细胞术检测方法从细胞生长曲线、细胞DNA合成以及细胞周期分布等方面观察高脂膳食喂养的雌性大鼠血清对癌细胞增殖活性的影响。结果(1)加入细胞培养液中血清浓度为15%时,人肺癌细胞生长较好,并且未灭活组好于灭活组。(2)从MTT比色法、3HTdR掺入实验以及流式细胞术结果来看,高脂膳食喂养的大鼠血清(RSTHFD)能促进肺腺癌细胞SPCA1的增殖和癌细胞DNA的合成,并能促使细胞进入活跃的有丝分裂状态。结论(1)用血清生理学方法可以直接在细胞水平上研究膳食因素对人肺腺癌细胞系SPCA1增殖活性的影响。(2)高脂膳食能促进人肺腺癌细胞SPCA1的增殖。     

Induction of apoptosis and cell cycle arrest in cancer cells by in vivo metabolites of teas

The present study was conducted to determine in vivo possibilities of inducing apoptosis and cell cycle arrest in rat cancer cells by green, oolong, and black teas and also to further identify the mechanisms inhibiting cancer cell proliferation by the sera from tea-treated rats. The tea extracts from these three kinds of tea, the rat sera obtained after oral intubation of the tea extracts, and the tea polyphenolic compounds, (-)-epigallocatechin-3-gallate, (-)-epigallocatechin, (-)-epicatechin-3-gallate, and the aflavins, were used in the related tests. The extracts, the sera from the treated rats, and the polyphenolic compounds significantly inhibited the proliferation of a rat hepatoma cell line (AH109A) and murine B16 melanoma cells but not normal rat mesothelial (M) cells. (-)-Epicatechin exhibited synergistic effects with (-)-epigallocatechin-3-gallate, (-)-epicatechin-3-gallate, and theaflavins against AH109A cell proliferation. The fluorescence staining of the nuclei, electrophoresis detection of DNA fragmentation, and analysis of cell cycle indicated that the sera from the tea-treated rats, the tea extracts, and the related tea components resulted in loss of viability, apoptosis, and cell cycle arrest at the G1 phase in AH109A and/or B16 cells, but not in normal M cells. Our results suggest that induction of apoptosis and cell cycle arrest may be important mechanisms of in vivo proliferation inhibition of AH109A and other cancer cells by these teas.     

Protein malnutrition: effect on rat peritoneal mast cell number, histamine content, and IgE receptors

To examine the effects of protein malnutrition on mast cells, rats were fed a protein-deficient diet (0.5% protein ad libitum) or normal diet (27% protein ad libitum or pair fed) for 16, 21, 27, or 57 d. Male rats in the different groups showed no significant differences in mast cell number or histamine content per mast cell. IgE binding sites as measured by flow cytometry were decreased in rats on the deficient diet. Even after stripping receptors of endogenous IgE and then labeling with fluorescent IgE, the difference remained, thus confirming the lower number of mast cell IgE receptors in rats maintained on the protein-deficient diet.     

Inhibitory effect of coffee on hepatoma proliferation and invasion in culture and on tumor growth, metastasis and abnormal lipoprotein profiles in hepatoma-bearing rats

We have already reported that instant coffee powder (ICP) and ICP-loaded rat sera could suppress proliferation and invasion of rat ascites hepatoma cell line of AH109A in vitro. In this report, we examined the mechanisms for suppression of tumor cell proliferation and invasion by ICP, and the effect of ICP on in vivo tumor growth, metastasis and abnormal lipoprotein profiles in hepatoma-bearing rats. ICP, when directly added to the culture media, induced cell cycle arrest (elongation of S phase) at a lower concentration (0.3 mg/mL) and apoptosis at a higher concentration (0.6-1.2 mg/mL). ICP and ICP-loaded rat sera showed reactive oxygen species (ROS)-scavenging property and canceled the enhancement of invasive activity of hepatoma cells induced by ROS in vitro. These results suggest that ICP suppresses the proliferation by inducing cell cycle arrest and apoptosis, and the invasion by scavenging ROS and that ICP could retain these properties after their gastrointestinal absorption. The hepatoma-bearing rats were fed with a 20% casein diet (20C) or 20C supplemented with 0.1%, ICP for 14 d. Dietary ICP significantly reduced solid tumor growth and tended to reduce hepatoma metastases to lung and lymphatic nodes, suggesting that ICP could suppress tumor cell proliferation and invasion in vivo. In addition, dietary ICP significantly increased serum high-density lipoprotein (HDL)-cholesterol and tended to reduce very low-density and low-density lipoprotein (VLDL+LDL)-cholesterol, resulting in amelioration of abnormal lipoprotein profiles occurred in hepatoma-bearing rats. In conclusion, ICP has the ability to induce cell cycle arrest and apoptosis in hepatoma cells and to suppress tumor cell invasion by reducing oxidative stresses in vitro, and it could also exhibit these effects in vivo, leading to the inhibition of tumor growth and metastases.     

Hydroxymatairesinol and its mammalian metabolite enterolactone reduce the growth and metastasis of subcutaneous AH109A hepatomas in rats

Both epidemiological and experimental evidence is accumulating to show that a lignan-rich diet may reduce the risk of human breast cancer. Possible anti-cancer effects of dietary lignans on hepatomas or hepatoma cells have not been the topic of earlier studies. In the present study, we examined the effect of 7-hydroxymatairesinol (HMR) and its mammalian metabolite, enterolactone (ENL), on AH109A hepatoma cell proliferation and invasion in vitro. HMR and ENL inhibited the proliferation and invasion of AH109A hepatoma cells in vitro. The 50% inhibitory concentration (IC50) of hepatoma cell proliferation was lower for ENL (10 microM) than HMR (> 200 microM). Likewise, IC50 of hepatoma cell invasion was lower for ENL (9 microM) than HMR (144 microM). ENL suppressed hepatoma cell proliferation by accumulating cells in G1 phase and elongating doubling time of these cells, and by increasing the rate of apoptosis. Subsequently, we investigated in vivo the effect of dietary HMR and ENL on growth and metastasis of AH109A hepatomas in rats. Both of these compounds reduced the growth and metastasis of solid AH109A hepatomas in rats. These in vitro and in vivo findings suggest that HMR has inhibitory activities on tumor growth and metastasis in the hepatoma-bearing rats, and that this anti-tumor effect is mediated at least partially by ENL, a metabolite of HMR.     

Hydroxymatairesinol and Its Mammalian Metabolite Enterolactone Reduce the Growth and Metastasis of Subcutaneous AH109A Hepatomas in Rats

Both epidemiological and experimental evidence is accumulating to show that a lignan-rich diet may reduce the risk of human breast cancer. Possible anti-cancer effects of dietary lignans on hepatomas or hepatoma cells have not been the topic of earlier studies. In the present study, we examined the effect of 7-hydroxymatairesinol (HMR) and its mammalian metabolite, enterolactone (ENL), on AH109A hepatoma cell proliferation and invasion in vitro. HMR and ENL inhibited the proliferation and invasion of AH109A hepatoma cells in vitro. The 50% inhibitory concentration (IC ₅₀ ) of hepatoma cell proliferation was lower for ENL (10 μ M) than HMR (> 200 μ M). Likewise, IC ₅₀ of hepatoma cell invasion was lower for ENL (9 μ M) than HMR (144 μ M). ENL suppressed hepatoma cell proliferation by accumulating cells in G ₁ phase and elongating doubling time of these cells, and by increasing the rate of apoptosis. Subsequently, we investigated in vivo the effect of dietary HMR and ENL on growth and metastasis of AH109A hepatomas in rats. Both of these compounds reduced the growth and metastasis of solid AH109A hepatomas in rats. These in vitro and in vivo findings suggest that HMR has inhibitory activities on tumor growth and metastasis in the hepatoma-bearing rats, and that this anti-tumor effect is mediated at least partially by ENL, a metabolite of HMR.     

Comparison of lycopene and tomato effects on biomarkers of oxidative stress in vitamin E deficient rats

Background Cohort studies suggested that individuals with higher intake of tomatoes and tomato products have a lower risk of degenerative diseases. Lycopene, an antioxidant and antiproliferative carotenoid, has been hypothesized to be responsible for the health benefits of tomatoes. However, studies demonstrated a higher potential of tomatoes compared to lycopene to reduce oxidative stress or carcinogenesis. Aim of the study Our study aimed at distinguishing lycopene effect from that of tomato on oxidative stress, by using yellow tomato, a tomato variety devoid of lycopene. Methods Effects of feeding with none (control), 16% freeze-dried yellow tomato (YT), 16% freeze-dried red tomato (RT) or 0.05% lycopene beadlets (LB) were compared in a rat model with mild oxidative stress induced by low vitamin E diet (LVED). Four groups of 10 rats were fed ad libitum for 6 weeks. Physiological parameters such as ingesta, body, spleen and liver weights, cholesterol and triglycerides (TG) levels were assessed. Lycopene and vitamin E concentrations and oxidative stress biomarkers were measured in the plasma and/or liver and/or heart tissue of the rats. Results RT, YT, and LB had no effect on rats’ ingesta, body and spleen weights. RT, YT and LB had no effect on plasma cholesterol concentration. RT decreased TG level compared to control, YT and LB (P < 0.05). Rats fed RT or LB accumulated lycopene in plasma in contrast with rats fed YT. Heart level of thiobarbituric reactive species (TBARS) in rats fed RT or YT was lower than that in the control and the LB fed rats (P < 0.05). Despite similar concentrations of lycopene in plasma and liver, rats fed LB showed a significantly higher heart level of TBARS than rats fed tomatoes. RT increased erythrocyte superoxide dismutase (eSOD) activity compared with LB and nitric oxide (NO) level compared with control and LB. LB decreased ferric reducing ability of plasma (FRAP) level compared with control, RT and LB (P < 0.05). Conclusion Our study showed for the first time that tomatoes, containing or not containing lycopene, have a higher potential than lycopene to attenuate and or to reverse oxidative stress-related parameters in a mild oxidative stress context.     

Sera fatty acid effects on cultured rat splenocytes

Rats were fed either a stock diet or purified diets containing either 10% by weight corn oil or linseed oil for 8 weeks. Splenocytes from rats on the stock ration were cultured for 48 hours in media containing either serum from the rats fed stock diet, corn oil or linseed oil, or fetal bovine serum (FBS). Populations were cultured without stimulation and with stimulation by leucogglutinin (PHA), and the production of prostaglandin F2 alpha by the cells was determined. The serum from the corn oil-fed rats differed markedly in composition from that of the linseed oil-fed rats notably in the higher level of arachidonic acid (20:4 omega 6) and lower level of timnodonic acid (20:5 omega 3). FBS also had a lower level of 20:4 omega 6. These changes were reflected in the fatty acid composition of the spleen choline glycerophosphatide. PGF2 alpha production was significantly depressed in the medium from linseed oil-fed rats compared to the corn oil group. This effect was due to the competition of 20:5 omega 3 for the cyclooxygenase. Viability of cells was better in rat serum than in FBS. The study shows that when studying functions in cultured cells obtained from rats fed different dietary fats the dietary effect will be abrogated or modified by use of FBS in the medium.     

In vitro and in vivo effects of exogenous nucleotides on the proliferation and maturation of intestinal epithelial cells.

To determine the nutritional role of nucleotides, the in vitro and in vivo effects of exogenous nucleotides on the development of intestine were investigated. First, the in vitro effects of nucleotides on the proliferation and maturation of enterocytes were studied by using a human colon tumor cell line (Caco-2) and a rat normal small intestinal crypt cell line (IEC-6). Second, the in vivo effects of nucleotides were also studied in early weaned rats fed nucleotide-unsupplemented or high-nucleotide-supplemented diet. Nucleotide composition resembled that of human milk (CMP:UMP:AMP:IMP:GMP = 10:1:1:1:1, in weight). Nucleotide supplement did not enhance Caco-2 cells proliferation; however, it significantly enhanced maltase and sucrase activities. In contrast, nucleotides supplement enhanced ICE-6 cells proliferation and maltase activity. CMP, predominantly contained in the mixture, enhanced most effectively the proliferation and maturation of cells. In the in vivo experiment, nucleotides significantly enhanced sucrase activity in the intestinal mucosa of early weaned rats. The results presented here suggest that a nucleotide supplement may enhance enterocyte proliferation and/or maturation in vivo and in vitro. Therefore exogenous nucleotides may play an important role in the development of the intestine.     

Effect of gender on the response to a high fat diet in aging Fischer 344 rats

The purpose of this study was to describe the effects of high fat (HF) and low fat (LF) diets in male and female Fischer 344 (F344) rats ages 5, 23 and 27 mo. Rats were fed the diet for 3 mo, and then resting metabolic rate, body composition and adipose tissue cellularity were evaluated. Although body mass was greater in rats fed the HF diet, this difference was due to a rapid increase in mass within the first 2 wk. There was no difference in the rate of body mass gain after this period. Resting mass-independent metabolic rate did not significantly differ due to age, diet or gender. In general, percentage fat mass was greater in rats fed the HF diet and in female than in male rats in both diet groups. However, lean body mass (%) was not altered due to diet or age. Cell number of the retroperitoneal depot increased with age and diet between 5 and 23 mo of age in both male and female rats. There was no effect of age, diet or gender on retroperitoneal cell size or gonadal cell number and size. These data suggest that age, gender and diet do not significantly alter the ability of F344 rats to regulate body composition or fat cell proliferation.     

应激对缺锌大鼠免疫功能的影响

目的 观察应激和缺锌双重因素作用下机体免疫功能的变化，并初步了解机体在不同锌水平下的应激反应能力。方法 将Wistar大鼠胺体重随机分为缺锌组（ZD），缺锌应激组（SZD）；对喂组（PF），对喂应激组（SPF）；常锌组（CT），常锌应激组（SCT）。缺锌组以缺锌饲料9锌含量2.0mg/kg），对喂组和常锌组饲以正常饲料（锌含量38.5mg/kg）。喂养1周后，各应激组大鼠接爱光－电刺激，连续15d。然后，取血测定血清皮质醇，取胸腺和脾脏称重，并制备脾脏细胞以测定T细胞增列反应。结果 缺锌或应激时皮质醇含量均明显上升，以缺锌应激组最为明显。缺锌级大鼠食欲减退，生长发育迟缓，出现缺锌体征。应激和非应激条件下，缺锌均可以使胸`腺脾脏萎缩，脏体指数明显下降；各应激组珉春对应的非应激组比较，上述免疫器官的重量和指数均有不同程度的下降，其中，SZD组的胸腺重量和指数、脾脏指数，SPF组的胸腺指数均明显低于对应的非应激组。应激时T细胞增殖能力下降，以缺锌组最为明显。结论 应激和缺锌均可使机体的免疫功能下降；机体锌营养不良使得应激对其免疫功能的损害更为严重。     

Effects of geophagia (kaolin ingestion) on the maternal blood and embryonic development in the pregnant rat

Geophagia, in the form of clay-eating, is often observed during pregnancy in the human population. The intent of this study was to determine the effects of kaolin (clay) ingestion on the maternal blood and embryonic development of the pregnant rat. Thirty-six Sprague-dawley female rats were divided into three groups: control diet, 20% kaolin diet, and iron-supplemented 20% kaolin diet. The diets were fed 37 to 68 days, 69 to 95 days, and 96 to 117 days prior to fertilization, and the same diets were fed for the duration of the gestation period. The rats fed the kaolin diet exhibited significant reductions in hemoglobin, hematocrit, and red blood cell levels, thus indicating maternal anemia. There was also a significant reduction in the birth weight of the pups born to kaolin fed rats. The kaolin fed rats receiving an iron supplement maintained hematocrit, hemoglobin, red blood cell levels, and pup weight within the normal range.     

Marginal nutritional status of zinc, iron, and calcium increases cadmium retention in the duodenum and other organs of rats fed rice-based diets

Dietary minerals Zn, Fe, and Ca are antagonistic to Cd absorption. We showed earlier that rats fed a rice-based diet with a marginal content of these nutrients absorbed more Cd than rats fed adequate Zn-Fe-Ca (Environ. Sci. Technol., 36 (2002) 2684-2692). The present experiment was designed to determine the effects of marginal dietary Zn, Fe, and Ca on the uptake and turnover of Cd in the gastrointestinal tract. Two groups of weanling female rats (six per treatment) were fed a diet containing 40% cooked, dried rice containing 0.6 mg Cd/kg. The diet of one group contained adequate Zn (35 mg/kg), Fe (30 mg/kg), and Ca (5000 mg/kg), while that of the other group contained marginal Zn (6 mg/kg), Fe (9 mg/kg), and Ca (2500 mg/kg). Rats were fed for 5 weeks and then orally dosed with 1g of diet containing rice extrinsically labeled with 109Cd. From 0.25 to 64 days after dosing, 109Cd and total Cd concentrations were determined in intestinal segments. Shortly after dosing, 109Cd, as a percentage of the dose, was about 4 times higher in the duodenum of marginally fed rats than in that of control rats (10% vs 40%, respectively). Sixty-four days after dosing, 109Cd was 10 times higher in marginally fed rats than in controls; however, of the amount at day 1, <0.1% remained at day 64. After 5 weeks, the concentration of elemental Cd in the duodenum of the marginally fed rats was 8 times higher than that of control rats (24 microg/g dry wt. vs 2.9 microg/g dry wt., respectively). Cd concentrations in liver and kidney were 5 times higher in the marginally fed rats than those in controls (liver, 0.81 microg/g dry wt. vs 0.14 microg/g dry wt.; kidney, 4.7 microg/g dry wt. vs 0.92 microg/g dry wt., respectively). These data suggest that marginal intakes of Zn, Fe, and Ca cause the accumulation of Cd in the duodenum, which results in a greater rate of Cd absorption and a greater accumulation in the internal organs. Results are discussed in relation to mineral nutrient status and risk assessment of Cd in natural food sources.     

Effects of stock or purified diet on rat liver enzymes involved in the synthesis of dimethyl selenide.

Rats fed either a stock deit or a purified diet based on casein were tested for their ability to convert 75Se-sodium selenite to volatile selenium (dimethyl selenide) in vivo. This conversion was also studied in liver and kidney in vitro. When injected with a subacute dose of selenite (2 mg Se/kg), rats previously fed stock diet volatilized more than twice as much of the dose compared to rats fed the purified diet, confirming earlier findings. Parallel dietary effects were also observed in vitro using subcellular fractions incubated with 75Se-selenite, glutathione, TPNH, and S-adenosylmethionine. The 9-000 X g supernate prepared from rats fed stock diet synthesized dimethyl selenide at approximately twice the rate of that prepared from rats fed purified diet. A fourfold higher activity was observed with liver microsomal fractions from rats fed the stock diet, whereas cytosol was slightly more active in rats fed the purified diet. Kidney fractions showed analogous changes with diet, although the activity of kidney microsomal fraction was very low. Only minor differences in the levels of glutathione reductase, nonspecific disulfide reducatse, and non-protein thiols were observed in liver and kidney from rats fed the two diets. Considering the effects of diet on the various enzymes known from our previous studies to be involved in dimethyl selenide synthesis, it was concluded that the enhanced ability of rats fed stock diet to synthesize dimethyl selenide results from the induction of a liver microsomal enzyme, apparently a Se-methyltransferase, caused by unknown substances in the stock diet.