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Showing papers on "7,12-Dimethylbenz[a]anthracene published in 2007"


Journal ArticleDOI
TL;DR: Oral administration of MEOT remarkably reduced the lipid peroxidation activity and increased the antioxidants level in drug treated animals and decreased the tumour weight significantly (P<0.05) in the DMBA+MEOT groups.

80 citations


Journal ArticleDOI
TL;DR: Eugenol has a potent protective effect against DMBA‐induced genotoxicity, presumably through the suppression of the DMBA activation and the induction of its detoxification.

60 citations


Journal ArticleDOI
TL;DR: leaf extract of O. sanctum provides protection against chemical carcinogenesis in one or more of the following mechanisms: (i) by acting as an antioxidant; (ii) by modulating phase I and II enzymes; (iii) by exhibiting antiproliferative activity.

56 citations


Journal ArticleDOI
TL;DR: The results indicate that anti-progestins should be developed for the chemoprevention and treatment of hormone-responsive breast cancer.
Abstract: In this report, we evaluate the effects of a 21-substituted-19-nor-progestin, CDB-4124, on 7,12,-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinogenesis in rats in comparison with RU486. Sprague-Dawley female rats were treated with DMBA at 50 days of age in order to induce mammary tumors. When the tumors reached the size of 10-12 mm, the animals were treated for 28 days with the vehicle, RU486, progesterone, CDB-4124 at various doses, or CDB-4124 plus progesterone. Anti-progestins resulted in the regression in the size of the existing tumors, and in the suppressed development of new tumors and tumor multiplicity. Progesterone treatment, however, increased the size and multiplicity. Progesterone rendered an increased number of growing tumors as compared to the regression in the anti-progesterone treatment groups. The combination of CDB-4124 and high doses of progesterone opposed the efficacy of CDB-4124. The growth inhibitory effects of the anti-progestins were correlated with increased apoptosis and reduced cell proliferation. These results indicate that anti-progestins should be developed for the chemoprevention and treatment of hormone-responsive breast cancer.

51 citations


Journal ArticleDOI
TL;DR: Results suggest that asiatic acid may exert anti-tumorigenesis through inhibitory actions in NO and COX-2 signals.
Abstract: Asiatic acid, a pentacyclic triterpene, has been reported to induce apoptosis of various human cancer cells In the present study, we assessed the anti-tumor promoting effect of asiatic acid against 12-O-tetradecanoylphorbol 13-acetate (TPA)-mediated skin tumorigenesis in 7,12-dimethylbenz[a]anthracene (DMBA)-initiated ICR mice Topical application of asiatic acid prior to each application of TPA resulted in a significant reduction in skin tumor formation We also found that pre-application of asiatic acid alleviated TPA-induced [3H]thymidine incorporation, which is a conventional marker for skin tumor promotion In addition, asiatic acid inhibited the TPA-induced generation of nitric oxide (NO) and expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), which are known to play important roles in tumor growth, especially in the promotion stage In addition, topical application of aminoguanidine (AG), a selective iNOS inhibitor, and N(G)-nitro-L-arginine-methyl ester (NAME), another iNOS inhibitor, 30 min prior to TPA treatment significantly inhibited the TPA-induced COX-2 expression These results suggest that asiatic acid may exert anti-tumorigenesis through inhibitory actions in NO and COX-2 signals

48 citations


Journal ArticleDOI
TL;DR: Results demonstrate that mEH (EPHX1 gene) is a crucial enzyme for metabolic activation of DMBA in vivo leading to immunosuppression of spleen cells.

44 citations


Journal ArticleDOI
TL;DR: Pretreatment with GEN by gavage could enhance host resistances to the B16F10 tumor and DMBA-induced carcinogenesis, suggesting that GEN modulation of immune response was, at least partially, responsible for the antitumor effect of this compound.
Abstract: The objective of this study was to determine if genistein (GEN) modulation of the immune responses might contribute to the increased host resistances to tumors. A time-course study was performed in adult female B6C3F1 mice that had been exposed to GEN for 1-4 weeks at the dose level of 20 mg/kg by gavage. A significant increase in ex vivo cytotoxic T lymphocyte (CTL) activity was observed in the periods of 2 weeks and 4 weeks. Moreover, increased activities of CTLs were associated with a decrease in the percentage of CD4 + CD25 + T cells and an increase in the production of interferon-γ and activation of STAT1 (signal transducer and activator of transcription 1) and STAT4. Additionally, exposure of mice to GEN increased the activities of in vivo CTLs. An increased activity of natural killer (NK) cells was also observed. Further study in the B16F10 tumor model suggested that GEN-mediated enhancement in host resistance to B16F10 tumor was partially related to its potentiating effect on NK cells. Finally, 7,12-dimethylbenz[a]anthracene (DMBA)-induced tumor model was employed to determine the chemopreventive effect of oral GEN treatment. Mice pretreated with GEN for 2 weeks by gavage, the time when an enhanced CTL activity had been produced, had a decreased susceptibility toward DMBA-mediated carcinogenesis, while treatment with GEN after tumor induction conferred no protection. In conclusion, pretreatment with GEN by gavage could enhance host resistances to the B16F10 tumor and DMBA-induced carcinogenesis, suggesting that GEN modulation of immune response was, at least partially, responsible for the antitumor effect of this compound.

39 citations


Journal ArticleDOI
TL;DR: It is suggested that ethanolic O. sanctum leaf extract inhibits DMBA-induced genotoxicity and oxidative stress by modulating xenobiotic-metabolizing enzymes, reducing the extent of lipid and protein oxidation and up-regulating antioxidant defenses.
Abstract: The present study was designed to evaluate the protective effects of ethanolic Ocimum sanctum leaf extract against 7,12-dimethylbenz[a]anthracene (DMBA)-induced genotoxicity, oxidative stress, and imbalance in xenobiotic-metabolizing enzymes. Four different concentrations of ethanolic O. sanctum leaf extract (100, 200, 300, and 400 mg/kg of body weight) were administered to Wistar rats by intragastric intubation for five consecutive days followed by intraperitoneal injection of DMBA (35 mg/kg of body weight) 90 minutes after the final dose of the extract. Administration of DMBA increased bone marrow micronuclei, phase I enzymes, lipid peroxidation, and protein carbonyl formation. This was accompanied by a significant decrease in the activities of phase II detoxification enzymes and antioxidants in the liver, erythrocytes, and bone marrow. Pretreatment with ethanolic O. sanctum leaf extract at a concentration of 300 mg/kg of body weight significantly reduced micronuclei formation and phase I enzymes as well as lipid and protein oxidation with enhanced antioxidant and phase II enzyme activities. The results of the present study suggest that ethanolic O. sanctum leaf extract inhibits DMBA-induced genotoxicity and oxidative stress by modulating xenobiotic-metabolizing enzymes, reducing the extent of lipid and protein oxidation and up-regulating antioxidant defenses.

37 citations


Journal ArticleDOI
TL;DR: Findings suggest that DAS can effectively check the mutations induced by environmental toxicants, including cancer preventive properties, through DNA strand breakage.
Abstract: Mutations that occur through DNA strand breaks are the prerequisites for the development of tumors, which ultimately leads to various genetic disorders including cancer A number of naturally occurring compounds including certain dietary constituents play an important role in causation and prevention of a number of genetic diseases Diallyl sulfide (DAS), a volatile organosulfur compound present in garlic has been shown to possess various pharmacological effects including cancer preventive properties Now we are reporting the antimutagenic properties of DAS on 7,12- dimethylbenz[a]anthracene (DMBA), a carcinogenic polycyclic aromatic hydrocarbon, induced DNA strand breaks in mouse skin, using an alkaline unwinding assay DAS (25-10 mg/kg body-weight) was applied topically, prior and post to DMBA (5 mg/kg body-weight) at the sampling time of 24, 48, 72 and 96 h DAS application resulted in a significant (p < 0001) protection in DMBA-induced DNA strand breaks The pre-treatment of DAS (10 mg/kg body-weight) showed 6835% protection and post-treatment showed 5949% protection, at an intermittent period of 48 h, against DMBA-induced DNA strand breakage These findings suggest that DAS can effectively check the mutations induced by environmental toxicants

34 citations


Journal ArticleDOI
TL;DR: Results of the study indicate that the anticarcinogenic activity of KA during DMBA-initiated mammary carcinogenesis is mediated through alteration of hepatic antioxidant status as well as modulation of TCA cycle enzymes.

31 citations


Journal ArticleDOI
Y.S. Kim1, K.N. Bahn1, C.K. Hah1, H.I. Gang1, Y.L. Ha1 
TL;DR: Artemisia capillaris was the most effective anticarcinogenic medicinal herb for DMBA-induced mouse epidermal carcinogenesis among 4 medicinal herbs tested, and the effect might be attributed to chemical compounds of camphor, 1-borneol, coumarin, and achillin.
Abstract: Anticarcinogenic activity of medicinal herbs (Artemisia capillaris, Taxus cuspidata, Anthriscus sylveatris, and Curcuma longa) was examined for 7,12-dimethylbenz[a]anthracene (DMBA)-induced mouse skin carcinogenesis. Four types of solvent fractions (hexane, chloroform, ethyl acetate, and butanol) were prepared from the methanolic extract of medicinal herbs. The cytotoxicity and anticarcinogenic activities of solvent fractions were examined for mouse leukemia L1210 cancer cells and for female ICR mouse epidermal carcinogenesis induced by DMBA, respectively. The chloroform fraction of Artemisia capillaris, Taxus cuspidata, and Anthriscus sylveatris was more toxic to L1210 cells than other solvent fractions. The chloroform fraction of Artemisia capillaris markedly reduced the number of tumors/mouse and tumor incidence relative to that of other medicinal herbs tested. Major active chemical constituents in the chloroform fraction of Artemisia capillaries were found to be camphor, 1-borneol, coumarin, and achillin when analyzed by TLC and GC-MS. These results suggest that Artemisia capillaris was the most effective anticarcinogenic medicinal herb for DMBA-induced mouse epidermal carcinogenesis among 4 medicinal herbs tested, and the effect might be attributed to chemical compounds of camphor, 1-borneol, coumarin, and achillin.

Journal ArticleDOI
TL;DR: Oral administration of CiELet for 25 weeks significantly prevented the tumor incidence, volume and burden of the tumor and showed potent antilipidperoxidative effect as well as enhanced the antioxidant defense mechanisms in DMBA painted mice.
Abstract: The present study has investigated the chemopreventive and antilipidperoxidative effects of the ethanolic extract of Clerodendron inerme leaves (CiELet) in DMBA induced skin carcinogenesis in Swiss albino mice. The skin squamous cell carcinoma was induced in the shaved back of mice, by painting with DMBA (25 microg 0.1 mL(-1) acetone) twice weekly for 8 weeks. We have observed 100% tumor formation in the fifteenth week of experimental period. Elevated lipid peroxidation and decline in enzymatic and non-enzymatic antioxidants status was observed in tumor bearing mice. Oral administration of CiELet (300 mg kg(-1) bw) for 25 weeks significantly prevented the tumor incidence, volume and burden of the tumor. The CiELet also showed potent antilipidperoxidative effect as well as enhanced the antioxidant defense mechanisms in DMBA painted mice. The present study thus demonstrated the chemopreventive and antilipidperoxidative efficacy of CiELet in DMBA induced mouse skin carcinogenesis.

Journal ArticleDOI
TL;DR: It is suggested that the administration of a relatively low dose (1 μg) of DES during neonatal period may increase TEBs, thus resulting in a stimulatory effect on the initiation of MCs.
Abstract: Various doses of diethylstilbestrol (DES) were administered to rats once at birth. Thereafter, at 50 days after birth, the rats in all groups were given 10 mg 7, 12-dimethylbenz[a]anthracene (DMBA) and undergone necropsy at 300 days after birth. The incidence of mammary carcinomas (MCs) were 50, 54, 91, 39, 19% at 175 days after birth, and 77, 87, 100, 85, 75% at necropsy in the 0, 0.1, 1, 10, 100 μg groups, respectively. The incidence of rats without corpus luteum were 0, 0, 0, 30, 100% at 50 days after birth, and 0, 40, 53, 93, 100% at necropsy in the 0, 0.1, 1, 10, 100 μg groups, respectively. Observation of the whole mount specimens showed a higher number of terminal end buds (TEBs) in the 1 μg group and a lower number in the 100 μg group compared with the control at 50 days after birth. It suggested that the administration of a relatively low dose (1 μg) of DES during neonatal period may increase TEBs, thus resulting in a stimulatory effect on the initiation of MCs.

Journal ArticleDOI
TL;DR: The results suggest that the diet supplement of Se-enriched sprout after DMBA-dosing provides a significant chemoprevention against chemical-induced mammary cancer and may be a useful dietary ingredient for preventing breast cancer.
Abstract: Breast cancer is one of the major cancers in women, and dietary intake must be controlled to prevent it. Selenium (Se), especially Se compound in vegetables, is thought to be a promising chemopreventive dietary ingredient for preventing breast cancer. In this study, we developed Se-enriched Japanese radish sprout using a special Se-additional fertilizer, and identified the Se chemical forms. The newly developed Se-enriched sprout is produced within a week by the tank forming method, and the major chemical form was identified as Se-methylselenocysteine (MeSeCys) (80%). Then, the chemopreventive effects of the Se-enriched sprout were investigated using Sprague-Dawley female rats with mammary cancer, induced by a single oral dose of 10 mg or 14 mg of 7, 12-dimethylbenz[a]anthracene (DMBA). Mammary tumors were found in 11, 16 and 2 rats treated with DMBA and thereafter fed the basal (n = 34), sprout-added basal (n = 30) and Se-enriched sprout-added test diets (n = 30), respectively. The incidence of mammary tumors was significantly lower in the Se-enriched sprout-added test diet group (7%) than in the basal diet group (32%) or sprout-added basal diet group (53%). In contrast, no significant difference was detected in the numbers and incidence of the tumor between the basal diet group and Se-enriched sprout-added test diet group before DMBA-dosing. These results suggest that the diet supplement of Se-enriched sprout after DMBA-dosing provides a significant chemoprevention against chemical-induced mammary cancer. Thus, Se-enriched sprout may be a useful dietary ingredient for preventing breast cancer.

Journal ArticleDOI
TL;DR: The findings suggest that the cancer preventive effect of soy-based diets is mediated in part by reduction in AhR protein level posttranslationally, which reduces procarcinogen-induced CYP1A1 induction and metabolic activation.
Abstract: Consumption of a soy diet has been found to reduce cancer incidence in animals and is associated with reduced cancer risk in humans. In this study, the effect of consuming soy protein isolate (SPI) on the aryl hydrocarbon receptor (AhR)-mediated signaling pathway was investigated. Female Sprague-Dawley rats were fed AIN-93G diets with (+) or without (-) SPI-bound phytochemicals or casein (CAS) protein and gavaged orally with 7,12-dimethylbenz[a]anthracene (DM BA) or sesame oil. We found reduced (P 20 d. Experiments in which SPI + -fed rats were weaned to CAS diets demonstrated that AhR reduction by SPI + is not imprinted metabolically. To determine the molecular mechanisms of SPI + -mediated AhR reduction, an ex vivo model was developed using FGC-4 cells treated with serum from CAS- or SPI + -fed rats. SPI + serum treatment of FGC-4 cells reduced AhR expression and DMBA-induced CYP1A1 expression (P < 0.05). The reduction in AhR expression was in part due to the shorter half-life of AhR protein. Our findings suggest that the cancer preventive effect of soy-based diets is mediated in part by reduction in AhR protein level posttranslationally, which reduces procarcinogen-induced CYP1A1 induction and metabolic activation.



Journal ArticleDOI
TL;DR: The consumption of milk promoted the development of DMBA-induced mammary tumors in rats independent of the fat level, and this finding was found to be consistent with previous studies.

Journal ArticleDOI
TL;DR: How flow cytometry can be used to measure cytotoxicity by earthworm coelomocytes cultured and exposed to DMBA in vitro to study the immunosuppressive effects of DMBA on NK-like effector cells of E. fetida is demonstrated.

Journal ArticleDOI
TL;DR: It can be inferred that LCLE possesses potential chemopreventive activity in this experimental model of cancer, and this results were supported by histopathologic studies.
Abstract: The chemopreventive effect of Lantana camara. L. (Verbenaceae) methanol leaf extract (LCLE) on 7,12-dimethylbenz[a.]anthracene (DMBA)-induced skin cancer was investigated in Swiss albino mice. The skin lesions were induced by the twice-weekly topical application of DMBA (100 nmol/100 µL acetone) for 8 weeks on the shaved backs of mice. LCLE was administered at the maximal tolerated dose of 400 mg/kg twice a week, 1 week before DMBA application, and continued for 20 weeks thereafter. The results of the study revealed a significant decrease in incidence of skin papillomas in mice, slight weight gain in mice, and reduced death rate in comparison with DMBA alone at the end of 20 weeks. These results were supported by histopathologic studies. The skin section of LCLE-treated mice showed hyperplastic papillomatous lesions without the evidence of infiltration or cytological atypia. From the current study, it can be inferred that LCLE possesses potential chemopreventive activity in this experimental model...


Journal ArticleDOI
TL;DR: It is indicated that milk as well as estrone sulfate promotes the development of DMBA-induced mammary tumors in rat and could be associated with the occurrence of adenocarcinoma.
Abstract: To assess the effect of milk on the development of 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors, 48 female Sprague-Dawley rats treated with DMBA were divided into 3 groups and given 1 of 3 test solutions for 20 weeks as their drinking liquid: milk, estrone sulfate solution or tap water. The milk group showed a significantly great incidence (75%) in tumor development compared with the water group (38%) and was comparable to the estrone sulfate group (69%). Mean tumor number per rat in the milk group was significantly higher than that in the water group (p=0.009). We classified the mammary tumors into three histological types: intraductal papilloma, fibroadenoma, and adenocarcinoma. Although the percent of intraductal papilloma and fibroadenoma was almost same among the three groups, malignant tumor was found only in the milk and estrone sulfate groups. In conclusion, our results indicate that milk as well as estrone sulfate promotes the development of DMBA-induced mammary tumors in rat and could be associated with the occurrence of adenocarcinoma.

Journal ArticleDOI
TL;DR: It is suggested that DMBA-induced mammary tumors are more prevalent in milk-fed groups due in part to the contribution of estrogen and progesterone in milk.


Journal Article
01 Jul 2007-in Vivo
TL;DR: The results suggest that commercial soy milk enhanced the development of DMBA-induced mammary tumors in rats, and careful consideration should be given when explaining the beneficial effects of soy food.
Abstract: Background: Soy milk is a major soy food in China and Japan. Isoflavones in soy food are considered to protect women again breast cancer. Materials and Methods: The effects of soy milk consumption on 7,12-dimethylbenz(a) anthracene (DMBA)-induced mammary tumors in adult female rats was investigated. Sprague-Dawley rats were given 5 mg DMBA via intragastric intubation and then assigned to receive soy milk or water in addition to a normal rodent diet. Body weights, liquid and food intake, tumor number, location and development were recorded. After 20 weeks, liver, uterus and mammary tumors were removed from the sacrificed animals and examined. Plasma 17‚-estradiol concentration was also determined. Results: After 20 weeks of DMBA administration, all of the rats that drank soy milk developed mammary tumors, while the incidence in the control group was 70% (p 0.05). Uterine weight and plasma 17‚-estradiol concentrations were similar in the two groups. Conclusion: Our results suggest that commercial soy milk enhanced the development of DMBA-induced mammary tumors in rats. Thus, careful consideration should be given when explaining the beneficial effects of soy food. Breast cancer is by far the most common cancer of women, comprising 23% of all female cancers, with an estimated 1.15 million new cases in 2002 (1). Although the introduction of screening programs has perturbed the preexisting trends in incidence, a steady increase in the number of cases of breast cancer continues almost everywhere (2). Incidence rates are high in the developed

Journal ArticleDOI
TL;DR: Obesity enhances the risk for DMBA-induced mammary tumor development in rats and principal component analysis indicated class separation between tumors from lean and obese rats based on their metabolic profiles, illustrating the potential for using 1 H-NMR metabolomic methods for identifying altered metabolic pathways.
Abstract: t. Obesity increases mammary tumor development in Zucker rats following a single administration of the pro-carcinogen 7,12-dimenthylbenz(a)anthracene (DMBA). Fifty-day-old obese and lean female Zucker rats were orally gavaged with 65 mg/kg DMBA and sacrificed 139 days post DMBA treatment. At the end of the experiment, mammary tumors were detected in 68% of the obese rats compared to 32% of the lean group (P<0.001). 1 H nuclear magnetic resonance ('H-NMR) spectra obtained for hydrophilic and lipophilic extracts from excised tumors illustrated fundamental differences in metabolic profiles between the two groups. Differences were observed for key choline compounds, namely phosphocholine and glycerophosphocholine, both markers of malignancy and apoptosis. In addition, levels of lactate, creatine, myo-inositol, α-glucose, alanine, leucine, glutamate, glutamine, tyrosine, phenylalanine, and NADH varied between the lean and obese groups. Principal component analysis indicated class separation between tumors from lean and obese rats based on their metabolic profiles, illustrating the potential for using 1 H-NMR metabolomic methods for identifying altered metabolic pathways. Our results suggest that obesity enhances the risk for DMBA-induced mammary tumor development in rats. However, the mechanism for this increase in risk is currently unknown and will require further studies for elucidation.

Journal ArticleDOI
TL;DR: The results reveal that dietary supplementation of Polyphenon B exerts protection against DMBA-induced genotoxicity and oxidative stress by augmenting bone marrow antioxidant defense mechanisms.
Abstract: This study was designed to evaluate the protective effect of black tea polyphenols (Polyphenon B) against genotoxicity and oxidative stress during 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis. Since the bone marrow reflects hematopoietic stress caused by tumor cells, we used the frequency of micronuclei, the extent of lipid peroxidation, and the status of antioxidants in the bone marrow plasma as intermediate biomarkers of oxidative stress. All the hamsters painted with DMBA alone for 14 weeks developed buccal pouch carcinomas with a 75.4% increase in the incidence of bone marrow micronuclei as compared to untreated control (group 4). This was accompanied by an increase in lipid peroxidation as evidenced by the formation of thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides (LOOH) (61.3% and 17.8%, respectively) and a decrease in the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG) and the activities of GSH-dependent...


Journal ArticleDOI
TL;DR: The results suggest that formononetin might be considered as a natural ligand to bind on AhR and consequently produces a potent protective effect against DMBA-induced genotoxicity.
Abstract: Formononetin is an isoflavonoid phytoestrogen found in certain foodstuffs such as soy and red clover. In this study, we examined the action of formononetin with the carcinogen activation pathway mediated through the aryl hydrocarbon receptor (AhR) in MCF-7 breast carcinoma cells. Treating the cells with formononetin alone caused the accumulation of CYP1A1 mRNA as well as elevation in CYP1A1-specific 7-ethoxyresorufin O-deethylase (EROD) activity in a dose dependent manner. However, a concomitant treatment with 7,12-dimethylbenz[a]anthracene (DMBA) and formononetin markedly reduced both the DMBA-inducible EROD activity and CYP1A1 mRNA level. Under the same conditions, formononetin inhibited the DMBA-induced AhR transactivation, as shown by reporter gene analysis using a xenobiotic responsive element (XRE). Additionally, formononetin inhibited both DMBA-inducible nuclear localization of the aryl hydrocarbon receptor (AhR) and metabolic activation of DMBA, as measured by the formation of the DMBA-DNA adducts. Furthermore, formononetin competed with the prototypical AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), for binding to the AhR in an isolated rat cytosol. These results suggest that formononetin might be considered as a natural ligand to bind on AhR and consequently produces a potent protective effect against DMBA-induced genotoxicity. Therefore, that’s the potential to act as a chemopreventive agent that is related to its effect on AhR pathway as antagonist/agonist.

Journal ArticleDOI
TL;DR: Weak inhibitory effects of arctiin on DMBA-induced mammary tumor development were suggested in OVX rats, but any further assessment is needed to obtain conclusive results.
Abstract: Arctiin, a plant lignan, is metabolized to hormone-like compounds with weak estrogenic and antioxidative activity in experimental animals and man. To clarify its influence on mammary carcinogenesis, female rats were administrated 7,12-dimethylbenz(a)anthracene (DMBA) once, and when the incidence of palpable mammary tumors reached 50%, subjected to ovariectomy (OVX) and divided into tumor-bearing [DMBA-Tumor (+)] and no-tumor-bearing [DMBA-Tumor (-)] groups, subgroups of each then being fed soybean-free diet containing 0, 40, 200, and 1000 ppm of arctiin for 31 wk. The incidence and multiplicity of palpable tumors in the 200 ppm DMBA-Tumor (+) subgroup from week 12 of arctiin treatment tended to be decreased as compared to the 0 ppm subgroup and at terminal sacrifice, the volume of histopathologically defined mammary tumors was decreased in the 40 ppm DMBA-Tumor (-) subgroup, but again without statistical significance. In conclusion, weak inhibitory effects of arctiin on DMBA-induced mammary tumor development were suggested in OVX rats, but any further assessment is needed to obtain conclusive results.