To evaluate in vitro the antiprotozoal and cytotoxic activities of 80% methanol extract from 45 medicinal plants collected in Sankuru (Democratic Republic of Congo) against Trypanosoma brucei brucei, Trypanosoma cruzi and the chloroquine-sensitive Ghanaian strain of Plasmodium falciparum, and MRC-5 cell lines respectively.
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An ethanol extract of leaves from M. charantia was prepared. To research in vitro antiepimastigote activity, T. cruzi CL-B5 clone was used. Epimastigotes were inoculated at a concentration of 1 × 10(5) cells/mL in 200 µl tryptose-liver infusion. For the cytotoxicity assay, J774 macrophages were used. The antifungal activity was evaluated by microdilution using strains of Candida albicans, Candida tropicalis, and Candida krusei.
Diabetes, a common metabolic disorder, is characterized by hyperglycemia. Insulin is the principal mediator of glucose homeostasis. In a previous study, we identified a trypsin inhibitor, named Momordica charantia insulin receptor (IR)-binding protein (mcIRBP) in this study, that might interact with IR. The physical and functional interactions between mcIRBP and IR were clearly analyzed in the present study. Photo-cross-linking coupled with mass spectrometry showed that three regions (17-21, 34-40, and 59-66 residues) located on mcIRBP physically interacted with leucine-rich repeat domain and cysteine-rich region of IR. IR-binding assay showed that the binding behavior of mcIRBP and insulin displayed a cooperative manner. After binding to IR, mcIRBP activated the kinase activity of IR by (5.87 ± 0.45)-fold, increased the amount of phospho-IR protein by (1.31 ± 0.03)-fold, affected phosphoinositide-3-kinase/Akt pathways, and consequently stimulated the uptake of glucose in 3T3-L1 cells by (1.36 ± 0.12)-fold. Intraperitoneal injection of 2.5 nmol/kg mcIRBP significantly decreased the blood glucose levels by 20.9 ± 3.2% and 10.8 ± 3.6% in normal and diabetic mice, respectively. Microarray analysis showed that mcIRBP affected genes involved in insulin signaling transduction pathway in mice. In conclusion, our findings suggest that mcIRBP is a novel IRBP that binds to sites different from the insulin-binding sites on IR and stimulates both the glucose uptake in cells and the glucose clearance in mice.
All the patients used their regular conventional medications together with herbal remedies. The most commonly used medication was metformin (91.4%). Ivy gourd (Coccinia grandis) was the most commonly used herbal remedy (32%), followed by crepe ginger (Costus speciosus) (25%) and bitter gourd (Momordica charantia) (20%). Herbal remedies used less frequently were finger millet (Eleusine corocana) (5%), anguna leaves (Wattakaka volubilis) (5%), goat weed (Scoparia dulcis) (4%), Salacia reticulata (4%), fenugreek (Trigonella foenum-graecum) (3%) and tree turmeric (Coscinium fenestratum) (0.5%). None of the patients used commercially available over-the-counter herbal products. The common preparations were salads (72.8%), curries (12.8%), herbal tea (6%), and herbal porridges (6%).
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This study investigated the hypocholesterolaemic effects of bitter melon aqueous extracts (BMAE) in vitro, the inhibitory effects of BMAE on pancreatic cholesterol esterase (CEase) and incorporation of cholesterol into micelles were investigated. BMAE decreased the in vitro micellar solubility of cholesterol in a dose-dependent manner. The conformation of CEase was investigated by means of circular dichroism (CD) and fluorescence. The result revealed the decrease of α-helix contents, increase of β-sheet and exposure of aromatic amino acid residuals. The incorporation of cholesterol into micelles was inhibited by BMAE. A complex was observed by transmission electron microscopy (TEM), which indicated interaction between cholesterol and BMAE. The result revealed that BMAE can play a role in decreased intestinal cholesterol absorption via inhibition of CEase, and of micelle formation.
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TST led to significant development of cold allodynia, mechanical and heat hyperalgesia, dynamic mechanical allodynia, and functional deficit in walking along with rise in the levels of TBARS and TNF-alpha. Administration of MC (200, 400, and 800 mg/kg) significantly attenuated TST-induced behavioural and biochemical changes. Furthermore, pretreatment of BADGE (120 mg/kg, intraperitoneally) abolished the protective effect of MC in TST-induced neuropathic pain.
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Serine proteinase inhibitors of the squash family were isolated from bitter gourd (Momordica charantia LINN.) seeds by the conventional purification method. Heat treatment of the extract of the seeds allowed removal of large amounts of protein without loss of trypsin and elastase inhibitory activities. From the supernatants thus obtained, the inhibitors were isolated to homogeneity by ion-exchange chromatography, gel filtration, and reversed phase chromatography. One trypsin inhibitor (Momordica charantia trypsin inhibitor-III; MCTI-III) and three elastase inhibitors (Momordica charantia elastase inhibitor-II, -III, and -IV; MCEI-II, -III, and -IV) were newly isolated in addition to trypsin inhibitors MCTI-I and -II and elastase inhibitor MCEI-I previously reported [Hara, S. et. al. (1989). J. Biochem. 105, 88-92]. The primary structures of the four new inhibitors were determined as follows. [sequence: see text] The dissociation constants, Ki, of MCTI-III complex with bovine beta-trypsin, and of MCEI-II, -III, -IV with porcine elastase were determined to be 1.9 x 10(-7) M, 9.4 x 10(-9) M, 4.0 x 10(-9) M, and 4.7 x 10(-9) M, respectively. Although MCTI-III differed from MCTI-I in only two amino acids, having Gly(3) and Gln(13) in place of Arg(3) and Arg(13), the Ki value of MCTI-III was 20-fold larger than that of MCTI-I. Addition of an amino terminal Glu residue, a dipeptide (Glu-Glu-), and a tripeptide (Glu-Glu-Glu-) to MCEI-I strengthened its elastase inhibitory activity by 200-fold.
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The aim of the study was to examine whether Momordica fruit extract (MFE) and Momordica leaves extract (MLE) might exert any chemopreventive effect in a two stage protocol in skin carcinogenesis with Swiss albino mice. The tumour incidence, tumour yield, tumour burden and cumulative no. of papillomas were found to be higher in the controls (without either extract) as compared to the MFE or MLE treated experimental groups. In a melanoma model, the mice which received fruit and leaf extracts of Momordica at the doses of 500 and 1000 mg/kg body weight for 30 days showed increase in life span of animals and tumour volume was significantly reduced as compared to control values. In cytogenetic studies, a single application of Momordica extracts at doses of 500, 1000 and 1500 mg/kg body weight, 24 hours prior the i.p. administration of cyclophosphamide, significantly prevented micronucleus formation and chromosomal aberrations in a dose dependent manner in bone marrow cells of mice. The present study demonstrate chemopreventive potential of Momordica fruit and leaf extracts on DMBA induced skin tumorigenesis, melanoma tumour and cytogenicity.
Ginsenosides Rb1, Rb2, Rc and Rg1 inhibited steroidogenesis induced by a maximally active dose of corticotropin in isolated rat adrenal cells. The galactose-binding lectins from Momordica charantia seeds and Trichosanthes kirilowii tubers and mannose-binding concanavalin A did not affect basal corticosterone production. The lectins potentiated steroidogenesis induced by a submaximal dose of corticotropin but were without effect on steroidogenesis induced by a maximally active dose of corticotropin. Momordica charantia insulin-like peptide did not affect steroidogenesis.
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Graded concentrations (1.25-100 μg/mL) of the crude methanolic and water extracts and fractions (dichloromethane, ethyl-acetate, n-butanol and water) were evaluated for abilities to scavenge 2,2-diphenyl-2-picrylhydrazyl hydrate (DPPH), nitric oxide (NO), superoxide (SO) radicals and to inhibit lipoxygenase and formation of advanced glycation endproduct (AGE) in vitro. The MTT (3-(4, 5-dimethylthazol-2-yl)-2,5-diphenyl tetrazonium bromide) cytotoxicity test was performed on 3T3 cell line.
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Subchronic study of MCE in alloxan induced diabetic rats showed significant antihyperglycemic activity by lowering blood glucose and GHb%, percent glycosylated haemoglobin. Pattern of glucose tolerance curve was also altered significantly. MCE treatment enhanced uptake of glucose by hemidiaphragm and inhibited glycogenolysis in liver slices in vitro. A significant reduction in the serum cholesterol and glyceride levels of obese rats following MCE treatment was also observed.
Salt-fractionated bitter gourd (Momordica charantia) proteins were employed for the decolorization of disperse dyes in the presence of H2O2. The effect of various experimental conditions such as concentration of enzyme, H2O2, phenol, reaction time, pH and temperature on the decolorization of dyes was investigated. Dyes were recalcitrant to the decolorization catalysed by bitter gourd peroxidase. However, these dyes were decolorized significantly in the presence of a redox mediator, phenol. Bitter gourd peroxidase (0.215 U/mL) could decolorize about 60% of Disperse Red 17 in the presence of 0.2 mM phenol, whereas Disperse Brown 1 was decolorized by only 40% even in the presence of 0.4 mM phenol. Maximum decolorization of dyes was achieved in the presence of 0.75 mM H2O2 in a buffer ofpH 3.0 and 40 degrees C within 30 min. The K(m) values obtained were 0.625 mg/(L x h) and 2.5 mg/(L x h) for Disperse Red 17 and Disperse Brown 1, respectively. In all the experiments, Disperse Brown 1 was found to be more recalcitrant to decolorization catalysed by bitter gourd peroxidise, as compared to Disperse Red 17.
Our survey showed significant retention of traditional knowledge of medicinal plants in rural Trinidad. More interestingly, a large remnant of medico-cultural concepts such as "cooling/cleanser", "afterbirth", "stoppage-of-water" and "womb infection" persist in the rural population. Although the scientific literature show that some of the cited plants possessed antimicrobial, anti-inflammatory and related pharmacological activities in laboratory studies, these results must be taken with caution until clinical trials are conducted to establish safety and efficacy.
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MAP30 is an anti-HIV plant protein that we have identified and purified to homogeneity from bitter melon (Momordica charantia). It is capable of acting against multiple stages of the viral life cycle, on acute infection as well as replication in chronically infected cells. In addition to antiviral action, MAP30 also possesses anti-tumor activity, topological inactivation of viral DNA, inhibition of viral integrase and cell-free ribosome-inactivation activities. We have cloned and expressed the MAP30 gene. The objective of this study is to characterize recombinant MAP30 (re-MAP30) and to determine its anti-HIV, anti-tumor and other activities. We report here that re-MAP30 inhibits HIV-1 and certain human tumors to the same extent as its native counterpart, natural MAP30 (nMAP30). The anti-HIV activity was measured by quantitative focal syncytium formation on CEM-ss cell monolayers, viral core protein p24 expression and viral-associated reverse transcriptase activity in HIV-1-infected H9 cells. The anti-tumor activity was measured by metabolic labeling of protein synthesis in tumor cells. In the dose range of the assay, re-MAP30 exhibits little toxicity to the uninfected viral target cells and other normal human cells. Identical to nMAP30, re-MAP30 is also active in topological inactivation of viral DNA, inhibition of viral DNA integration and cell-free ribosome inactivation. The cloning and expression of the gene encoding biologically active re-MAP30 provides an abundant source of homogeneous material for clinical investigations, as well as structure-function studies of this novel antiviral and anti-tumor agent.
In total, 72 Sprague-Dawley rats were used for the study. The animals were subdivided into two groups: a nondiabetic group (n = 36) and a group with diabetes induced by streptozotocin (n = 36). Both groups were subdivided further into a nontreated control group (n = 18), and a topically treated group with MC extract administered daily (n = 18). The wound was inflicted with a 6-mm punch-biopsy needle on the dorsal aspect of the thoracolumbar region. The animals were killed on the days 1, 5 and 10 after wound creation. The rate of wound closure and the total protein content was estimated. Histological study of the wound tissue at days 5 and 10 was also performed.
The leaf extracts increased the intracellular accumulation of [3H]-vinblastine in KB-V1 cells in a dose-dependent manner, but extracts from the fruits and tendrils had no effect. By modulating Pgp-mediated vinblastine efflux, the leaf extracts decreased the [3H]-vinblastine efflux in KB-V1 cells in a dose-dependent manner, but not in KB-3-1 cells. Treatment of drug-resistant KB-V1 cells with bitter melon leaf extracts increased their sensitivity to vinblastine, but similar treatment of KB-3-1 cells showed no modulating effect. The fruit and tendril extracts did not affect the MDR phenotype in either cell line.
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Effects of three different varieties (Koimidori, Powerful-Reishi, and Hyakunari) of bitter melon (Momordica charantia) and those of methanol fraction extract of Koimidori variety on serum and liver triglycerides were studied in rats. Feeding of diets containing either bitter melon or various fractions isolated by organic solvents caused no adverse effects on food intake or growth of rats. When the effect of three different varieties of bitter melon was compared, the Koimidori variety was found to be the most effective in lowering hepatic triglyceride levels as compared to the other two varieties, suggesting a variety-dependent difference in their activity. Furthermore, the active component(s) responsible for the liver triglyceride lowering activity of Koimidori variety was assumed to be concentrated in the methanol fraction, but not in other fractions such as the n-hexane, the acetone, or the residual fraction. The triglyceride lowering activity was furthermore confirmed by the dose-dependent reduction of hepatic triglyceride, resulting the lowest level in rats fed 3.0% supplementation. In these experiments, the effects on serum lipids were marginal. The results of the present and previous studies clearly show that bitter melon, especially Koimidori variety, exhibits a potent liver triglyceride-lowering activity.
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In recent years, use of environment friendly and biodegradable natural insecticides of plant origin have received renewed attention as agents for vector control. In this study, essential oils extracted by steam distillation from leaves of five plant species Centella asiatica L., Ipomoea cairica L., Momordica charantia L., Psidium guajava L. and Tridax procumbens L. were evaluated for their topical repellency effects against malarial vector Anopheles stephensi in mosquito cages. All essential oils were tested at three different concentrations (2, 4 and 6%). Of these, the essential oils of I. cairica, M. charantia and T. procumbens exhibited relatively high repellency effect (>300 minutes at 6% concentration), followed by C. asiatica and P. guajava which showed less effective (< 150 minutes at 6 % concentration). However, the ethanol applied arm served as control provided maximum 8.0 minutes repellency in this study. In general, clear dose-response relationships were established in all essential oils, with the highest concentration of 6% provided high repellency effect. The results obtained from this study suggest that essential oils of I. cairica, M. charantia and T. procumbens are promising as repellents at 6% concentration against An. stephensi and could be useful in the search for new natural repellent compounds.
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New York University School of Medicine.
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Based on the sequence reported by Lee-Huang,S, we cloned the MAP30 gene of Momordica charantia (balsam pear) into a prokaryotic expression vector pET28a (+). A method by using PCR for rapid identification of positive clone was developed. Result showed this screening method can be used to detect positive colonies from samples of bacterial, purified plasmid, liquid culture,and liquid culture treated with mixture of phenol/Chloroform. The result from liquid-culture-treated- PCR (LCT-PCR) is very close to that of by plasmid-PCR. LCT-PCR is reliable and much easier to used than plasmid-PCR, therefore the LCT-PCR can be used for clone screening during the molecular cloning.
Compared to baseline, mean reduction in HbA1-c at the endpoint was significant among patients of group I, group II and group III (p ≤ 0.05, p ≤ 0.02 and p < 0.005 respectively) and same was the case for FPG (p ≤ 0.05, p < 0.04, p < 0.003 respectively), but the improvement in 2 hour OGTT was significant only in group III (p < 0.03). The decrease in PSA was observed only among group I and group II with the later showing significant reduction from baseline (p < 0.01). In group III, the level slightly increased. Parameters including blood lipids, atherogenic index, body weight and SBP improved among patients of group I and group II but deteriorated among group III patients.
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Momordica charantia L., also known as bitter melon, has been shown to ameliorate obesity and insulin resistance. However, metabolic changes regulated by M. charantia in obesity are not clearly understood. In this study, serums obtained from obese and M. charantia-treated mice were analyzed by using gas and liquid chromatography-mass spectrometry, and multivariate statistical analysis was performed by Orthogonal partial least squares discriminant analysis. The results from this study indicated that body weight fat and insulin levels of obese mice are dramatically suppressed by 8 weeks of dietary supplementation of M. charantia. Metabolomic data revealed that overproductions of energy and nutrient metabolism in obese mice were restored by M. charantia treatment. The antiinflammatory and inhibition of insulin resistance effect of M. charantia in obesity was illustrated with the restoration of free fatty acids and eicosanoids. The findings achieved in this study further strengthen the therapeutic value of using M. charantia to treat obesity. Copyright © 2016 John Wiley & Sons, Ltd.
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PEGylation could reduce the hepatotoxicity of alpha-MMC to rats.
Previous studies showed that the two forms of momorcharins which are isolated from seeds of Momordica charantia L. are effective in inducing early and midterm abortions in the mouse. Momorcharins were found to be teratogenic to the cultured mouse embryos at the early organogenesis stage. Morphological abnormalities were seen in the head, trunk and limbs. Ultrastructural studies on the visceral yolk sac of the momorcharin-treated embryos showed that the endodermal layer was deranged, membrane invaginations at the apical surface were decreased and intercellular space became distended. It is likely that the teratogenic action of momorcharins on mouse embryos in vitro is mediated through the deleterious effects on the visceral yolk sac, which functions as a vital transport organ for the conceptus at the immediate post-implantation period.
Momordica charantia Linn. (Cucurbitaceae), also called bitter melon, has traditionally been used as a natural anti-diabetic agent for anti-hyperglycemic activity in several animal models and clinical trials. We investigated the differences in the anti-diabetic properties and mechanism of action of Taiwanese M. charantia (MC) between type 1 diabetic (T1D) and type 2 diabetic (T2D) mice. To clarify the beneficial effects of MC, we measured non-fasting glucose, oral glucose tolerance, and plasma insulin levels in KK/HIJ mice with high-fat diet-induced diabetes (200 mg/kg/day of charantin-rich extract of MC [CEMC]) and in ICR mice with STZ-induced diabetes. After 8 weeks, all the mice were exsanguinated, and the expression of the insulin-signaling-associated proteins in their tissue was evaluated, in coordination with the protective effects of CEMC against pancreatic β-cell toxicity (in vitro). Eight weeks of data indicated that CEMC caused a significant decline in non-fasting blood glucose, plasma glucose intolerance, and insulin resistance in the KK/HIJ mice, but not in the ICR mice. Furthermore, CEMC decreased plasma insulin and promoted the sensitivity of insulin by increasing the expression of GLUT4 in the skeletal muscle and of IRS-1 in the liver of KK/HIJ mice; however, CEMC extract had no effect on the insulin sensitivity of ICR mice. In vitro study showed that CEMC prevented pancreatic β cells from high-glucose-induced cytotoxicity after 24 h of incubation, but the protective effect was not detectable after 72 h. Collectively, the hypoglycemic effects of CEMC suggest that it has potential for increasing insulin sensitivity in patients with T2D rather than for protecting patients with T1D against β-cell dysfunction.
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Lectin isolated from the seeds of Momordica charantia (MCL) is a galactose-specific glycoprotein. To investigate the effects of MCL on cell activation, we analyzed the responses of BALB/c splenocytes, thymocytes, T cells and B cells on MCL stimulation. Proliferation assays showed that MCL selectively stimulates the B cell subset of splenocytes (p<0.05) in a dose and time dependent manner and that this activation proceeds without the involvement of T cells. Flow cytometric analysis revealed that the fluorescein isothiocyanate (FITC)-labeled MCL binds to B cells, which was inhibited by specific sugars, including galactose. Mouse immunoglobulin (Ig) was able to inhibit MCL-induced proliferation of mouse B cells, suggesting MCL stimulates B cell activation via membrane Ig in the B cell surface. Moreover, after 96-h co-culture, MCL triggered splenocytes to produce a large amount of non-specific IgM in culture supernatants (p<0.01). Additionally, MCL was shown to up-regulate the cell activation marker CD86, in a B cell subpopulation distinct from that affected by LPS. These data suggest that MCL is a T cell-independent B cell activator and a polyclonal Ig inducer, and provide further information on the immunomodulatory effect of MCL.
The binding of 4-methylumbelliferyl beta-D-galactopyranoside (MeUmb-Galp), to Mormordica charantia lectin was studied by equilibrium dialysis and quenching of ligand fluorescence. The fluorescence of MeUmb-Galp decreases as a function of solvent polarity. On binding to M. charantia lectin, its fluorescence was nearly 100% quenched, showing that the binding of the glycoside takes place in hydrophobic environment. The binding of the fluorescent sugar was saccharide-specific as evidenced by reversal of MeUmb-Galp fluorescence quenching by lactose. The association constant is independent of the experimental method used and at 25 degrees C the value is (1.96 +/- 0.05) X 10(4) M-1. The number of binding sites as determined by equilibrium dialysis and fluorescence quenching agree very well with each other; n being equal to 1.98 +/- 0.02. The Ka value for the glycoside was also determined by competition studies employing reversal of fluorescence quenching of MeUmb-Galp by lactose. The value of ka obtained for lactose is 1.21 X 10(4) M-1 at 30 degrees C. The internal consistency of the association constant and number of binding site values at low and high saturation indicates the absence of additional subsite on M. charantia lectin. The thermodynamic parameters do not differ greatly with change in temperature; the values of - delta H degrees and - delta S degrees are equal to 30 +/- 9.63 kJ mol-1 and 21 +/- 0.3 J mol-1 K-1 respectively in the range of 15--35 degrees C indicting that the binding of M. charantia lectin to saccharide is exothermic in nature.
Momordica charantia fruits are used as a vegetable in many countries. From time immemorial, it has also been used for management of diabetes in the Ayurvedic and Chinese systems of medicine. Information regarding the standardization of this vegetable for its usage as an antidiabetic drug is scanty. There are many reports on its effects on glucose and lipid levels in diabetic animals and some in clinical trials. Reports regarding its mechanism of action are limited. So in the present review all the information is considered to produce some concrete findings on the mechanism behind its hypoglycemic and hypolipidemic effects. Studies have shown that M. charantia repairs damaged β-cells, increases insulin levels, and also enhance the sensitivity of insulin. It inhibits the absorption of glucose by inhibiting glucosidase and also suppresses the activity of disaccharidases in the intestine. It stimulates the synthesis and release of thyroid hormones and adiponectin and enhances the activity of AMP-activated protein kinase (AMPK). Effects of M. charantia like transport of glucose in the cells, transport of fatty acids in the mitochondria, modulation of insulin secretion, and elevation of levels of uncoupling proteins in adipose and skeletal muscles are similar to those of AMPK and thyroxine. Therefore it is proposed that effects of M. charantia on carbohydrate and fat metabolism are through thyroxine and AMPK.
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Our previous short-term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in cis(c)9, trans(t)11, t13-conjugated linolenic acid (CLN), inhibited the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF). In our study, the possible inhibitory effect of dietary administration of BMO on the development of colonic neoplasms was investigated using an animal colon carcinogenesis model initiated with a colon carcinogen AOM. Male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks to induce colon neoplasms. They also received diets containing 0.01%, 0.1% or 1% BMO for 32 weeks, starting 1 week before the first dosing of AOM. At the termination of the study (32 weeks), AOM induced 83% incidence (15/18 rats) of colonic adenocarcinoma. Dietary supplementation with 0.01% and 0.1% BMO caused significant reduction in the incidence (47% inhibition by 0.01% BMO, p<0.02; 40% inhibition by 0.1% BMO, p<0.05; and 17% inhibition by 1% BMO) and the multiplicity (64% inhibition by 0.01% BMO, p<0.005; 58% inhibition by 0.1% BMO, p<0.02; and 48% inhibition by 1% BMO, p<0.05) of colonic adenocarcinoma, though a clear dose response was not observed. Such inhibition was associated with the increased content of CLA (c9,t11-18:2) in the lipid composition in colonic mucosa and liver. Also, BMO administration in diet enhanced expression of peroxisome proliferator-activated receptor (PPAR) gamma protein in the nonlesional colonic mucosa. These findings suggest that BMO rich in CLN can suppress AOM-induced colon carcinogenesis and the inhibition might be caused, in part, by modification of lipid composition in the colon and liver and/or increased expression of PPARgamma protein level in the colon mucosa.