cytellin and Colonic-Neoplasms

All the currently available cancer therapeutic options are expensive but none of them are safe. However, traditional plant-derived medicines or compounds are relatively safe. One widely known such compound is beta-sitosterol (BS), a plant derived nutrient with anticancer properties against breast cancer, prostate cancer, colon cancer, lung cancer, stomach cancer, ovarian cancer, and leukemia. Studies have shown that BS interfere with multiple cell signaling pathways, including cell cycle, apoptosis, proliferation, survival, invasion, angiogenesis, metastasis and inflammation. Most of the studies are incomplete partly due to the fact that BS is relatively less potent. But the fact that it is generally considered as nontoxic, the opposite of all currently available cancer chemo-therapeutics, is missed by almost all research communities. To offset the lower efficacy of BS, designing BS delivery for "cancer cell specific" therapy hold huge potential. Delivery of BS through liposome is one of such demonstrations that has shown to be highly promising. But further research did not progress neither in the field of drug delivery of BS nor in the field on how BS mediated anticancer activities could be improved, thus making BS an orphan nutraceutical. Therefore, extensive research with BS as potent anticancer nutraceutical is highly recommended.

Topics: Apoptosis; Breast Neoplasms; Cell Cycle; Colonic Neoplasms; Dietary Supplements; Drug Delivery Systems; Female; Humans; Leukemia; Liposomes; Lung Neoplasms; Male; Neoplasms; Orphan Drug Production; Phytoestrogens; Prostatic Neoplasms; Signal Transduction; Sitosterols

Substantial attention has been given to primary cancer prevention in daily life. Dietary factors are through to contribute to as much as one-third of the factors influencing the development of cancer. Ones of the components of a plant-based diet are beta-sitosterol and taraxasterol, compounds attracting our specific attention. This review summarizes the biological activities of presented phytosterols (anti-inflammatory, cholesterol-lowering, anti-microbial, anti-bacterial, anti-fungal effects). Our interest has been focussed especially on their anti-tumor and chemopreventive activity. They have been shown experimentally to inhibit colon and breast cancer development. They act at various stages of tumor development, including inhibition of tumorigenesis, inhibition of tumor promotion, and induction of cell differentiation. They effectively inhibit invasion of tumor cells and metastasis. With regard to toxicity, no obvious side effects of phytosterols have been observed in studies to date, with the exception of individuals with phytosterolemia. The exact mechanism by which dietary phytosterols act is not fully understood. However, some mechanisms have been offered. Therefore, they have a bright future in clinical application. Further investigation to explore their potential in tumor treatment may prove to be worthwhile.

Topics: Animals; Anti-Inflammatory Agents; Anticarcinogenic Agents; Antineoplastic Agents; Antioxidants; Breast Neoplasms; Colonic Neoplasms; Diet; Drugs, Chinese Herbal; Female; Humans; Phytosterols; Sitosterols; Sterols; Triterpenes

Adenoma formation in the colon has been shown to be initiated by an alteration in the genetic make-up which controls the repopulation of the mucosa. This defect is recognized primarily by an upward displacement of the major zone of DNA synthesis within one or a few crypts. Progression to a microadenoma involves an elevation of cell proliferation within these glands and may be hastened by mucosal responses to environmental and dietary factors which enhance cell turnover. The high proliferative activity of epithelial cells within these select crypts allows the unmasking of the neoplastic genotype and the expansion of these cells with a proliferative advantage. Continued rapid cell proliferation within the adenoma either indigenous to the excrescence or fueled additionally by luminal conditions may contribute to the evolution of a malignant genotype, the establishment of a severely dysplastic clone and ultimately to the production of invasive colon cancer.

Topics: Adult; Animals; Antioxidants; Colon; Colonic Neoplasms; Humans; Intestinal Polyps; Mice; Middle Aged; Neoplasms, Experimental; Precancerous Conditions; Rats; Sitosterols

The detrimental impact of reactive oxygen species on D.N.A. repair processes is one of the contributing factors to colon cancer. The idea that oxidative stress may be a significant etiological element for carcinogenesis is currently receiving more and more support. The goal of the current study is to evaluate the anti-inflammatory and anticancer activity of three powerful phytocompounds-sitosterol, amyrin, and epiafzelechin-alone and in various therapeutic combinations against colon cancer to identify the critical mechanisms that mitigate nickel's carcinogenic effect. To evaluate the ligand-protein interaction of four selected components against Vascular endothelial growth factor (VEGF), Matrix metalloproteinase-9 (MMP9) inhibitor and Interleukin-10 (IL-10) molecular docking approach was applied using PyRx bioinformatics tool. For in vivo analysis, hundred albino rats were included, divided into ten groups, each containing ten rats of weight 160-200 g. All the groups were injected with 1 ml/kg nickel intraperitoneally per week for three months, excluding the negative control group. Three of the ten groups were treated with β-sitosterol (100 mg/kg b wt), β-amyrin (100 mg/kg b wt), and epiafzelechin (200 mg/kg b wt), respectively, for one month. The later four groups were fed with combinatorial treatments of the three phyto compounds for one month. The last group was administered with commercial drug Nalgin (500 mg/kg b wt). The biochemical parameters Creatinine, Protein carbonyl, 8-hydroxydeoxyguanosine (8-OHdG), VEGF, MMP-9 Inhibitor, and IL-10 were estimated using ELISA kits and Glutathione (G.S.H.), Superoxide dismutase (S.O.D.), Catalase (C.A.T.) and Nitric Oxide (NO) were analyzed manually. The correlation was analyzed through Pearson's correlation matrix. All the parameters were significantly raised in the positive control group, indicating significant inflammation. At the same time, the levels of the foresaid biomarkers were decreased in the serum in all the other groups treated with the three phytocompounds in different dose patterns. However, the best recovery was observed in the group where the three active compounds were administered concomitantly. The correlation matrix indicated a significant positive correlation of IL-10 vs VEGF (r = 0.749**, p = 0.009), MMP-9 inhibitor vs SOD (r = 0.748**, p = 0.0 21). The study concluded that the three phytocompounds β-sitosterol, β-amyrin, and epiafzelechin are important anticancer agents which can target

Topics: Animals; Biomarkers; Colonic Neoplasms; Interleukin-10; Matrix Metalloproteinase 9; Molecular Docking Simulation; Nickel; Rats; Sitosterols; Vascular Endothelial Growth Factor A

Oxidative stress has become widely viewed as an underlying condition in diseases such as ischemia/reperfusion disorders, central nervous system disorders, cardiovascular disease, cancer, diabetes, etc. The role that antioxidants play in the process of carcinogenesis has recently gained considerable attention. β-Sitosterol, a naturally occurring sterol molecule, is a relatively mild to moderate antioxidant and exerts beneficial effects in vitro by decreasing the level of reactive oxygen species. The present study evaluated the antioxidant potential of β-sitosterol in 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis. The enzymatic and nonenzymatic antioxidants and lipid peroxides in colonic and hepatic tissues were evaluated. Generation of reactive oxygen species, beyond the body's endogenous antioxidant capacity, causes a severe imbalance of cellular antioxidant defense mechanisms. Elevated levels of liver lipid peroxides by DMH induction were effectively decreased by β-sitosterol supplementation. β-Sitosterol also exhibited a protective action against DMH-induced depletion of antioxidants such as catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione S-transferase, and reduced glutathione in colonic and hepatic tissues of experimental animals. Supplementation with β-sitosterol restored the levels of nonenzymatic antioxidants (vitamin C, vitamin E, and glutathione). Histopathological alterations in DMH-induced animals were restored to near normal in rats treated with β-sitosterol. Thus, β-sitosterol by virtue of its antioxidant potential may be used as an effective agent to reduce DMH-induced oxidative stress in Wistar rats and may be an effective chemopreventive drug for colon carcinogenesis.

Topics: 1,2-Dimethylhydrazine; Animals; Anticarcinogenic Agents; Antioxidants; Ascorbic Acid; Catalase; Colon; Colonic Neoplasms; Glutathione; Glutathione Peroxidase; Glutathione Reductase; Glutathione Transferase; Lipid Peroxidation; Male; Oxidative Stress; Rats; Rats, Wistar; Reactive Oxygen Species; Sitosterols; Superoxide Dismutase; Vitamin E

Asclepias curassavica Linn. is a traditional medicinal plant used by tribal people in the western ghats, India, to treat piles, gonorrhoea, roundworm infestation and abdominal tumours. We have determined the protective effect of beta-sitosterol isolated from A. curassavica in colon cancer, using in vitro and in vivo models.. The active molecule was isolated, based upon bioassay guided fractionation, and identified as beta-sitosterol on spectral evidence. The ability to induce apoptosis was determined by its in vitro antiradical activity, cytotoxic studies using human colon adenocarcinoma and normal monkey kidney cell lines, and the expression of beta-catenin and proliferating cell nuclear antigen (PCNA) in human colon cancer cell lines (COLO 320 DM). The chemopreventive potential of beta-sitosterol in colon carcinogenesis was assessed by injecting 1,2-dimethylhydrazine (DMH, 20 mg/kg b.w.) into male Wistar rats and supplementing this with beta-sitosterol throughout the experimental period of 16 weeks at 5, 10, and 20 mg/kg b.w.. beta-sitosterol induced significant dose-dependent growth inhibition of COLO 320 DM cells (IC50 266.2 microM), induced apoptosis by scavenging reactive oxygen species, and suppressed the expression of beta-catenin and PCNA antigens in human colon cancer cells. beta-sitosterol supplementation reduced the number of aberrant crypt and crypt multiplicity in DMH-initiated rats in a dose-dependent manner with no toxic effects.. We found doses of 10-20 mg/kg b.w. beta-sitosterol to be effective for future in vivo studies. beta-sitosterol had chemopreventive potential by virtue of its radical quenching ability in vitro, with minimal toxicity to normal cells. It also attenuated beta-catenin and PCNA expression, making it a potential anticancer drug for colon carcinogenesis.

Topics: Adenocarcinoma; Animals; Antineoplastic Agents, Phytogenic; Antioxidants; Apoptosis; Asclepias; beta Catenin; Cell Line; Cell Line, Tumor; Colon; Colonic Neoplasms; Disease Models, Animal; Dose-Response Relationship, Drug; Haplorhini; Humans; Kidney; Male; Phytotherapy; Plant Extracts; Proliferating Cell Nuclear Antigen; Rats; Rats, Wistar; Sitosterols

We reported previously that 7beta-hydroxysitosterol and 7beta-hydroxycholesterol induced apoptosis in Caco-2 cells. Apoptosis caused by 7beta-hydroxysitosterol but not by 7beta-hydroxycholesterol was related to a caspase-dependent process. In the present report, we compared the effects of both compounds on mitochondria integrity and on various modulators of apoptosis. When Caco-2 cells were exposed to both hydroxysterols, no changes in Bcl-2 and Bax expressions were detected indicating a Bcl-2/Bax-independent cell death pathway, whereas loss of mitochondrial membrane potential and cytochrome c release were observed. Endonuclease G expression and enhanced production of reactive oxygen species were detected in 7beta-hydroxycholesterol treated cells, but not with 7beta-hydroxysitosterol. Loss of mitochondrial membrane potential and cell death produced by both hydroxysterols were prevented by vitamin C. Lysosomal membrane integrity was altered with both hydroxysterols, but 7beta-hydroxysitosterol was significantly more active on than 7beta-hydroxycholesterol. Both hydroxysterols induced apoptosis by mitochondrial membrane permeabilization. However, 7beta-hydroxycholesterol exhibited a specific enhancement of oxidative stress and of endonuclease G expression despite its closely related chemical structure with 7beta-hydroxysitosterol. The two hydroxysterols exhibit different lipophilic properties which may explain their different biological effects.

Topics: Apoptosis; Ascorbic Acid; bcl-2-Associated X Protein; Caco-2 Cells; Colonic Neoplasms; Cytochromes c; Endodeoxyribonucleases; Humans; Hydroxycholesterols; Lysosomes; Membrane Potential, Mitochondrial; Mitochondria; Oxidative Stress; Proto-Oncogene Proteins c-bcl-2; Reactive Oxygen Species; Sitosterols

Recently several plant derived natural compounds have been screened for their anticancer activity in order to identify putative compounds with novel structures or mechanism of action. In the present study, fruits of Poncirus trifoliata were extracted with acetone and loaded onto silica gel column chromatography. The column was eluted with different solvents to obtain two bioactive compounds. The purity of compounds was analyzed by HPLC and their structures were identified by 1H and 13C NMR experiments as beta-sitosterol and 2-hydroxy-1,2,3-propanetricarboxylic acid 2-methyl ester (HPCME). beta-Sitosterol, HPCME, and trolox were tested for their antioxidant capacity by oxygen radical absorbance capacity (ORAC) measurement. Further, these compounds were tested for their inhibition of cancer cell proliferation and apoptosis using human colon cancer cell line (HT-29). These results were compared with the corresponding activity on non-cancerous (COS-1 fibroblast) cells. Cell proliferation and induction of apoptosis were determined by MTT assay and nuclear staining. The MTT assay indicated that both the compounds exhibited differential inhibition at various concentrations. Significant arrest of cell growth was observed with beta-sitosterol even at low concentration such as 0.63 microM in 48 h and none of the compounds exerted any apparent cytostatic effects on the non-cancerous COS-1 fibroblast cells. Growth inhibition assay suggested the potential use of bioactive compounds as cancer chemopreventive and therapeutic agents. This is the first report on HPCME isolation and identification from Rutaceae family and beta-sitosterol from P. trifoliata.

Topics: Animals; Antioxidants; Carboxylic Acids; Cell Extracts; Cell Line; Cell Proliferation; Chlorocebus aethiops; Chromatography, High Pressure Liquid; Colonic Neoplasms; Esters; Humans; Magnetic Resonance Spectroscopy; Molecular Structure; Poncirus; Sitosterols

7beta-OHsitosterol and 7beta-OHcholesterol are natural compounds of plant and animal cells with high structural similarity. Recently it was reported that both compounds induced apoptosis on human colon cancer cells by targeting different signalling pathways. Our study aimed at comparing their effects on polyamine metabolism and its relation to apoptosis. When human colon cancer cells were exposed to 7beta-OHsitosterol and to 7beta-OHcholesterol at concentrations inhibiting growth by the same degree, both compounds caused a reduction of polyamine biosynthetic enzyme activity, of the polyamine pools, and an increase of N1-acetylspermidine concentration indicating the enhancement of polyamine catabolism. Exogenous putrescine did not prevent cell death caused by 7beta-OHsitosterol, whereas 7beta-OHcholesterol-induced apoptosis was inhibited. MDL 72527, an inhibitor of polyamine oxidase, an enzyme of the polyamine catabolic pathway, potentiated the antiproliferative effects of 7beta-OHcholesterol by increasing the N1-acetylspermidine pool and enhanced the accumulation of apoptotic cells. In contrast, MDL 72527 did not change the apoptosis rate and the N1-acetylspermidine content in cells treated with 7beta-OHsitosterol. These data indicate that polyamine metabolic perturbations triggered by 7beta-OHcholesterol but not by 7beta-OHsitosterol are related to cell death.

Topics: Biogenic Polyamines; Caco-2 Cells; Cell Death; Cell Growth Processes; Colonic Neoplasms; Drug Synergism; Flow Cytometry; Humans; Hydroxycholesterols; Putrescine; Sitosterols; Spermidine

Plant sterols are found in fruits and vegetables. Their cholesterol-lowering effect is well documented. Our study aimed at comparing antiproliferative effects of 7beta-hydroxysitosterol (7beta-OHsito) versus 7beta-hydroxycholesterol (7beta-OHchol) on the human colon cancer cell line Caco-2. When cells were exposed for 32 h to 60 microM 7beta-OHsito or to 30 microM 7beta-OHchol, both compounds caused 50% growth inhibition. Cells treated with 7beta-OHsito showed enhanced caspase-9 and -3 activities followed by DNA fragmentation. In contrast, 7beta-OHchol did not activate caspase-3 and activation of caspase-9 and DNA fragmentation were delayed. The treatment of cells with the caspase inhibitor Z-VAD.fmk retarded the 7beta-OHsito-induced apoptotic process but not that triggered by 7beta-OHchol. Our data suggest that the two compounds in spite of their structural similarities target different cellular pathways, which lead to cell death.

Topics: Amino Acid Chloromethyl Ketones; Apoptosis; Caco-2 Cells; Caspase 3; Caspase 9; Caspase Inhibitors; Caspases; Cell Cycle; Cell Proliferation; Colonic Neoplasms; Cysteine Proteinase Inhibitors; DNA Fragmentation; Humans; Hydroxycholesterols; Sitosterols

This study examined the effects of lyophilized black raspberries (BRB) on azoxymethane (AOM)-induced aberrant crypt foci (ACF), colon tumors, and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in male Fischer 344 rats. AOM was injected (15 mg/kg body wt i.p.) once per week for 2 wk. At 24 h after the final injection, AOM-treated rats began consuming diets containing 0%, 2.5%, 5%, or 10% (wt/wt) BRB. Vehicle controls received 5% BRB or diet only. Rats were sacrificed after 9 and 33 wk of BRB feeding for ACF enumeration and tumor analysis. ACF multiplicity decreased 36%, 24%, and 21% (P < 0.01 for all groups) in the 2.5%, 5%, and 10% BRB groups, respectively, relative to the AOM-only group. Total tumor multiplicity declined 42%, 45%, and 71% (P < 0.05 for all groups). Although not significant, a decrease in tumor burden (28%, 42%, and 75%) was observed in all BRB groups. Adenocarcinoma multiplicity decreased 28%, 35%, and 80% (P < 0.01) in the same treatment groups. Urinary 8-OHdG levels were reduced by 73%, 81%, and 83% (P < 0.01 for all groups). These results indicate that BRB inhibit several measures of AOM-induced colon carcinogenesis and modulate an important marker of oxidative stress in the Fischer 344 rat.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Adenocarcinoma; Adenoma; Animals; Anthocyanins; Anticarcinogenic Agents; Azoxymethane; Calcium; Cholesterol; Colonic Neoplasms; Coumaric Acids; Deoxyguanosine; Diet; Ellagic Acid; Freeze Drying; Fruit; Oxidative Stress; Rats; Rats, Inbred F344; Rosaceae; Sitosterols

Work from our laboratory, as well as others, suggests a protective role of phytosterols (PS), especially beta-sitosterol, from colon, prostate, and breast cancer. Asians and vegetarians consume higher amounts of PS than Western societies. The latter societies have a higher incidence of these cancers than Asians and vegetarians. The aim of this study was to evaluate peanuts and its products as sources of PS in the American diet. Roasted peanuts contain 61-114 mg PS/100 g depending on the peanut variety, 78-83% of which is in the form of beta-sitosterol. Unrefined peanut oil contains 207 mg PS/100 g, which is similar to that of the US Department of Agriculture Nutrient Database. This value is higher than that of unrefined olive oil. Refining these oils results in reduction in PS concentration in the oil. This loss is greater in the case of olive oil than peanut oil. Further refining, such as deodorization, results in significant loss in PS, but hydrogenation after refining has a minimal effect on PS loss. Peanut butter, which represents 50% of the peanuts consumed in the United States, contains 144-157 mg PS/100 g. Peanut flour, which results from partial removal of oil from peanuts, contains 55-60 mg PS/100 g. The data suggest that peanuts and its products, such as peanut oil, peanut butter, and peanut flour, are good sources of PS.

Topics: Antineoplastic Agents; Arachis; Breast Neoplasms; Colonic Neoplasms; Female; Humans; In Vitro Techniques; Male; Phytosterols; Phytotherapy; Prostatic Neoplasms; Sitosterols

Fecal bile acids and neutral sterols of spontaneous colon cancer-bearing Wistar-Furth strain rats were examined and compared with those of control rats of the same strain by gas chromatography and gas chromatography-mass spectrometry. The amount of total fecal bile acids and the percentage of fecal lithocholic acid were almost similar in both groups, but the percentage of fecal deoxycholic acid was significantly higher in the colon cancer group than in the controls. The amount of total fecal neutral sterols and the percentage of fecal coprostanol were also markedly higher in the colon cancer group than in the controls. The percentage of cholesterol and the amount of beta-sitosterol were, however, almost similar in the two groups. These results indicate that fecal deoxycholic acid and fecal coprostanol are notably higher in rats with colon cancer than in controls.

Topics: Animals; Bile Acids and Salts; Cholestanol; Cholesterol; Colonic Neoplasms; Feces; Rats; Rats, Inbred WF; Sitosterols; Sterols

Cholesterol and fat are implicated as dietary factors enhancing the risk for colon carcinogenesis. Plant sterols such as beta-sitosterol when added to diets of experimental animals treated with colon carcinogens reduce tumor yields and counteract the proliferative changes associated with carcinogenesis. The question of whether the diet of human populations at low risk for colon cancer is mirrored in their sterol composition is addressed in this study. Four study groups consisting of 18 Seventh-day Adventist (SDA) pure vegetarians, 50 SDA lacto-ovo vegetarians, 50 SDA nonvegetarians, and 50 general population nonvegetarians were selected from the greater Los Angeles basin, and 3-day composite diets were analyzed for their sterol composition. The most significant index of dietary sterol status is the ratio, beta-sitosterol + stigmasterol/cholesterol (plant sterol/cholesterol ratio). The values for the four groups ranged from 0.49 to 16.0 (general population nonvegetarians = 0.49; SDA-nonvegetarians = 0.98; SDA lacto-ovo vegetarians = 3.26; SDA pure vegetarians = 16.0). The data also show that the absolute amounts of cholesterol consumed as a factor by itself might not be as significant as its relationship to total plant sterols in the diet.

Topics: Adult; Age Factors; Cholesterol, Dietary; Colonic Neoplasms; Diet; Diet, Vegetarian; Energy Intake; Female; Humans; Male; Middle Aged; Phytosterols; Sex Factors; Sitosterols; Stigmasterol

The effect of dietary supplementation with beta-sitosterol (0.2% of diet) was followed in Fischer rats after both acute and chronic feeding. Compared to controls after 3 and 7 days, the number of epithelial cells per crypt column in both plant sterol fed groups was shifted to lower values; moreover, fewer cells above cell position 12 were engaged in DNA synthesis. Continued feeding of beta-sitosterol for 28 weeks revealed the number and position of 3HTdR-labeled cells per crypt column after 1 pulse labeling to be similar to that seen in the acute phase. However, differences were more marked after 24 h showing the maximum number of labeled cells per column to be at least 25% less than the untreated group and the leading edge of labeled cells moving more slowly up the crypt wall. Rats treated with N-methyl-N-nitrosourea (MNU) intrarectally (8 mg/animal) while simultaneously consuming beta-sitosterol demonstrated a reduction in the size of the proliferative compartment as well as the number of labeled cells per crypt column as compared to rodents receiving just the carcinogen (3.3 and 5.4 mean labeled cells per column, respectively). At this time, MNU-treated rats fed beta-sitosterol had a significantly decreased colonic tumor incidence (Raicht et al. 1980). This plant sterol which passes through the digestive tract relatively unabsorbed appears to slow colonic epithelial cell proliferation resulting in a reduced expression of neoplastic transformation.

Topics: Animals; Cell Division; Cell Transformation, Neoplastic; Colonic Neoplasms; DNA; Kinetics; Male; Methylnitrosourea; Neoplasms, Experimental; Nitrosourea Compounds; Rats; Sitosterols

Diets rich in vegetables are associated with a low incidence of colon cancer. Since plant sterols are plentiful in vegetarian diets, we studied the effect of beta-sitosterol on colon tumor formation in rats treated with the carcinogen N-methyl-N-nitrosourea. We demonstrated that beta-sitosterol nullified in part the effect of this direct-acting carcinogen on the colon. We suggest that plant sterols may have a protective dietary action action to retard colon tumor formation. The beneficial effects of vegetarian diets may be enhanced because of the presence of these compounds.

Topics: Animals; Bile Acids and Salts; Cholesterol; Colonic Neoplasms; Diet; Diet, Vegetarian; Feces; Humans; Male; Methylnitrosourea; Neoplasms, Experimental; Nitrosourea Compounds; Rats; Sitosterols

A method is described for the analysis of fecal neutral steriods with a dual-column gas-liquid chromatography (GLC) system. After saponification of the fecal slurry, the neutral steroids were extracted with hexane. The GLC separation of the compounds and quantitation were achieved by simultaneous injection of the derivatized and derivatized aliquots of the extract onto dual colmuns under identical conditions. The neutral steroids of interest were than identified by matching the retention times with those of known standards, and identification was confirmed by use of an interfaced GLC high-resolution mass spectrometry system. The detection limit was 0.003 mg of steroid/g of fecal slurry. The pricision of the method is illustrated by a relative standard diviation of 2-10% and a recovery of neutral steroids from 73-96%. The method was applied to the determination of fecal neutral steroids in a "High protein diet in colon cancer study". A considerably larger level of coprostanone than of coprostanol was observed. Data on neutral steroids in fecal samples from subjects on different diets are the subject of a separate publication.

Topics: Cholestanes; Cholestanol; Cholestanones; Cholesterol; Chromatography, Gas; Colonic Neoplasms; Dietary Proteins; Feces; Humans; Male; Sitosterols; Stigmasterol