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PubMed1994

Experimental studies of the inhibitory effects of green tea catechin on mice large intestinal cancers induced by 1,2-dimethylhydrazine.

Three hundred Kunming mice were randomly divided into six groups (half males and half females in each group). Group 1 was the positive control group, Groups 2, 3, 4 and 5 were experimental groups and Group 6 was used as the solvent control group. Mice in Groups 1-4 were injected with 1,2-dimethylhydrazine (1,2-DMH) (20 mg/kg body wt.) solution subcutaneously once a week from the 2nd week to the 20th week. From the 1st week to the 23rd week, mice in Groups 2, 3 and 4 were given catechin (1 mg/mouse), catechin (2 mg/mouse) and EGCG (2 mg/mouse), respectively, five times a week. Mice in Group 5 received only catechin (3 mg/mouse) five times a week from the 1st to the 23rd week. Mice in Group 6 were injected with an equal volume of 1 mmol EDTA solution subcutaneously once a week from the 2nd to the 20th week. At the end of the 27th week, all the mice were killed by cervical dislocation (Zhu, Q.H. and Zhu, Q.F. (1991) Laboratory Animal Science, 1st edition. The Junior Educational Publisher, Guangdong). Pathological examinations indicated that the incidence of large intestinal cancers occurring in Group 1 was 80%, significantly higher than that in Groups 2, 3 and 4 (p < 0.001). No tumors were found in Groups 5 and 6. This might suggest that green tea has preventive effects on large intestinal cancer induction in spite of the different doses of catechin. Immunohistochemistry studies showed that green tea catechins could enhance the activity of superoxide dismutase (SOD) in tissues.

1,2-Dimethylhydrazine↗
PubMed1994

Effect of aspirin on incidence and growth of aberrant crypt foci induced in the rat colon by 1,2-dimethylhydrazine.

The aim of this work was to investigate if the possible chemopreventive effect of aspirin (ASA) on rat colon carcinogenesis could be detected with a medium-term assay. The end-point chosen was the inhibition of incidence and growth of putative preneoplastic lesions, the aberrant crypt foci (ACF) induced in the rat colon by two administrations of 1,2-dimethylhydrazine (DMH, 25 mg/kg p.o.). At both 4 and 8 weeks after the starting of the carcinogenic treatment the incidence of total ACF was reduced of 60% in rats receiving ASA (10 mg/kg/day p.o.) for 12 consecutive days during the initiation treatment with DMH. Also the number of the larger foci (with 3 or more crypts) was significantly lower in ASA-treated rats at both time-points (about 70% reduction). Moreover, concomitant ASA treatment determined a significant decrease of the mean number of crypts per focus at week 8. These results indicate that the chemopreventive effect of ASA on chemically-induced rat colon carcinogenesis observed in long-term studies may be detected in this relatively short assay.

1,2-Dimethylhydrazine↗
PubMed1994

Effect of beta-carotene, sodium ascorbate and cellulose on 1,2-dimethylhydrazine-induced intestinal carcinogenesis in rats.

Male Sprague-Dawley rats were fed a diet containing either 0.005% beta-carotene, 0.02% sodium ascorbate or 1.5% cellulose for 14 weeks. Beginning on day 3, all animals were also given weekly subcutaneous injections of 1,2-dimethylhydrazine (DMH; 20 mg/kg body wt.) throughout a 12-week period. The experimental diet was continued for an additional 14 weeks. At the end of the 26th week, surviving animals were sacrificed and the incidence of intestinal carcinomas was examined. A significantly lower incidence of carcinomas was observed in the beta-carotene-fed group (55.0%), compared with that in the control group given DMH (82.1%).

1,2-Dimethylhydrazine↗
PubMed1996

Inhibition of mucosal lipid hyperoxidation by green tea extract in 1,2-dimethylhydrazine-induced rat colonic carcinogenesis.

Phosphatidylcholine hydroperoxide (PCOOH) measured using a chemiluminescence detector to examine colonic mucosal lipid hyperoxidation increased after injection of 1,2-dimethylhydrazine and green tea extract (GTE), which we previously showed inhibited carcinogenesis and oxidative DNA damage in the gastrointestinal tract. Therefore, the hyperoxidation of membrane phospholipids reflected well the degree of DNA damage and carcinogenic alteration, and may be a useful intermediate biomarker for initiation of carcinogenesis.

1,2-Dimethylhydrazine↗
PubMed1985

The effect of carbon black ingestion on 1,2-dimethylhydrazine-induced colon carcinogenesis in rats and mice.

The possible co-carcinogenic effect of ingestion of industrial carbon black was examined in female Sprague-Dawley rats and female CF1 mice treated with 1,2-dimethylhydrazine (DMH) to induce adenocarcinomas of the colon. Carbon black was added to the diet at 2.05 g/kg feed and fed for 52 weeks. No differences (P greater than 0.05) in tumor incidences were seen in rats or mice. Simultaneous 2-year feeding experiments with carbon black alone showed no increase in the development of spontaneous tumors. These findings are consistent with the belief that carbon blacks are ineffective as carcinogens because of their adsorptive properties.

1,2-Dimethylhydrazine↗
PubMed1989

Dose- and time-response of colon carcinogenesis in Fischer-344 rats after a single dose of 1,2-dimethylhydrazine.

The purpose of this experiment was to examine the development of colon tumors after the injection of a single dose of 1,2-dimethylhydrazine (DMH) in rats. Male Fischer-344 rats were injected with 0, 10, 30, 100 or 200 mg/kg of DMH dihydrochloride. No tumors were seen after 3 or 5 months at any dose, but were seen after 7 or 9 months. At 9 months, tumors were induced in a dose-dependent manner, with 64.7% of rats receiving the 200 mg/kg dose developing tumors. This study shows that a high incidence of colon tumors can be induced by a single dose of DMH after a 9-month latency period.

1,2-Dimethylhydrazine↗
PubMed1991

Alterations in lectin binding in the proximal and distal colon of Sprague-Dawley rats with 1,2 dimethylhydrazine administration.

Sequential changes in rhodamine or fluorescein isothiocyanate-conjugated lectin binding of proximal and distal colonic crypts were studied during and after the administration of the 1,2 dimethylhydrazine (DMH). Five adult its unexposed to DMH or vehicle served as baseline controls. Tissue from normal appearing colon and tumor tissue was incubated with Ulex europaeus agglutinin 1 (UEA), Arachis hypogaea (PNA), Dolichos biflorus (DBA) and Griffonia simplicafolia 1 (GSA1). Distinct regional differences were noted in the baseline controls. UEA, PNA and DBA binding were absent in the distal colonic crypt cells. In the proximal colon minimal UEA and PNA binding was noted in the lower crypt whereas DBA binding was intense. GSA1 binding was diffuse in the upper and lower crypt of both regions. During carcinogenesis a progressive increase in PNA binding was noted in normal appearing colonic crypts from both regions. A progressive increase in PNA binding in proximal and distal colonic tumors was noted over time. Similar to normal tissue, DBA bound markedly to proximal colon tumors but was absent in most distal colonic tumors. UEA stained all proximal tumors intensely at all time points. In distal colonic tumors, UEA staining was diminished at 30 weeks compared to tumors analyzed at 16, 22 and 26 weeks. Mucin depletion was also a feature of tumor tissue compared to adjacent normal and hyperplastic glands. This study documents the region specific changes in lectin binding in normal and neoplastic colonic crypts induced by DMH.

1,2-Dimethylhydrazine↗
PubMed1985

Comparison of immune status and 1,2-dimethylhydrazine induced tumorigenesis in brown--Norway and Fischer rats. Emphasis on splenic and colonic lymphocyte function.

Sym 1,2-dimethylhydrazine (DMH)-induced colon tumorigenesis was studied in immunologically different strains of rat: the Brown--Norway which is known to be immunologically a low-responder and the Fischer a high-responder. Brown--Norway rats received a total dose of 75, 150 or 225 mg DMH/kg or vehicle and Fischer rats received 150 mg DMH/kg or vehicle over a 3-week period. Rats were killed 5 months after the final treatment. Lymphocytes were isolated from the spleen and colon from rats treated with 150 mg DMH/kg or vehicle. Natural killer (NK) cell activity and the autologous mixed lymphocyte response (AMLR) as well as colon tumor incidence were compared between the two strains. Splenic and colonic intraperithelial lymphocytes (IEL) from the Brown--Norway strain demonstrated low NK activity and reduced splenic T lymphocyte proliferation in response to autologous non-T lymphocytes. As well, colonic lamina propria lymphocyte (LPL) proliferation was low and Brown--Norway rats had a low incidence of DMH-induced colon neoplasms (7%). In comparison, the Fischer rats had more effective splenic and IEL NK killing, enhanced splenic AMLR, enhanced LPL proliferation and a higher incidence of colon tumors (20%).

1,2-Dimethylhydrazine↗
PubMed1997

Specific species of intestinal bacteria influence the induction of aberrant crypt foci by 1,2-dimethylhydrazine in rats.

To shed light on the association of intestinal microflora with the development of colon cancer, we studied the modifying effects of intestinal microflora on the occurrence of 1,2-dimethylhydrazine (DMH)-induced colonic aberrant crypt foci (ACF) in germfree (GF), gnotobiotic (GB) and conventionalized (Cvd) rats. In the first part of this study, 10 week old germfree Fischer-344 rats were randomly assigned to three groups and two groups of rats were orally inoculated with mixtures of pure culture of Escherichia coli, Enterococcus faecium, and several strains of Bacteroides and Clostridium species (GB), or feces from conventional rats (Cvd). Inoculated rats were given two weekly i.p. injections of DMH (20 mg/kg body wt) at 13 and 14 weeks of age. Rats were sacrificed 11 or 34 weeks after the last DMH injection for ACF scoring. The total number of ACF, ACF with four or more crypts/focus, and mean number of aberrant crypts per focus (crypt multiplicity) in GB rats sacrificed at week 34 were 168% (P < 0.001), 442% (P < 0.001) and 138% (P < 0.001) of those in GF rats, respectively. On the other hand, the same values in Cvd rats were 42% (P < 0.001), 147% (P = 0.246) and 159% (P < 0.001) of those in GF rats, respectively. Similar results were observed in rats that were sacrificed at week 11. In the second part of this study, the effect of colonization of Bifidobacterium breve on the ACF profiles was examined in GB rats. The number of ACF with four or more crypts/focus and crypt multiplicity in GB plus B. breve rats at week 11 were significantly lower than those of GB rats (P < 0.01, and P < 0.05, respectively), although the former was not statistically significant at week 34. These findings suggest that some intestinal bacteria might behave as promoters and some as anti-promoters in colon carcinogenesis.

1,2-Dimethylhydrazine↗
PubMed1993

Uterine sarcomas in CBA mice induced by combined treatment with 1,2-dimethylhydrazine and estradiol dipropionate. Light and electron microscopy.

Three uterine sarcomas induced by combined treatment (1,2-dimethylhydrazine and estradiol dipropionate) in CBA mice were examined by light and electron microscopy. Histologically the tumours consisted either of loose areas with stellate cells or of solid cellular areas. These were formed of elongated cells of the fibroblastic type and rounded cells with clear nuclei and abundant cytoplasm without clearly discernible bodies. Ultrastructurally, undifferentiated mesenchymal cells and cells with the features of fibroblasts and myofibroblasts were distinguished. The tumours described bear resemblance to human endometrial stromal sarcomas and are interpreted as sarcomas originating from immature mesenchymal cells differentiating mainly in the direction of cells of the fibroblastic type. Certain similarities with fibrous histiocytomas are noted.

1,2-Dimethylhydrazine↗
PubMed1997

Aspirin, but not sodium salicylate, indomethacin, or nabumetone, reversibly suppresses 1,2-dimethylhydrazine-induced colonic aberrant crypt foci in rats.

The aim of this study was to determine if selective inhibition of cyclooxygenase isozymes affects the initiation of carcinogen-induced colon cancer using aberrant crypt foci (ACF) as a surrogate biomarker. Male Sprague-Dawley rats (18 per group) were given single subcutaneous injections of saline (4 ml/kg), aspirin (50 mg/kg body wt) sodium salicylate (50 mg/kg), indomethacin (4 mg/kg), nabumetone (100 mg/kg), or 16,16-dimethyl-prostaglandin E2 (50 mg/kg) for three days. On day 4, 12 rats per group were given a subcutaneous injection of 1,2-dimethylhydrazine (12 mg base/kg body wt) and six rats per group received vehicle alone (4 ml/kg) every week for eight weeks, after which drug treatment ceased. Control and six carcinogen-treated rats per group were killed at this time and the remaining six rats per group killed 22 weeks later. Colons were scored for ACF number and size. Only aspirin caused a significant reduction in total ACF and ACF formation at the early time point, but at the later time, there were no significant differences between groups. ACF from all treatment groups increased in size at similar rates at both time points. Thus, only aspirin demonstrated a significant, although reversible, suppression of carcinogen-induced ACF. Possible mechanisms of action and the clinical implications of aspirin chemoprevention are discussed.

1,2-Dimethylhydrazine↗
PubMed1981

Kinetics of the non-neoplastic mucosa of the large bowel of dimethylhydrazine-treated rats.

Administration of 1,2 dimethylhydrazine (DMH) to rats by weekly s.c. injections causes the development of multiple epithelial tumours of the large bowel. These appear to arise as localized dysplastic abnormalities in hitherto apparently morphologically normal crypts. This study was undertaken in order to examine cell proliferation in such apparently normal crypts of DMH-treated animals. A number of proliferative abnormalities are evident, including changes in the size of the crypts, changes in the disposition of proliferating cells within them and reduced cell-cycle times. The nature and the extent of the abnormalities vary from site to site along the length of the bowel, and reflect the vulnerability of the different segments of the bowel, not only to the carcinogenic effects of DMH, but also to short-term toxicity.

1,2-Dimethylhydrazine↗
PubMed1984

Morphological studies on the long-term organ culture of colonic mucosa from normal and dimethylhydrazine treated rats.

Mucosal explants were prepared from the colons of normal rats and from the non-neoplastic colonic mucosa of rats which had been treated chronically with the intestinal carcinogen dimethylhydrazine. They were maintained in an organ culture system which permitted survival up to at least 25 days. Morphological preservation of the mucosa was excellent up to 6 days in culture and thereafter changes began to occur. But even at 25 days normal crypt structures were still evident. The hyperplastic and dysplastic changes seen in pre-culture samples of DMH-treated mucosae remained recognisable during the first two days in culture. They were no longer seen in explants examined after this time however and, indeed, there appeared to be no difference in the morphology and survival of control and DMH-treated mucosae. It is possible that our culture system does not permit further neoplastic progression, but an alternative explanation is that the system discriminates specifically against the survival of neoplastic elements.

1,2-Dimethylhydrazine↗
PubMed1986

Vanadate supplements and 1,2-dimethylhydrazine induced colon cancer in mice: increased thymidine incorporation without enhanced carcinogenesis.

Because vanadate ion is a potent mitogen and accumulates in the gut of rodents fed vanadate supplements, effects of ammonium metavanadate in drinking water (10 ppm or 20 ppm) were studied on the development of large bowel neoplasms in mice treated with 1,2-dimethylhydrazine (DMH) (20 mg kg-1 weekly for 20 weeks). In the colon at 30 weeks DMH treatment caused a 14% increase in RNA content, an 18% increase in DNA content, and 33% deeper crypts. Vanadate at either 10 ppm or 20 ppm decreased RNA content by approximately 11%. Although vanadate increased thymidine incorporation 210% to 550% compared with controls, it had no influence on the attack rate, incidence, or histological type of tumours induced by DMH.

1,2-Dimethylhydrazine↗
PubMed1996

Comparison of resistant starch with cellulose diet on 1,2-dimethylhydrazine-induced colonic carcinogenesis in rats.

BACKGROUND & AIMS: Epidemiological and experimental studies have shown that dietary fiber may prevent colon cancer. Resistant starch, like dietary fiber, is not subject to digestion in the small intestine. However, it is unknown whether resistant starch inhibits colonic carcinogenesis. In vitro studies have shown that butyrate slows the growth of cultured colon cancer cells. The effect of resistant starch diet on 1,2-dimethylhydrazine-induced colonic carcinogenesis in rats was evaluated, and the colonic butyrate concentration was measured. METHODS: Sprague-Dawley rats were randomly divided into five groups that were fed diets containing no fiber, 3% cellulose, 10% cellulose, 3% resistant starch, or 10% resistant starch. Colonic carcinogenesis and butyrate concentration of colonic contents and feces in each diet group were compared. RESULTS: Total cancer volume per rat in the 10% cellulose group was significantly lower than that in the basal group (109 +/- 54 mm3 and 247 +/- 83 mm3; P < 0.05), but the other groups showed no significant differences. The butyrate concentration in colonic content and in feces were higher in the resistant starch groups than in the cellulose groups. CONCLUSIONS: The resistant starch diet increased butyrate concentration but did not inhibit colonic carcinogenesis. It remains doubtful whether butyrate inhibits the proliferation of colon cancer cells.

1,2-Dimethylhydrazine↗
PubMed1993

Effects of kampo (Japanese herbal) medicine "sho-saiko-to" on DNA-synthesizing enzyme activity in 1,2-dimethylhydrazine-induced colonic carcinomas in rats.

Sho-Saiko-To (SST) is a modified Japanese traditional Chinese herbal medicine containing seven medical plants: Bupleuri radix, Pinelliae tuber, Suxtallariae radix, Zizyphi fructus, Ginseng radix, Glycyrrhizae radix, and Zingiberis recens rhizoma. This preparation has been used in the treatment of some inflammatory diseases of the respiratory system and chronic hepatitis. In the present study, the effects of SST were investigated on the activities of DNA-synthesizing enzymes in 1,2-dimethylhydrazine (DMH)-induced colonic carcinomas in rats. Six-week administration of SST prevented nearly 100% of the body weight loss and the final number of the colonic carcinomas compared to those in the rats treated with DMH alone, and suppressed the enhanced activities of thymidylate synthetase (TS) and thymidine kinase (TK) which were involved in the de novo and salvage pathways of pyrimidine synthesis, respectively, in DMH-induced colonic carcinomas. These results indicate that SST may show directly and/or indirectly inhibitory effects on the development of colonic carcinomas.

1,2-Dimethylhydrazine↗
PubMed1983

Effects of wheat, rice, corn, and soybean bran on 1,2-dimethylhydrazine-induced large bowel tumorigenesis in F344 rats.

This study was designed to determine the relative effects of four dietary brans on large bowel tumorigenesis in rats treated with 1,2-dimethylhydrazine (DMH). Four-week-old F344 rats were fed a 20% bran (either wheat, rice, corn, or soybean) semisynthetic diet or a no-fiber-added control diet for life. All rats except for one control diet for life. All rats except for one control group were infected with DMH (2SC doses; approximately 150 mg/kg body weight) at 8 and 10 weeks of age. Two additional groups were fed the control diet and then at 4 and 18 weeks, respectively, after the second DMH dose, were fed the wheat bran diet. All surviving rats were killed 9 months following the first DMH dose. Survival was increased in all groups receiving bran diets. Large bowel tumor incidences in the DMH group were as follows: control, 95%; wheat, 75%; rice 86%; corn, 100%; soybean, 84%; wheat after 4 weeks, 62% (lower than control group, p less than 0.05); wheat after 18 weeks, 84%. All but one of the DMH groups had approximately two tumors/tumor-positive rat; the corn group had four. The effect of bran on large bowel carcinogenesis appears to depend both on the source of bran and when it is fed in relation to tumor initiation.

1,2-Dimethylhydrazine↗
PubMed1983

Modification of dimethylhydrazine-induced carcinogenesis in rats by dietary cholesterol.

Diets capable of affecting serum cholesterol levels were examined for effects on tumorigenesis in male Fischer 344 rats given 1,2-dimethylhydrazine dihydrochloride (DMH). Four regimens were used: Group A was maintained on a semipurified diet; Group B was maintained on the same diet with cholesterol and bile salts added; Group C was fed the cholesterol and bile salt diet and then switched to the semipurified diet; and Group D was fed the cholesterol and bile salt diet and then placed on a semipurified diet containing bile salts. Six months after DMH administration, Group B and D exhibited similar tumor incidence (77% and 83%, respectively) and yield (2.3 and 2.4 tumors/tumor-bearing rat). These yields were significantly greater than those seen in Group A (70% incidence and 1.4 tumors/tumor-bearing rat) or Group C (52% incidence and 1.7 tumors/tumor-bearing rat). Tumors in Groups B and D were larger in size and closer to the rectum than those seen in the other groups. In each of Groups A, C, and D, approximately 26% of the tumors were malignant; in Group B, 42% were malignant. Colonic epithelial cell kinetics in rats from Groups C and D not given DMH were determined using autoradiographic study of [3H]thymidine incorporation. Group D showed enhanced cell proliferation and expansion of the crypt cell population. These results suggest that dietary bile salts increase cell turnover and frequency of tumors, and that the addition of cholesterol to a cocarcinogenic diet can be associated with a significantly higher percentage of invasive tumors.

1,2-Dimethylhydrazine↗