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PubMedDate not supplied

Effects of 5-methoxypsoralen (5-MOP) on arylamine N-acetyltransferase activity in the stomach and colon of rats and human stomach and colon tumor cell lines.

BACKGROUND: It has been shown that cytochrome P450 enzymes (CYPs) and acetyltransferase can be used as biomarkers of carcinogen-DNA adduct levels and human cancer susceptibility. The gastrointestinal tract is the portal of entry of foreign compounds and presents xenobiotic metabolizing N-acetyltransferase (NAT) and CYPs activities. 5-Methoxypsoralen (5-MOP) has been used in combination with UV radiation in skin photochemotherapy for decades. A number of studies have demonstrated that 5-MOP is inhibitory towards mouse and human CYP isoforms, but investigations on the direct effects on NAT activity in laboratory animals and human cancer cells are limited. The main objective of this study was to document the effects of 5-MOP on the modulation of NAT activities in the stomach and colon of rats and human stomach and colon tumor cell lines. MATERIALS AND METHODS: N-Acetylation of 2-aminofluorene (AF) to 2-acetylaminofluorene (AAF) by NAT in the stomach and colon of Sprague-Dawley (SD) rats and in human stomach (SC-M1) and colon (COLO 205) tumor cell lines was investigated. RESULTS: The data show that the metabolic activity of NAT in the rat colon was higher than that in the rat stomach, and the further metabolism of AAF was slower in the stomach than in the colon. 5-MOP increased the activity of NATand also increased the further metabolism of AAF at 24 h in the rat stomach. In the rat colon, no statistically significant changes caused by 5-MOP were observed in NAT activity, but 5-MOP increased the further metabolism of AAF at 24 to 72 h. 5-MOP decreased the activity of NAT only at 72-h incubation in SC-M1 cells. In COLO 205 cells, however, 5-MOP decreased the activity of NAT between 24 h and 72 h. The optimal concentrations of 5-MOP to induce decreased NAT activity in SC-M1 cells were 0.05 mM to 25 mM. In COLO 205 cells, the data indicate that the higher the concentrations of 5-MOP, the higher the acetylation of AF; a promotion effect of NAT activity occured at a higher dose (50 mM) of 5-MOP and an inhibition effect occured at lower doses (0.05-0.5 mM) of 5-MOP, while concentrations of 5-25 mM of 5-MOP showed no significant difference compared with the control regimen. CONCLUSION: The metabolic activity of NAT in the rat colon was higher than that in the rat stomach, and the results also showed a high degree of correspondence with SC-M1 cells and COLO 205 cells. 5-MOP more efficiently inhibited NAT activity in human stomach and colon tumor cell lines than in the stomach and colon of rats.

2-Acetylaminofluorene↗
PubMed1986

Activation of the colon carcinogen 1,2-dimethylhydrazine in a rat colon cell-mediated mutagenesis assay.

Suspensions of rat colon epithelial cells metabolized the potent colon carcinogen, 1,2-[14C]dimethylhydrazine (DMH), into 14C-labeled, alkali-soluble volatile products, presumably CO2. The colon cell suspensions, however, were less effective than rat hepatocyte suspensions. In addition, we used a cell-mediated mutagenesis assay to test rat colon epithelial cells grown from tissue explants for their ability to metabolize DMH into products mutagenic for human P3 teratoma cells. Mutagenesis in the P3 cells was indicated by an acquired resistance to 6-thioguanine. Cocultivation of the colon cells with the P3 cells in the cell-mediated assay resulted in mutagenesis, whereas in the absence of the colon cells, no mutagenesis by DMH was observed. Similar results were obtained in a hepatocyte-mediated mutagenesis assay. Colon cells were also able to activate another carcinogen, benzo(a)pyrene, into products mutagenic for the P3 cells. Individual epithelial clonal populations isolated from the colon cultures grown from tissue explants, however, expressed different capacities to activate DMH and benzo(a)pyrene into mutagens, and a high degree of DMH activation by cells from a colon clone was not necessarily associated with a similar degree of benzo(a)pyrene activation. Our results indicate that the colon itself contains epithelial cell types capable of effectively converting DMH into mutagenic (and presumably carcinogenic) products without necessarily involving intermediary metabolism by hepatocytes as previously thought.

1,2-Dimethylhydrazine↗
PubMed1995

Characterization of the major sialyl-Lex-positive mucins present in colon, colon carcinoma, and sera of patients with colorectal cancer.

The expression of the mucin-bound sialyl-Lewisx epitope is increased in the tissue of most colorectal carcinomas and in the sera of about 30% of tumor patients. In colon cancer, a portion of the sialyl-Lex groups detectable with the monoclonal antibody AM-3 is located on MUC1 (C. Hanski et al., Cancer Res., 53: 4082-4088, 1993). In order to characterize the major colon carcinoma-associated sialyl-Lex-positive glycoprotein components, the tissue- and serum-derived antigens were investigated. The buoyant densities of the sialyl-Lewisx-positive antigens from tumor and normal colonic tissues and from sera of patients with colon carcinoma and healthy donors correspond to that of mucins (1.40 g/ml). The sialyl-Lex-positive mucins purified from both tissues elute under nonreducing conditions in the void volume of a Sepharose CL-2B column, indicating a molecular mass more than 2 x 10(7) daltons. They yield in immunoblot after SDS gel electrophoresis under reducing conditions a main band at an apparent M(r) 880,000. Radioactive labeling revealed that the band at M(r) 880,000 is the major protein component in sialyl-Lewisx-positive mucins both from tumor and normal colonic tissue. In sera of colon carcinoma patients, the sialyl-Lex moiety is also detectable mainly on a M(r) 880,000 glycoprotein band and, additionally, on a M(r) 140,000 molecule as well as on alpha 1-acid glycoprotein. Sera from healthy donors exhibited only a sialyl-Lex-positive glycoprotein with the apparent M(r) 140,000. Sandwich ELISA as well as immunoblots of mucins purified from the colon carcinoma cell line LS174T indicated that the sialyl-Lex moiety migrating in the M(r) 880,000 band is located on MUC2 protein core. Together, these data suggest that sialyl-Lex antigen in colon, colon carcinoma, and the sera of patients with this tumor is located on the MUC2 molecule, consisting of several subunits with an apparent M(r) 880,000, linked via disulfide bridges. The increase of sialyl-Lex expression in colon carcinomas appears to be mainly due to a more frequent transfer of sialyl-Lex moieties onto the mucin core in tumor tissue.

Antibodies, Monoclonal↗
PubMed1997

Dietary fat and colon cancer: modulating effect of types and amount of dietary fat on ras-p21 function during promotion and progression stages of colon cancer.

Although epidemiological and experimental studies have indicated a strong relationship between types and amount of dietary fat and colon tumorigenesis, the modulating effects of these nutritional factors at the molecular level have not been fully elucidated. Transforming proteins encoded by activated ras genes have been implicated in the etiology of many human malignancies, including colon cancer. It is now well established that the transforming ability of ras-p21 critically depends on its correct localization in plasma membrane. The posttranslational processing of the cytosolic precursor (pro-ras), as it is synthesized in the cytoplasm, and its proper anchorage to the cytoplasmic face of plasma membrane are determined by an important intermediate metabolite of dietary fat and an enzyme system that includes farnesyl protein transferase. To provide an understanding of the molecular basis of the relationship between the types and amount of dietary fat and the transforming function of ras, especially during the stages of promotion and progression of colon tumor development, we investigated the effect of various types and amount of dietary fat on the expression of ras-p21 during azoxymethane (AOM)-induced colon carcinogenesis. Male F344 rats were fed the semipurified American Institute of Nutrition-76A diet containing low-fat corn oil and were given s.c. injections of AOM dissolved in normal saline at a dose rate of 15 mg/kg body weight, once weekly, for 2 weeks. Control animals received s.c. injections of equal volumes of normal saline. Beginning 1 day after the second AOM or saline injection, groups of animals intended for the treatment with different types of high-fat dietary regimens were fed the semipurified American Institute of Nutrition-76A diets containing high levels of high-fat corn oil (HFCO) rich in omega-6 fatty acids or high levels of high-fat fish oil (HFFO) rich in omega-3 fatty acids; the remaining animals in experimental and control groups were continued on the low-fat corn oil diet until termination of the experiment. Groups of animals were sacrificed 1, 12, or 36 weeks after the last AOM or saline injection, and their colonic mucosa and grossly visible colon tumors from rats sacrificed 36 weeks after the last AOM injection were analyzed for the levels of expression of ras-p21. We found that AOM induced increasingly higher levels of ras-p21 expression with advancing stages of colon tumor development. The HFCO diet resulted in enhanced expression of AOM-induced ras-p21 as observed 36 weeks after the last AOM injection. In contrast, feeding the HFFO diet inhibited AOM-induced ras-p21 expression. These results correlate with increased incidence and multiplicity of grossly visible colon tumors in AOM-treated animals fed a HFCO diet versus decreased incidence and lower multiplicity of colon tumors in their counterparts on the HFFO diet. Further analysis of ras-p21 levels in cytosol and plasma membrane revealed that feeding a HFFO diet resulted in increasing accumulation of ras-p21 in cytoplasm with a concomitant decrease in membrane-bound ras-p21 levels as observed in animals sacrificed 12 and 36 weeks after the last AOM injection. Thus, the dietary HFCO may promote colon tumorigenesis by increasing ras-p21 expression, whereas HFFO appears to exert its antitumor activity by interfering with posttranslational modification and membrane localization of ras-p21.

Animals↗
PubMed1987

Analysis of pp60c-src tyrosine kinase activity and phosphotyrosyl phosphatase activity in human colon carcinoma and normal human colon mucosal cells.

We have compared the level of phosphotyrosyl phosphatase activity in lysates from normal human colon mucosal cells and human colon carcinoma cells and analyzed the effect of incubating these cells with sodium orthovanadate, an inhibitor of phosphotyrosyl phosphatase activity, on the relative abundance of acid-stable phosphotyrosine and on in vitro protein kinase activity of pp60c-src. Additionally, we compared the effect of lysing these cells in buffer containing only nonionic detergents with RIPA buffer, which contains both sodium dodecyl sulfate and deoxycholate, on the in vitro kinase activity of pp60c-src. Our results show that the level of detectable phosphotyrosyl phosphatase activity in lysates derived from normal colon cells and colon carcinoma cells is very similar. Additionally, the abundance of acid-stable phosphotyrosine in these cells cultured in the absence or presence of vanadate is not significantly different. However, incubation of these cells with vanadate significantly stimulates the activity of pp60c-src derived from the normal colon cells in immune-complex kinase assays, while having no detectable effect on the activity of pp60c-src from the colon tumor cells. The in vitro protein kinase activity of pp60c-src derived from RIPA buffer lysates of colon carcinoma cells was found to be elevated five- to sevenfold when compared with pp60c-src from these same cells lysed in buffer containing only Nonidet-P 40 as a detergent. The type of lysis buffer did not effect the activity of pp60c-src from normal colon mucosal cells. These results provide additional evidence that the activity of pp60c-src may be regulated differently in colon carcinoma and normal colon mucosal cells.

Adenocarcinoma↗
PubMed1997

Aspirin effects on colonic mucosal bleeding: implications for colonic biopsy and polypectomy.

BACKGROUND: Many patients who require endoscopic treatments such as biopsy and polypectomy are given antiplatelet agents reluctantly. We have studied the effects of aspirin on colonic mucosal hemostasis. METHODS AND PATIENTS: We developed a new endoscopic device to make a standard incision (7-mm length) on the colonic mucosa to study colon bleeding time. We measured the colon bleeding time of normal colonic mucosa in 47 cases. The colon bleeding time and skin bleeding time (Simplate method) were measured before and one hour after aspirin ingestion (990 mg) in ten healthy subjects. RESULTS: The bleeding time of normal colonic mucosa was 156 +/- 71 (mean +/- standard deviation) seconds. Significant prolongation was noted in both skin bleeding time (357 +/- 192 vs. 477 +/- 183 seconds; P < 0.05) and colon bleeding time (155 +/- 47 vs. 244 +/- 169 seconds; P < 0.05) after aspirin ingestion. CONCLUSIONS: Bleeding time was measured safely under direct colonoscopic visualization. Aspirin prolonged the colon bleeding time. Therefore, endoscopists should be aware of a risk of abnormal bleeding after endoscopic biopsy and polypectomy in patients with aspirin use. Two days were necessary for colon bleeding time to become normalized in patients with aspirin use.

Aspirin↗
PubMed2006

Impact of adenoma size in distal colon on risk for advanced adenoma of the proximal colon.

Adenomas of the rectosigmoid colon are considered markers of risk for advanced adenomas of the proximal colon. However, studies report a wide variation in risk. This study was designed to determine the risk for advanced adenomas in the proximal colon in patients from a large, homogeneous population with an advanced or nonadvanced adenoma of the distal colon. We designed a prospective study of 7157 patients who were evaluated for neoplasia by flexible sigmoidoscopy and, when adenomas were found, by colonoscopy. Adenomas were considered advanced if they were > or =10 mm in size or had villous or dysplastic features. Ninety-seven patients had an advanced adenoma of the distal colon (Group A) and were compared with 183 patients who had a nonadvanced adenoma (Group B). Seven patients (7.2%) in Group A had an advanced adenoma of the proximal colon, compared with four patients (2.2%) in Group B (P < 0.05, relative risk = 3.3). When patients with adenomas of the distal colon >5 mm (Group C) were compared to patients with adenomas < or =5 mm (Group D), the prevalence of advanced adenomas of the proximal colon remained at 7% (10/143) for Group C but fell to 0.73% (1/137) for Group D (P = 0.011, relative risk = 9.6). By expanding the criteria for risk from adenomas of the distal colon to include all adenomas >5 mm, the relative risk for advanced adenoma of the proximal colon was increased threefold.

Adenoma↗
PubMed1998

Colonic endocrine cells in patients with carcinoma of the colon.

OBJECTIVE: To investigate the colonic endocrine cells in patients with colon carcinoma in order to establish a possible abnormality. PATIENTS: Twelve patients with colon adenocarcinoma (eight women and four men; mean age 69 years; range 52-88 years) were studied. As controls, macroscopically and histologically normal tissues from the colon of 12 patients (eight women and four men; mean age 66 years; range 34-86 years) were examined. These patients suffered from polyps, prolapsus, chronic diverticulitis, volvulus or haemorrhoids. METHODS: Macroscopically and histologically normal tissues from the colon of the patients, about 10 cm from the tumour, and of the controls were examined. Endocrine cells were immunostained with the avidin-biotin-complex method, and were quantified by computer image analysis using an automatic standard sequence analysis operation. Three parameters were used: (1) the number of endocrine cells per mm3 of epithelial cells; (2) the cell secretory index (CSI); and (3) the nuclear volume. RESULTS: The numbers of somatostatin- and serotonin-immunoreactive cells were significantly reduced in patients with colon carcinoma (P = 0.03 and 0.009, respectively). There was no difference between patients and controls regarding the numbers of PYY-, PP-, and enteroglucagon-immunoreactive cells. The CSI of somatostatin- and serotonin-immunoreactive cells were significantly decreased. There was no difference in the CSI between the patients and controls regarding PYY-, PP- or enteroglucagon-immunoreactive cells. The nuclear volumes of PYY- and enteroglucagon-immunoreactive cells increased significantly in the patients. The nuclear volume of PP-, somatostatin- and serotonin cells did not differ from those of the controls. CONCLUSION: The present results support the assumption that a disturbance in the colonic neuroendocrine system occurs in patients with colon carcinoma, which might affect the development of the tumour. The decrease in the number and CSI of somatostatin cells may account for the decrease of the colonic content of this peptide observed previously in these patients. The decrease in the number and CSI of serotonin-immunoreactive cells in patients with colon adenocarcinoma might be a method by which the body defends itself against this mitogenic substance.

Adenocarcinoma↗
PubMed1997

Colonic mucin discharge by a cholinergic agonist, prostaglandins, and peptide YY in the isolated vascularly perfused rat colon.

UNLABELLED: The model of the isolated, vascularly perfused rat colon was assessed in the present study to investigate the nervous, hormonal, and local/paracrine pathways involved in colonic mucin secretion. A colonic loop was perfused via the superior mesenteric artery with a Krebs-Henseleit buffer containing 25% washed bovine erythrocytes at a rate of 2.5 ml/min. After a 10-min control period, each compound to be tested was infused intra-arterially for 30 min. Tissue samples from the proximal and midsegments of the perfused rat colon were then fixed and stained for mucus cell count. Intra-arterial administration of bethanechol evoked a concentration-dependent decrease in the number of stained mucus cells per crypt section over the range 2 x 10(-6) to 2 x 10(-4) M: 16.6 +/- 1.4 stained mucus cells per crypt in the midportion of the perfused rat colon (n = 5) with bethanechol 2 x 10(-4) M versus 28.8 +/- 1.5 for controls (n = 6). After infusion of 1.25 and 2.5 microM 16,16-dimethyl prostaglandin E2 (dmPGE2), the number of stained mucus cells per crypt section was significantly reduced: 21.6 +/- 0.6 (n = 6) and 20.6 +/- 1.4 (n = 7), respectively. An increase in the number of cavitated mucus cells was also observed (22.1 +/- 6.7 and 38.5 +/- 4.1% of cavitated mucus cells in the midsegment of the perfused rat colon with 1.25 and 2.5 microM dmPGE2, respectively, vs. 12.3 +/- 4.1% for controls). In contrast, prostaglandin F2alpha did not significantly affect mucus discharge from colonic cells. Peptide YY (10(-10), 10(-9) and 10(-8) M) induced a dose-dependent increase in the percentage of cavitated mucus cells (16.7 +/- 2.8, 23.1 +/- 4.2, and 31.2 +/- 3.4% of cavitated mucus cells in the midsegment, respectively). The proximal and midsegments of the perfused rat colon were equally sensitive to each secretagogue. CONCLUSION: In the isolated, vascularly perfused rat colon, mucus cells strongly respond to the well-known mucin secretagogues, bethanechol and dmPGE2. This approach has already led to the identification of a novel stimulant of mucin secretion: peptide YY. Our ex vivo model, in which goblet cells are submitted to well-defined luminal and blood-borne stimuli is, therefore, reliable to investigate the nervous, hormonal, and local/paracrine pathways involved in the colonic mucin secretion.

Animals↗
PubMed1999

The protective effect of estrogen against chemically induced murine colon carcinogenesis is associated with decreased CpG island methylation and increased mRNA and protein expression of the colonic vitamin D receptor.

Epidemiological studies suggest that estrogen prevents neoplastic transformation in the intestinal mucosa. Estrogen was shown to increase the expression of vitamin D receptors (VDR) in a variety of tissues. 1,25-Dihydroxyvitamin D [1,25-(OH)2D] and several of its analogues are known as potent antineoplastic and prodifferentiative in many cell types, including colon-derived cells. The present study was designed to examine the effect of estradiol (E2) on dimethylhydrazine (DMH)-induced colon cancer in rats, and the possibility that E2 may exert its protective effect on the colon through modulation of the vitamin D-endocrine system. The in vivo effect of E2 on DMH-induced colorectal cancer was studied in four groups of ovariectomized female rats: (I) untreated control, (II) E2 treated, (III) DMH treated, and (IV) combined E2 and DMH treated. Significantly higher uterine weights and higher colonic estrogen receptor content confirmed the effectiveness of ovariectomy and E2 replacement. The number of malignant tumors in group IV was 2.3+/-1.1 (mean +/- SE) per rat, compared with 8.1+/-1.9 in group III (P < 0.001). Exposure to estrogen was associated with a marked increase in VDR mRNA content and VDR protein expression in the normal colonic mucosa. In tumor extracts VDR protein expression was considerably lower compared with normal mucosa. Estrogen treatment did not affect serum levels of 25(OH)D, 1,25(OH)2D, and PTH. Significant CpG island methylation in the VDR gene was observed in colonic tissue DNA harvested from rats treated with DMH, but not in colonic mucosae from rats treated with DMH + E2. The highest frequency of CpG methylation in the VDR gene was detected in DNA extracted from cancer tissue rims. In summary, the protective effect of estrogen against chemically induced colonic carcinogenesis is associated with reduced methylation of the VDR gene and with upregulation of both VDR gene transcription and protein expression. We suggest that estrogen may interfere with the process of CpG DNA methylation in the colonic mucosa to prevent silencing of the VDR gene. Increased VDR activity could be one of the mechanisms by which estrogen protects against neoplastic transformation in the colon.

Animals↗
PubMed1989

Hyperplastic colonic polyps as a marker for adenomatous colonic polyps.

Hyperplastic colonic polyps are generally regarded as being of little or no clinical consequence. Recently, however, hyperplastic polyps have been found to share numerous functional similarities with colorectal carcinoma. To determine whether the presence of an isolated left-sided colonic hyperplastic (metaplastic) polyp could serve as a marker for more proximal synchronous adenomatous colonic polyps, we retrospectively analyzed all consecutive colonoscopic polypectomies performed over an 18-month period at two medical centers. It is the policy at both institutions to remove or biopsy all polyps, regardless of size. Indications for colonoscopy included known or previous colonic polyps or carcinoma, hemoccult positive stool, lower gastrointestinal bleeding, iron deficiency anemia, abnormal barium enema, inflammatory bowel disease, abdominal pain, and family history of colon cancer. The location of adenomatous polyps and hyperplastic polyps was recorded and compared. One hundred sixty-three of 845 consecutive patients (19.3%) had at least one colonic polyp. The prevalence of adenomatous polyps alone was 10.3%, hyperplastic polyps 9%, and both types 1.9%. The prevalence rate for an adenomatous polyp in patients without a hyperplastic polyp was 15%. In contrast, among patients with a hyperplastic polyp, 49% had a synchronous adenomatous polyp. Only 3.4% of patients had an adenomatous polyp proximal to the splenic flexure when no polyps were present in the left colon. Conversely, among the 29 patients in whom an isolated hyperplastic polyp was found in the left colon, there was a 32.5% prevalence of adenomatous polyps in the proximal colon (p less than 0.01). The results of this study suggest that left-sided hyperplastic colonic polyps (generally within the reach of a screening sigmoidoscopy) serve as a marker for neoplastic polyps.

Adolescent↗
PubMed1987

[Double-contrast colonic radiography. Comparative, randomized study of 4 colon preparations].

Since diagnostic value of double contrast colon imaging is dependent on the colon preparation used, tolerance and efficacy of 4 colon preparations were evaluated by a simple-blind, comparative, randomized study in 185 outpatients. Colon preparation involves variable combinations of 3 means: residue-free diet, laxatives and wash-out enemas. Principal criteria were evaluated under blind conditions by the same investigator during all examinations, with quantitative rating by segment (left, transverse and right colon) of adherence and colon cleanliness, and global assessment of quality of preparation. The 4 groups were comparable: mean age 44.7 years, sex ratio (male/female) 51.3%. Tolerance and compliance were elevated without significant inter-group differences. The colon preparations studied did not allow a homogeneous preparation to be obtained throughout the colon, efficacy in left colon being superior to right colon, whatever the method used. Analysis of cleanliness and adherence by segment failed to show significant differences between procedures, probably related to weak differences in their effectiveness and the strict nature of the study. The use of a global criterion tended to show value of wash-out enemas as a routine procedure, whether in outpatients or in the Radiology department.

Adolescent↗
PubMed1996

Alterations in colonic arterial and venous plasma neuropeptide concentrations in horses during low-flow ischemia and reperfusion of the large colon.

OBJECTIVE: To measure colonic arterial (CA) and colonic venous (CV) plasma neuropeptide concentrations during low-flow ischemia and reperfusion of the large colon in horses. ANIMALS: 10 adult horses. PROCEDURE: CA and CV plasma samples collected from anesthetized horses during experimentally induced low-flow colonic ischemia and reperfusion were assayed for vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and substance P (SP), using radioimmunoassays. In 6 anesthetized horses, colonic ischemia (20% of baseline (BL]) was maintained for 3 hours, then blood flow was restored and monitored for 3 hours. Hemodynamic variables were monitored continuously and recorded at 30-minute intervals. CA resistance was calculated from colonic blood flow (Q(colon)) and mean CA pressure values at each time. Blood was obtained from CA and CV catheters at 0, 1, 2, 3, 3.25, 3.5, 4, 5, and 6 hours; plasma VIP, CGRP, and SP concentrations were quantified, using radioimmunoassays. In 4 additional horses, VIP and CGRP were measured in CA and CV blood at 0, 0.25, 0.5, 0.75, and 1 hour. RESULTS: Heart rate was significantly increased at 5.5 and 6 hours; other alterations in systemic hemodynamic variables were not significant. Decrease in Q(colon) during ischemia was significant; Q(colon) rebounded to a value significantly greater than BL value within 5 minutes of reperfusion and was maintained above the BL value during 3 hours of reperfusion. Mean CA pressure was significantly decreased during ischemia, but returned to a value not different from the BL value by 3.25 hours. Mean CV pressure remained unchanged from the BL value during ischemia, but increased to a value significantly greater than the BL value by 3.25 hours and remained increased through 6 hours. CA resistance began to decrease during early ischemia and was significantly less than the BL value by 3.25 hours; it remained less than the BL value through 4 hours. Increase in CV VIP concentration was significant by 0.25 hour of ischemia, but decreased to a value not different from BL value by 3.25 hours. Increase in CV CGRP was significant at 3.25 hours, but this variable returned to a value not different from BL value by 3.5 hours. CONCLUSIONS: CV VIP concentration increases during low-flow colonic ischemia, and CV and CA CGRP and CA SP concentrations increase during early reperfusion.

Animals↗
PubMed2006

Colonic electrical stimulation regulates colonic transit via the nitrergic pathway in rats.

Gastrointestinal electrical stimulation has been proposed for the treatment of gastrointestinal motor disorders. However, little is known about potential roles of colonic electrical stimulation (CES). The aim of this study was to evaluate the effect and mechanism of CES on colonic transit in conscious rats. Male rats (N = 14) were equipped with a pair of colonic serosal electrodes for stimulation and a catheter in the colon. Colonic transit was assessed in four randomized sessions with or without CES and with or without nitric oxide synthesis blocker, L-NNA, by calculating the output of phenol red from the anus every 10 min for 90 min. Results were as follows. (1) CES with trains of short pulses significantly enhanced colonic transit. Colonic emptying was 57.3 +/- 6.1% in the control session and 81.9 +/- 4.6% with CES at 90 min, reflecting a 43% increase. (2) L-NNA delayed colonic transit compared with saline and prevented the accelerative effect of CES on colonic transit. We conclude that CES has an excitatory effect on colonic transit and this excitatory effect may be mediated via the nitrergic pathway.

Analysis of Variance↗
PubMed1999

Colonization of the respiratory and genital tracts of female mice with Mycoplasma pneumoniae and protection afforded to the genital tract by prior respiratory colonization.

Mycoplasma pneumoniae, strain MY 12763, colonized the throats of 6 BALB/c female mice for at least 18 days after intranasal inoculation. The same strain colonized, in high titre, the vagina of 9 of 10 progesterone-treated BALB/c mice for at least 35 days, but none of 10 oestradiol-treated mice. Mice were less susceptible to genital-tract colonization with the multiple broth-passed FH strain of M. pneumoniae, only 3 of 10 becoming colonized. The 6 mice inoculated intranasally with strain MY 12763 were immune to genital-tract colonization with the same strain, whereas 10 mice without respiratory-tract colonization were susceptible. Protection of the genital tract in this way was at least as effective as that afforded by previous genital-tract colonization. In a further experiment, 26 immunocompetent BALB/c mice colonized previously in the respiratory tract were resistant to vaginal colonization, whereas 20 BALB/c nude mice, similarly colonized in the respiratory tract, were susceptible in the vagina, illustrating the importance of cell-mediated immunity. The possible relevance of the findings to the human situation is discussed.

Animals↗
PubMed2004

Maternal genital colonization with Ureaplasma urealyticum promotes preterm delivery: association of the respiratory colonization of premature infants with chronic lung disease and increased mortality.

BACKGROUND: Infection of the chorioamnion with Ureaplasma urealyticum has been associated with low birth weight. Respiratory tract colonization in preterm infants has been associated with the development of chronic lung disease (CLD). The purpose of the present study was to determine the frequency of colonization of the mother's vagina and the preterm infant's respiratory tract and to associate U. urealyticum with premature birth and with development of CLD in the newborn. METHODS: The present prospective study involved 126 mothers with preterm delivery and 125 mothers with full-term delivery, as well as their offspring. Vaginal secretion specimens were obtained from each mother before delivery. Rhinopharyngeal secretion or tracheal lavage specimens were collected after the birth of each premature and full-term infant and then periodically during hospitalization. RESULTS: Vaginal Ureaplasma colonization occurred among 36.5% of mothers with preterm delivery and among 38% of mothers with full-term delivery. The rate of vertical transmission was 33% and 17% for mothers with preterm delivery and mothers with full-term delivery, respectively. The transmission rate for infants, according to birth weight, was as follows: 60%, for infants with a birth weight of <1000 g; 50%, for infants with a birth weight of 1000-1500 g; and 15.3%, for infants with a birth weight of > or =1500 g (P=.001). The median gestational age of preterm infants born to colonized mothers was 28.5 weeks, and that of preterm infants born to noncolonized mothers was 32 weeks (P<.0001). The median birth weight of colonized preterm infants was 1135 g, and that of noncolonized infants was 1670 g (P<.0001). Twenty-four percent of preterm infants and 10% of full-term infants were colonized with U. urealyticum. Of colonized preterm infants, 27% developed CLD, compared with 9% of noncolonized infants (P=.03). Mortality was significantly higher among colonized preterm infants (P=.003). CONCLUSIONS: The rate of vertical transmission is highest among preterm infants with a birth weight of <1500 g. Vaginal colonization with Ureaplasma organisms is associated with premature delivery. Colonization of the respiratory tract of infants is associated with the development of CLD and with increased mortality.

Adult↗
PubMed1984

Immunohistological evidence, obtained with monoclonal antibodies, of small intestinal brush border hydrolases in human colon cancers and foetal colons.

The expression of small intestinal hydrolases associated with the enterocyte brush border membrane was studied in human colon cancers and foetal colons, by means of monoclonal antibodies against human small intestinal sucrase-isomaltase (SI), maltase-glucoamylase (MGA), lactase (L), aminopeptidase N (APN), and dipeptidylpeptidase IV (DPP-IV). The enzymes were visualized by indirect immunofluorescence on cryostat sections of tumors developed in nude mice with 6 human colon carcinoma cell lines (HT-29, Caco-2, SW-480, HRT-18, HCT-8R, and Co-115), of 27 primary colorectal carcinomas from patients, and of human foetal (16 to 20 weeks of gestation) and normal adult small intestines and colons. All 5 monoclonals bound to the brush border of the adult small intestine, but not to that of the adult colon mucosa. Antibodies against SI, APN and DPP-IV also bound to the brush border of the foetal colons, to apical borders in HT-29 and Caco-2 tumors in nude mice, and to brush border-like structures in 7/27 tumors from patients. No binding was observed for MGA and L in either tumors or foetal colons. Binding of anti-SI antibodies to the brush border of the juxta-tumoral mucosal epithelium was observed in 9/11 samples tested. These data indicate that some colon tumors exhibit a typical pattern of enterocytic differentiation which is of foetal type and which involves at least 3 brush border membrane hydrolases. Monoclonal antibodies to small intestinal hydrolases may, therefore, be important tools for identification and characterization of some differentiated colonic tumors.

Antibodies, Monoclonal↗
PubMed1983

Induction of colon mucosal beta-glucuronidase production as a mechanism for 1,2-dimethylhydrazine colon carcinogenesis.

Although early studies in germ-free rats showed almost complete dependence on dimethylhydrazine (DMH) colon carcinogenesis upon the presence of colon bacteria, no adequate explanation was given for the 20% tumor incidence observed in germ-free animals. Bacterial activation of liver microsomal products releasing active proximate carcinogens has been the accepted reason for the exquisite specificity DMH has for the colon. Recent work, including the present study, show the colon mucosa is capable of metabolizing carcinogens and activating conjugating forms metabolized in the liver independent of the intestinal microflora. Mucosal beta-glucuronidase production was assayed in coded, scraped mucosa samples from the duodenum/jejunum, ileum, right colon, and left colon of normal and DMH-treated rats. Normal mucosal beta-glucuronidase production was highest in the left colon followed by the right colon, duodenum, and ileum, respectively. Enzyme production in the left colon was significantly increased 24 hours after injection of 25 mg/kg body weight DMH. No elevation was seen in other mucosal samples. Metabolism of DMH to oxidated forms conjugated to glucuronic acid is well established. Thus, this study offers a possible role for carcinogen, induction of a metabolic enzyme in its target tissue.

Animals↗