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G Caderni

Publications and source records attributed to G Caderni.

At least 55 records · Page 3Linked to original sources
PubMed1991

Starchy foods and colon proliferation in mice.

The effect of starch contained in different foods on colonic proliferation was studied in C57BL/6N mice after four weeks of feeding with 20% fat diets containing cornstarch, white bread, pasta, and rice; an equicaloric amount of sucrose was used in a control diet. Cell proliferation was evaluated in different subsites of the colon (rectal end, mid colon and cecal end) by colchicine arrest and [3H]thymidine incorporation. The following parameters were analyzed: mitotic index (MI), labeling index (LI), and the distribution of labeled cells along the crypt. Different results were obtained in the different subsites. At the rectal end of the colon, all diets containing starch lowered cell proliferation compared with the sucrose diet. The values for MI in the different diets were 2.56 +/- 0.22, 1.73 +/- 0.30, 1.37 +/- 0.19, 1.61 +/- 0.29, and 1.29 +/- 0.31 for control, cornstarch, white bread, pasta, and rice, respectively. Values are means +/- SE (n = 10). The values for LI showed a similar pattern. In the mid colon, the MI was significantly lowered only by the diet containing rice, whereas the DNA synthetic activity (LI) was lowered by cornstarch, pasta, and rice. Toward the cecal end, we observed a significant reduction in MI with diets containing pasta and rice and in the LI with diets containing pasta. The distribution of the LI along the crypt in the different subsites was not significantly affected by experimental dietary variations. The results suggest that starch from different dietary sources might reduce colon proliferation in the mouse.

Analysis of Variance↗
PubMed1991

Gastric hyperplastic changes and thymidine uptake after partial gastrectomy in rats.

Foveolar hyperplastic changes have been recently considered to be the most distinctive histological finding after partial gastrectomy, and their relationship with bile reflux has been proven. The present study was undertaken to establish whether an increase in 3H-thymidine uptake--which is an expression of increased gastric mucosal proliferative activity--might correspond to these hyperplastic changes. Histology and thymidine uptake values were assessed and compared in nineteen rats operated upon either by means of a Polya gastrectomy (11), or with a Roux-en-Y biliary diversion (8). Thymidine uptake values and the extent of gastric hyperplastic changes were greater in the Polya than in the Roux-en-Y group. Moreover, a significant correlation was found between thymidine uptake values and the extent of hyperplastic changes. The relationship between hyperplastic changes and post-gastrectomy increased mucosal proliferative activity would thus seem to have been demonstrated. Since bile acids have been shown to stimulate cell proliferation in ileal and colonic mucosa, a rôle for bile reflux can be hypothesized for the increased cell proliferation activity in the gastric stump.

Animals↗
PubMed1991

Gastric hyperplastic changes and thymidine uptake after partial gastrectomy in rats.

Foveolar hyperplastic changes have been recently considered to be the most distinctive histological findings following partial gastrectomy, and their relationship to bile reflux has been proven. The present study was undertaken in order to determine whether an increase in 3H-thymidine uptake, which is an expression of increased gastric mucosal proliferative activity, might correspond to these hyperplastic changes. Histology and thymidine uptake values were assessed and compared in nineteen rats operated upon either with a Polya gastrectomy (11) or with a Roux-en-Y biliary diversion (8). Thymidine uptake values and the extent of gastric hyperplastic changes were greater in the Polya than in the Roux-en-Y group. Moreover, a significant correlation was found between thymidine uptake values and the extent of hyperplastic changes. Therefore, the relationship between hyperplastic changes and increased mucosal proliferative activity post-gastrectomy would seem to have been proven. Since bile acids have been shown to be able to stimulate cell proliferation in ileal and colonic mucosa, a role for bile reflux in the increased cell proliferation activity in the gastric stump can be hypothesized.

Anastomosis, Roux-en-Y↗
PubMed1990

Effect of dietary lipids on hepatic and intestinal monooxygenases in mice.

The effect of dietary lipids on hepatic and intestinal monooxygenases was studied by feeding C57BL/6N mice (for 2 wks) diets containing 5% and 23.5% (wt/wt) olive oil or corn oil. At the end of the feeding period, we measured arylhydrocarbon hydroxylase (AHH) activity in S9 preparations from liver, small intestine, and colon; and, using the same S9 preparations from the liver, we observed the activation of the following three dietary promutagens: 2-amino-3-methylimidazo(4,5-f)quinoline, 2-amino-3,8-dimethylimidazo(4,5-f) quinoxaline, and 2-amino-6-methyldipyrido(1,2-a:3',2'-d)imidazole. The results showed that high-fat diets increased hepatic AHH activity both in corn oil and olive oil diets compared with the low-fat diets; also, a 5% corn oil diet had significantly higher AHH activity compared with the 5% olive oil diet. AHH activity was, respectively, 48.6 +/- 5.1 and 79.5 +/- 11.4 pmol 3OH-benzo[a]pyrene formed/mg/min in the 5% and 23.5% olive oil diets and 66.1 +/- 5.1 and 83.9 +/- 12.2 in the 5% and 23.5% corn oil diets; values are means +/- SE, n = 16. The results also showed a significant increase in the ability of hepatic S9 fractions from animals on high-fat diets to activate promutagens in the Salmonella/plate test. On the contrary, AHH activity in the small intestine and colon was not affected by the fat content of the diet.

Animals↗
PubMed1989

Proliferative activity in the colon of the mouse and its modulation by dietary starch, fat, and cellulose.

The effect of dietary starch, fat, and cellulose on colonic proliferation was studied in female C57Bl/6J mice after 4 weeks of feeding with diets containing various levels of starch (3, 36, and 57-65%), various levels of fat (corn oil, 5 and 29%) and various levels of cellulose (2 and 10%). Cell proliferation was measured by colchicine arrest and [3H]thymidine incorporation. The following parameters were analyzed: mitotic index, labeling index, and position of labelled cells along the crypt. Increasing starch content from 3 to 36% decreased cell proliferation both in low (5%) and high (29%) fat diets. By estimating simultaneously the effects of starch and fat with a single multiple regression model, we observed a decrease of mitotic index from 3.04 +/- 0.34 to 2.04 +/- 0.43 (means +/- SE) (P less than 0.05) when starch was increased from 3 to 36% regardless of the level of fat. Other proliferation parameters showed a similar pattern. Changes in dietary fat alone did not affect significantly cell proliferation. We also investigated the effect of starch at high levels (57-65%) and its interactions with cellulose. High starch (57-65%) increased the labeling index from 7.70 +/- 0.58 to 9.65 +/- 0.88 (P less than 0.05), when also considering the effect of cellulose in the multiple regression model. Cellulose by itself did not change the labeling index. Varying starch from 36 to 57-65% increased the number of cells/crypt column from 22.20 +/- 0.82 to 25.87 +/- 1.21 (P less than 0.05) and varying cellulose from 2 to 10% increased the number of cells/crypt column from 22.20 +/- 0.82 to 27.25 +/- 0.97 (P less than 0.01). The results indicate that either high or low fat diets, containing 36% starch, have the minimum proliferative effects in the mouse colon. However, diets containing high levels of both starch (57%) and cellulose (10%) may induce an increase in proliferation. These data suggest a potential beneficial effect of starch on colon proliferation.

Animals↗
PubMed1989

Effect of dietary fat, starch and cellulose on fecal bile acids in mice.

The effect of dietary fat, starch and cellulose on individual and total fecal bile acids was studied in mice after 4 wk of feeding diets containing different levels of fat (5 and 29%), starch (3, 36 and 57-65%) and cellulose (2 and 10%). Diet affected the fecal concentration of deoxycholic acid, beta-muricholic acid and total bile acids. Increasing dietary fat from 5 to 29% significantly increased the level of deoxycholic acid and total bile acids. An increase in dietary cellulose from 2 to 10% significantly decreased the level of deoxycholic acid, beta-muricholic acid and total bile acids. High levels of dietary starch (36 and 57-65%) did not significantly affect the excretion of deoxycholic, beta-muricholic and total fecal bile acids. Starch was able to bind bile acids in vitro and to affect the level of fecal free bile acids. In high fat diets, the level of free bile acids was lower in the feces of animals fed 36% starch diets than in those fed 3% starch diets. This reduction of free bile acids was accompanied by a reduction in colon proliferative activity. We suggest that free, rather than total, bile acids are the effective damaging agents for colon mucosa, and may represent a risk factor in the development of cancer.

Animals↗
PubMed1988

Nuclear aberrations and micronuclei induction in the digestive tract of mice treated with different iron salts.

Toxic effects of ferrous sulfate and of ferric chloride were determined in the gastrointestinal tract by measuring the induction of nuclear aberrations and micronuclei. In fasting animals ferric chloride induced a dose-related increase of nuclear aberrations in the stomach, whereas ferrous sulfate was not active. In normally feeding animals no increase of nuclear aberrations was observed. The effects of the iron compounds on the duodenum were minimal. In fasting animals a dose-related increase of nuclear aberrations was observed at the level of the colon, with no clear difference between ferrous and ferric compounds. A modest increase of nuclear aberrations of the colon was seen in feeding animals only with ferrous sulphate. By intrarectal administration, nuclear aberrations were induced especially by ferric chloride. An increase of the frequency of micronuclei was not observed at the level of the stomach, duodenum and colon, with the exception of ferric chloride, that induces a significant, although small increase of colon micronuclei when administered intra-rectally. The data demonstrate that iron compounds have an intrinsic cellular toxicity when not administered with food, but do not seem to carry any genotoxic potential for the gastrointestinal tract.

Animals↗
PubMed1988

Dietary factors affecting the proliferation of epithelial cells in the mouse colon.

Corn oil (CO), given as a bolus to female C57BL/6J mice, caused a marked increase in cell proliferation in the colon; this was assessed with a two-hour colchicine arrest for mitotic figures (MF) and with [3H]thymidine incorporation for labeled cells (LC) per crypt measured in histological preparations. In contrast, the same amount of fat given as a bolus in a high-fat diet mixture failed to increase cell proliferation. To determine whether a particular component in the diet was responsible for this protective effect, mice were treated with boluses of CO (0.4 ml) mixed with cellulose (CL), starch (ST), sucrose (SU), casein (CS), vitamin mix (VM) or mineral mix (MM). The results indicated that cellulose, starch, and minerals reduced the proliferative activity caused by CO (MF/crypt CO = 1.30 +/- 0.24; CO + CL = 0.55 +/- 0.10, CO + ST = 0.91 +/- 0.23, CO + MM = 0.63 +/- 0.16), whereas sucrose, casein, and vitamin mix did not. To test the implications of these findings in chronic feeding studies, groups of animals were fed (for 4 wks) diets "deficient" in starch and cellulose, calcium, and both the complex carbohydrates and calcium. The results showed that both calcium and complex carbohydrates affected the proliferation rate significantly (for instance, MF/crypt = 1.44 +/- 0.22 for both factors deficient vs. 0.48 +/- 0.05 for both factors present). We concluded that starch, cellulose, and calcium are protective for the toxic effect of CO on the mouse colon.

Animals↗
PubMed1987

A CHO cell line resistant to deoxycholic acid.

Spontaneous mutants resistant to deoxycholic acid (DCA) have been selected from a CHO cell line AuxBl. One of the colonies or 'lines' selected was subsequently mutagenized by ethylmethanesulfonate (250 micrograms/ml) and a more resistant cell, named alpha 3, has been selected. When AuxBl and alpha 3 were exposed to graded concentrations of DCA for 1 h, the LD50 for the mutant strain alpha 3 was 0.66 mM compared to 0.26 mM for the parental line. AuxBl. alpha 3 showed a cross-resistance compared to AuxBl with respect to cholic acid and chenodeoxycholic acid and to other acidic lipids such as linoleic and oleic acids. As an initial step in characterization of the cell lines, the amounts of different phospholipids from whole cell extracts of the parental and mutant strains have been measured after thin-layer chromatography (TLC) separation. The results obtained demonstrated that the fraction of sphingomyelin and phosphatidylcholine over the total phospholipids was slightly increased in the resistant cell line, alpha 3, compared to the parental line, AuxBl (54.9% +/- 1.04 compared to 51.2% +/- 0.3, P = 0.01). Further characterization of cell lines resistant to bile acids could lead to the identification of the cellular target of bile acid action.

Animals↗
PubMed1986

Nuclear damage of colon epithelial cells by the food carcinogen 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) is modulated by dietary lipids.

Intestinal damage in C57BL/6J female mice was quantified by measuring the frequency of nuclear aberrations in colonic crypts. The animals were maintained on the following diets: standard (5% lipids, 5% cellulose); low- and high-cellulose (0-20% cellulose); high lipids (20% maize oil or 20% olive oil). All groups of animals were treated by gavage either with saline or 250 mg/kg of the dietary carcinogen 2-amino-3-methylimidazo[4,5-f]quinoline (IQ). After 24 h their colons were removed and stained and the nuclear aberrations scored under the microscope. The administration of IQ markedly increased the number of colon aberrations in all of the treated animals. Variations in dietary fiber did not modify the colon-damaging activity of this compound. Maize oil slightly increased the colon-damaging activity, whereas significant protection was observed in the animals on a high-lipid olive-oil diet. These results show that composition of the diet may vary the genotoxic effect of this dietary carcinogen.

Animals↗
PubMed1985

Alkaline elution of DNA as a method for assessing genotoxic effects of drugs: its application to a series of antiviral compounds.

Various techniques are available for the evaluation of the genotoxic potential of drugs and chemicals, some of which utilize as targets mammalian cells grown in vitro. Among these techniques alkaline elution of DNA has the advantage of rapidity and low cost, and can be performed on easily grown leukemia cell lines. To test the applicability of the method to pharmaceutical compounds, we used DNA-alkaline elution with a series of antiviral agents with variable DNA-damaging activity. 5-Iodo-2'-deoxyuridine (5-IdU), 5-bromo-2'-deoxyuridine (5-BrdU) and 5-trifluoromethyl-2'-deoxyuridine (F3dT) increased the DNA elution rate over controls in a dose-dependent fashion, 9-beta-D-arabinofuranosyladenine (ARA-A) had a marginal effect. 9-(2-Hydroxyethoxymethyl)guanine(acyclovir,ACV) and 5-(2-bromovinyl)-2-deoxyuridine (5-BrVdU), selective antiviral compounds, did not vary alkaline elution profiles. These results fully support the use of alkaline elution of DNA as a standard procedure in the evaluation of the genotoxic effect of drugs.

Animals↗
PubMed1984

Urinary mutagens in humans after fried pork and bacon meals.

Urinary mutagenic activity on Salmonella typhimurium strain TA1538 with S9 was determined after morning meals of fried pork and bacon. Both in fasting and non-fasting subjects a very marginal elevation of urinary mutagenic activity was observed, accounting for a small fraction only of the total amount of mutagens ingested.

Animals↗
PubMed1983

The effect of cigarette smoke on aryl-hydrocarbon hydroxylase (AHH) activity of the human kidney.

AHH activity was measured in kidney cortex biopsies obtained during surgery from patients with hydronephrosis and from unaffected portions of kidneys with renal cell carcinomas. AHH activity was slightly, but not significantly, higher in the group of non-smoking cancer patients when compared to non-smoking hydronephrotic subjects. Smoking induced a significant increase of AHH activity in the hydronephrotic kidneys but not in cancer kidneys, probably due to the higher baseline values and scatter in the cancer group. Pooling cancer and non-cancer kidneys, smokers had a higher AHH activity than non-smokers, this increase being dose-related.

Adenocarcinoma↗
PubMed1983

DNA damage of mammalian cells by the beef extract mutagen 2-amino-3-methylimidazo[4,5-f]quinoline.

The beef-extract mutagen, 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), was shown, by alkaline elution procedures, to induce DNA damage in radiation-induced mouse leukaemia cells. The effect, which was dose related, occurred in incubations containing S-9 mix derived from polychlorinated biphenyl-induced rat liver but not in the absence of this metabolic activation system. An increased alkaline elution of DNA was also observed following IQ addition to cultures of hepatocytes from 3,3',4,4'-tetrachloroazobenzene-induced rat liver, and the DNA damage was again dose related. IQ has thus been shown to be genotoxic to mammalian cells in the presence of an effective activation system.

Animals↗