Effect of dietary chenodeoxycholic acid on intestinal carcinogenesis induced by 1.2 dimethylhydrazine in mice and hamsters

Martin, M S; Justrabo, E; Jeannin, Jean–François; Leclerc, Anne-Marie; Martı́n, Francisco

doi:10.1038/bjc.1981.130

Cited by 17 publications

(5 citation statements)

References 5 publications

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“…These crystalline structures are formed by concretion or accretion of cholesterol monohydrate plus an admixture of calcium salts, bile acids, bile pigments, proteins, fatty acids and phospholipids. Finally, some of the secondary bile salts generated by microorganisms are potentially toxic and/or mutagenic [29–31]. It is suggested that they can disturb the normal microbiota of the gut leading to diarrhoea, mucosal inflammation or activation of harmful drugs and carcinogens in the intestinal contents [32].…”

Section: Physiology Of Bile Production and Flowmentioning

confidence: 99%

The interaction between bacteria and bile

2005

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Commensal and pathogenic microorganisms must resist the deleterious actions of bile in order to survive in the human gastrointestinal tract. Herein we review the current knowledge on the mechanisms by which Gram-positive and Gram-negative bacteria contend with bile stress. We describe the antimicrobial actions of bile, assess the variations in bile tolerance between bacterial genera and examine the interplay between bile stress and other stresses. The molecular mechanisms underlying bile tolerance are investigated and the relationship between bile and virulence is examined. Finally, the potential benefits of bile research are briefly discussed.

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Section: Physiology Of Bile Production and Flowmentioning

confidence: 99%

The interaction between bacteria and bile

2005

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“…6.6.5. Products used in experimental carcinogenesis (Martin et al 1981). Spontaneous colorectal cancer is exceptional in animal models, but tumours can be created easily in rats, mice or hamsters using chemicals such as N-methylnitrosourea and N-methyl-N ' -nitro-N-nitrosoguanidine (Table 6).…”

Section: Cell Proliferationmentioning

confidence: 99%

Functional food science and gastrointestinal physiology and function

et al. 1998

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The gut is an obvious target for the development of functional foods, acting as it does as the interface between diet and the metabolic events which sustain life. The key processes in digestive physiology which can be regulated by modifying diet are satiety, the rate and extent of macronutrient breakdown and absorption from the small bowel, sterol metabolism, the colonic microflora, fermentation, mucosal function and bowel habit, and the gut immune system. The intestinal microflora is the main focus of many current functional foods. Probiotics are foods which contain live bacteria which are beneficial to health whilst prebiotics, such as certain non-digestible oligosaccharides which selectively stimulate the growth of bifidobacteria in the colon, are already on the market. Their claimed benefits are to alleviate lactose maldigestion, increase resistance to invasion by pathogenic species of bacteria in the gut, stimulate the immune system and possibly protect against cancer. There are very few reports of well-designed human intervention studies with prebiotics as yet. Certain probiotic species have been shown to shorten the duration of rotavirus diarrhoea in children but much more work is needed on the mechanism of immunomodulation and of competitive exclusion and microflora modification. The develop-ment of functional foods for the gut is in its infancy and will be successful only if more fundamental research is done on digestive physiology, the gut microflora, immune system and mucosal function.

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“…Oral administration of primary bile acids has increased tumour yields in various models: rats and mice given dimethylhydrazine (Martin et al, 1981) or methylnitrosourea , and rats with 'spontaneous' cancers arising at a colostomy (Sauer et al, 1980). Direct exposure of colorectal mucosa to primary or secondary bile acid solutions instilled per rectum also promotes carcinogenesis in response to the contact carcinogen N-methyl-N'-nitro-Nnitroso-guanidine (Narisawa et al, 1974;Reddy et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

The cocarcinogenic effect of intrarectal deoxycholate in rats is reduced by oral metronidazole

Rainey¹,

Maeda²,

Williams³

et al. 1984

Br J Cancer

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Summary Bile acids enhance colorectal carcinogenesis in animals and man, perhaps after degradation by faecal anaerobes. The promotional effect of sodium deoxycholate (SDC) and its relationship to bacteria was examined in male Sprague-Dawley rats (n = 115) which had received a 6-week course of azoxymethane (total dose 90mg kg 1 s.c.) Two groups received 3 x weekly intrarectal (i.r.) instillations of N saline or 0.12 M SDC for 18 weeks. Another group received SDC i.r. plus metronidazole (22.5mgkg-1) daily in the drinking water. Controls had no instillations or metronidazole alone. By 28 weeks SDC had increased mean colonic crypt depth by 9% (P<0.001), and had almost trebled colorectal tumour yields from 2.4+0.4 per rat (mean + s.e.) in controls to 6.4+0.5 (P<0.001). Tumour yields after SDC + metronidazole (4.2+0.5) remained 75% higher than in controls (P<0.01) but were 33% less than after SDC alone (P<0.01), and the increase in crypt depth was maintained at 7% (P<0.001). Neither metronidazole alone nor saline i.r. had any effect on tumour yield, but metronidazole alone reduced crypt depth by 9% (P<0.001). Deoxycholate is a potent cocarcinogen and also stimulates mucosal hyperplasia. Metronidazole reduces its tumour-promoting effect, suggesting that faecal anaerobes are important in bile acid cocarcinogenesis.

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Effect of dietary chenodeoxycholic acid on intestinal carcinogenesis induced by 1.2 dimethylhydrazine in mice and hamsters

Cited by 17 publications

References 5 publications

The interaction between bacteria and bile

The interaction between bacteria and bile

Functional food science and gastrointestinal physiology and function

The cocarcinogenic effect of intrarectal deoxycholate in rats is reduced by oral metronidazole

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