Bifidobacterium longum and lactulose suppress azoxymethane-induced colonic aberrant crypt foci in rats

Abstract

Bifidobacterium longum has been shown to afford protection against colon tumorigenesis. Lactulose, a keto analog of lactose, serves as a substrate for preferential growth of Bifidobacterium. It is not known whether feeding lactulose along with B. longum will have any advantage over feeding of B. longum alone. To test this combination effect, 61 male Fisher 344 weanling rats were divided into four groups of 15 rats each (16 in the control group) and assigned to one of the following four diets for 13 weeks: (i) AIN76A (control, C); (ii) C + 0.5% B. longum (C+Bl, containing 1 x 10(8) viable cells/g feed); (iii) C + 2.5% lactulose (C+L); (iv) C + 0.5% B. longum + 2.5% lactulose (C+Bl+L). All animals received a s.c. injection of azoxymethane at 16 mg/kg body wt at 7 and 8 weeks of age. Colons of 10 rats from each dietary group were analyzed for aberrant crypt foci (ACF), which are preneoplastic markers. Colonic mucosa and livers from five rats were analyzed for glutathione S-transferase (GST, a Phase II enzyme marker). Results indicate that feeding of lactulose and B. longum singly and in combination reduces the number of ACF (P = 0.0001) and the total number of aberrant crypts significantly (P = 0.0005). The total number of ACF in diets C, C+Bl, C+L and C+Bl+L were 187 +/- 9, 143 +/- 9, 145 +/- 11 and 97 +/- 11 respectively. There was no significant difference in weight gain among treatments. Colonic mucosal GST levels were significantly (P = 0.05) higher in the Bl and L groups compared with group C. Initially there was a mild diarrhea in lactulose-fed rats. There was a positive correlation between higher cecal pH and number of ACF. Results of the study indicate that Bifidobacterium and lactulose exert an additive antitumorigenic effect in rat colon.

Hydrolysed inulin alleviates the azoxymethane-induced preneoplastic aberrant crypt foci by altering selected intestinal microbiota in Sprague–Dawley rats

“…The previous studies by Verghese et al (2002a,b) also reported that the weight of the rat that fed on 10% inulin was reduced. However, some studies have reported no significant consequence of inulin or other prebiotics on body weight or feed intake (Challa et al 1997;Reddy et al 1997;Rowland et al 1998). Increase in cecal weight and decline in pH of the cecal content were observed among inulin-fed rats (Table 1), possibly, due to the fermentation of inulin by intestinal bacteria and short-chain fatty acid (SCFA) (Rossi et al 2005).…”

Lactulose ingestion increases faecal bifidobacterial counts: A randomised double-blind study in healthy humans

“…Increasing bifidobacterial counts can be perceived as beneficial, and this saccharolytic genus could be of interest in the prevention of colon carcinogenesis (Buddington et al, 1996). Experimental studies in rat have shown that feeding of lactulose and Bifidobacterium longum singly and in combination had an additive antitumorigenic effect in the rat colon (Challa et al, 1997;Singh et al, 1997). Under our experimental conditions, the partial replacement of other anaerobes with bifidobacteria did not alter the faecal pH, concentrations of bile acids and neutral sterols, which are factors potentially implicated in colon carcinogenesis (Nair, 1988;Owen, 1997).…”

“…Once in the caecum, lactulose is fermented by the colonic microflora resulting in changes in bacterial composition and metabolic activities of the colonic flora. After ingestion of a large dose of lactulose ranged 20-60 g/day (Berge Henegouwen et al, 1987), the following has been shown: (a) an increase of bifidobacterial counts (Ballongue et al, 1997); (b) an inhibition of bacterial degradation of primary to secondary bile acids (Nair, 1988) and (c) an inhibition of colon cancer in rats when administered alone or in conjunction with bifidobacteria (Hennigan et al, 1995;Challa et al, 1997).…”

Role of probiotics, prebiotics and synbiotics in chemoprevention for colorectal cancer

“…Lactic acid bacteria have been shown to increase colonic NADPH-cytochrome P-450 reductase activity [42] and glutathione S-transferase levels [43] and to reduce hepatic uridine diphosphoglucuronyl-transferase activity [19] , enzymes which are involved in the metabolism of carcinogens in rats.…”