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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.

The relative effectiveness of commercially available plain yogurt (Y), sweet acidophilus milk (SAM), hydrolyzed-lactose milk (HLM), a lactase tablet (LT), and whole milk (WM) was evaluated in 10 lactose-intolerant black subjects. In a 5 x 5 Latin square design, hourly breath hydrogen excretion (BHE) was measured for 5 h after the subjects consumed the above products (18 g lactose in each except HLM, which had 5 g). Mean BHE (ppm) for Y, SAM, LT, HLM, and WM were 12, 37, 29, 18, and 33, respectively. There was a significant (p less than 0.05) positive correlation of 0.808 between the symptoms reported and the mean peak BHE. However, the correlation between the symptoms and diagnosis by history was not significant. Although Y was as effective as HLM in minimizing lactose maldigestion, it was the least accepted by the subjects in sensory evaluations. Results of this study also indicate that microbial endogenous lactase in yogurt is superior to exogenous commercial lactase in alleviating lactose maldigestion.

Three experiments were conducted to study the effect of milk, Thermophilus milk and methanol solubles of milk and Thermophilus milk on the plasma cholesterol levels and hepatic cholesterogenesis using laboratory rats. In experiment I, white Wistar male rats of 3288 initial average weight were assigned to three dietary treatments consisting of: (1) commercial rat chow + water, (2) commercial rat chow + skim milk, and (3) commercial rat chow + Thermophilus milk. In the second experiment, the methanol solubles of whole milk and Thermophilus milk were given by gastric intubation to white Wistar male rats in six treatment groups. The methanol solubles were given at levels of 1 ml and 2 ml, and the control groups received similar quantities of H,O. In the third experiment, liver tissue from white Wistar male rats was used to study the in vitro hepatic cholesterol synthesis. Consumption of Thermophilus milk by the rats in experiment 1 resulted in a significant decrease in plasma cholesterol levels, The liver cholesterol levels were lower in the group receiving Thermophilus milk than the group receiving skim milk. Similar results were seen with feeding of methanol solubles. The in vitro hepatic cholesterogenesis was inhibited by methanol solubles from milk and Thermophilus milk, the inhibition being much more with methanol solubles from ThermophiZus milk. The metabolites produced during fermentation of milk may be responsible for the hypocholesterolemic effect of Thermophilus milk.

This study was designed to determine the effect of 10% dietary long-chain inulin on the azoxymethane (AOM)-induced colonic preneoplastic aberrant crypt foci (ACF) and small intestinal and colon tumors at the initiation (I), promotion (P) and I + P stages (20 rats per treatment) in Fisher 344 male weanling rats. After an acclimatization period of 1 wk, groups of Fisher 344 male weanling rats were assigned to consume AIN 93G diet (control) or AIN 93G diet containing 10% inulin. All the rats received 16 mg/kg body AOM dissolved in saline subcutaneously at 7 wk of age followed by a second injection at 8 wk of age. An additional group of five rats received only saline and consumed the control diet. The rats received the assigned diets until asphyxiation by CO(2) at 16 wk of age for the ACF experiment and 45 wk for the end-point tumor experiment. Feed intake, weight gain, diarrheal index, cecal weight, cecal pH, ACF and tumors in the colon were determined. Rats fed inulin had diarrhea after 2 wk of feeding and recovered by approximately 4 wk. Cecal weight was greater in rats fed inulin and cecal pH was lower. The inulin group had more than 66% fewer aberrant crypts and 60% fewer ACF compared with the control group. Tumor incidences in the small intestine and colon of rats in the control, I, P and I + P groups were: 78, 31, 0 and 11% and 90, 73, 69 and 50%, respectively. The corresponding values for the distal portion of the colon were 87, 63, 45 and 33%, respectively. Colon tumors per tumor-bearing rat were 4.2, 3.09, 1.36 and 1.2 for the control, I, P and I + P groups, respectively. All groups differed, P < 0.05. The results of this study indicate that dietary long-chain inulin suppresses AOM-induced ACF formation, an early preneoplastic marker of colon tumorigenesis in rats, and colon tumors, particularly at the promotion stage.

Skim milk fermented by various lactic cultures was tested for antimicrobial activity by agar diffusion technique, using Pseudomonas jluorescens, P. aeruginosa and Bacillus subtilis as test organisms. Lactobacillus bulgaricus, L. acidophilus and Streptococcus thermophilus strongly inhibited the growth of the test organisms. Other lactic cultures, singly or in combination, showed varying degrees of antimicrobial activity. A methanoi-acetone (M-A) extract was prepared by lyophilizing fermented milk and extracting the powder sequentially with cold methanol and acetone. The methanol-acetone (M-A) extract strongly inhibited the growth of B. subtilis, B. pumulis, P. aeruginosa, P. jluorescens, Flavobacterium capsulatum, Satmonella typhimurium, Escherichia coli, Shigella sp. and Streptococcus lactis. The antimicrobial activity of S. thermophilus was not reported in the literature previously. The M-A extract contained ninhydrin-positive materials and did not lose antimicrobial activity even when it was exposed to a temperature of 100°C for 10 min. Five milliliters of M-A extract were applied to 20 x 2.2 cm Sephadex G-10 column equilibrated with 0.05N HCl which later served as the eluant. Fractions of 15 ml were collected at a flow rate of 2.5 ml/mm Sephadex fractionation of M-A extract showed that there were at least three active fractions. One of the fractions appeared in the void volume followed closely by the other fractions indicating that the latter two fractions have compounds of molecular weight less than 700 daltons. The purification achieved was about 400-fold. The activity (recovery) of the compound(s) increased upon fractionation on Sephadex indicating the possible presence of inhibitor(s).

Antimutagenic activity of acetone or ethylacetate extracts of skim milk fermented by Streptococcus thermophilus, Lactobacillus bulgaricus, or a combination of both the organisms was studied using Salmonella typhimurium (TA 98 and TA 100). Mutagens used were 4-nitroquinoline-N-oxide (a direct-acting mutagen) and 2-aminofluorene (a mutagen requiring S9 activation). Extracts from all fermented milks showed significant (P less than .05) dose response in suppressing the number of revertants caused by NQNO and 2-aminofluorene in both tester strains, whereas extracts from unfermented milk had no effect. Extracts prepared from milk fermented by L. bulgaricus plus S. thermophilus showed significantly (P less than .05) more antimutagenic activity than extracts prepared from milk fermented by S. thermophilus alone. Solvent (acetone vs. ethyl acetate) effect was not significant with 4-nitroquinoline-N-oxide as mutagen. However, in the case of 2-aminofluorene, acetone extracts showed significantly (P less than .05) higher antimutagenic activity. The results of this and related studies strongly indicate that antimutagenic compounds are produced in milk during fermentation by S. thermophilus and L. bulgaricus.

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