Synergistic impact of Lactobacillus fermentum, Lactobacillus plantarum and vincristine on 1,2-dimethylhydrazine-induced colorectal carcinogenesis in mice

Abstract

Lactobacillus sp. is the most dominant probiotic strain of bacteria. Evidence indicates that the consumption of Lactobacillus sp. reduces the risk of colorectal cancer in animal models. The present study was carried out to determine whether administration of Lactobacillus fermentum/ Lactobacillus plantarum alone or in combination with vincristine have a synergistic impact on the control of colorectal cancer in an animal model. Mice with 1,2 dimethylhydrazine (DMH) hydrochloride-induced colon cancer were fed with L. fermentum and L. plantarum isolated along with vincristine. An increase in body weight, a decrease in ammonia concentration, a decrease in β glucosidase and β glucuronidase enzyme activity and a reduction in the number of crypts in the mice in the pre-carcinogen-induced group was noted when compared to these variables in the post-carcinogen-induced group. The body weight of the mice fed L. fermentum along with vincristine was increased (6.5 g), and was found to be 3.5 times higher compared to that of the control. A marked decrease in the ammonia concentration (240 mg), and β glucosidase (0.0023 IU) and β glucopyranose enzyme activity (0.0027 IU) was observed; 22.59% less ammonia concentration, 73.26% less β glucosidase activity and 56.46% less β glucuronidase enzyme activity was noted when compared to the control. A significant reduction in the number of aberrant crypt foci (ACF) (90%) was observed when compared to the control. Maximum protection was observed in the mice fed the probiotics and vincristine prior to cancer induction. Among the different dietary combinations tested in the present study, L. fermentum and vincristine showed a more extensive reduction in ammonia concentration, β glucosidase, β glucuronidase activity and the number of ACF.

Figure 1.

Concentration of ammonia. 1, normal diet (Control 1); 2, normal diet + DMH (Control 2); 3, Lf3 + DMH + normal diet; 4, DMH + Lf3 + normal diet; 5, Lp1 + DMH + normal diet; 6, DMH + Lp1 + normal diet; 7, Lf3 + Lp1 + VCR + DMH + normal diet; 8, DMH + Lf3 + Lp1 + normal diet; 9, VCR + normal diet (Control 3); 10, VCR + DMH + normal diet (Control 4); 11, DMH + VCR + normal diet (Control 5); 12, Lf3 + VCR + DMH + normal diet; 13, DMH + Lf3 + VCR + normal diet; 14, Lp1 + VCR + DMH + normal diet; 15, DMH + Lp1 + VCR + normal diet; 16, Lf3 + Lp1 + DMH + normal diet; 17, DMH + Lf3 + Lp1 + VCR + normal diet.

Figure 2.

Enzyme activity of β glucuronidase, β glucosidase and number of ACF in experimental mice. 1, normal diet (Control 1); 2, normal diet + DMH (Control 2); 3, Lf3 + DMH + normal diet; 4, DMH + Lf3 + normal diet; 5, Lp1 + DMH + normal diet; 6, DMH + Lp1 + normal diet; 7, Lf3 + Lp1 + VCR + DMH + normal diet; 8, DMH + Lf3 + Lp1 + normal diet; 9, VCR + normal diet (Control 3); 10, VCR + DMH + normal diet (Control 4); 11, DMH + VCR + normal diet (Control 5); 12, Lf3 + VCR + DMH + normal diet; 13, DMH + Lf3 + VCR + normal diet; 14, Lp1 + VCR + DMH + normal diet; 15, DMH + Lp1 + VCR + normal diet; 16, Lf3 + Lp1 + DMH + normal diet; 17, DMH + Lf3 + Lp1 + VCR + normal diet.

Figure 3.

Normal colonic cells at low magnification (×10) in the control group.

Figure 4.

Enlarged colonic cell without the crypt at low magnification (×10) in the Lf3 + VCR + DMH + normal diet group (Group 12).

Figure 5.

Larger tumor at low magnification (×10) in the normal diet + DMH group (Control 2).