Inhibitory effects of freeze-dried milk fermented by selected Lactobacillus bulgaricus strains on carcinogenesis induced by 1,2-dimethylhydrazine in rats and by diethylnitrosamine in hamsters

Balansky, Roumen; Gyosheva, B.; Ganchev, G.; Mircheva, Z.; Minkova, Svetlana; Georgiev, G.

doi:10.1016/s0304-3835(99)00287-6

Cited by 29 publications

(19 citation statements)

References 25 publications

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“…These protective effects were observed in colon cells (where direct positive effects of dietary probiotics could be expected) and, to a lesser extent (not statistically significant), in liver cells. A similar systemic chemopreventive activity has also been reported for L. bulgaricus; the role of resorbed protective agents has been hypothesized [Balansky et al, 1999]. Interestingly, the reduction of DNA damage to below the basal levels is in agreement with the marked decrease of b-glucuronidase activity in fecal samples from L. caseisupplemented rats.…”

Section: Discussionsupporting

confidence: 62%

“…The effect of L. casei dietary supplement in animals was studied using the experimental carcinogen DMH [Balansky et al, 1999;Li et al, 2000]. While the epithelial cells of the colonic mucosa are the main target of DMH genotoxicity with DMH inducing colorectal tumors in experimental animals, this xenobiotic is also a potent hepatocarcinogen [Hawks et al, 1974].…”

Section: Model Mutagenmentioning

confidence: 99%

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Modulatory activity of a Lactobacillus casei strain on 1,2‐dimethylhydrazine‐induced genotoxicity in rats

Villarini

Caldini

Moretti

et al. 2008

Environ and Mol Mutagen

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The present study was designed to investigate the putative antigenotoxic effects of supplementing the diet of rats treated with the colon carcinogen 1,2-dimethylhydrazine hydrochloride (DMH) with a Lactobacillus casei strain using an in vivo approach. The antigenotoxic response was evaluated in colon and liver cells using the alkaline comet assay. Since the balance between the bioactivation and detoxification metabolic pathways is crucial for the formation of toxic and genotoxic metabolites, alterations in the level of some xenobiotic metabolizing enzymes (XME) were studied in liver preparations. In the challenge group (L. casei + DMH), lactobacilli-supplemented diet, there was a decrease in the extent of DMH-induced DNA damage, especially in colon cells. Compared with control rats, there was less basal DNA damage in colon cells of rats fed on a lactobacilli-supplemented diet. These findings are the first to give clear evidence of DNA-protective effects of lactobacilli against basal DNA damage. Moreover, the chemopreventive effects were accompanied by changes in the activities of several XME. The observed decrease in the concentration of nonenzymatic antioxidants (i.e. GSH) and the reduced activity of enzymatic antioxidants (i.e., GST, GPx, and SOD) in liver could reflect an overall reduction in the level of oxidative stress in rats on a diet supplemented with the L. casei suspension compared with control rats (basal state). Thus, the concentrations of GSH and the activities of GST, GPx, and SOD could be downregulated by supplementing the diet with L. casei as a response to an improved antioxidant status.

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Section: Discussionsupporting

confidence: 62%

Section: Model Mutagenmentioning

confidence: 99%

Modulatory activity of a Lactobacillus casei strain on 1,2‐dimethylhydrazine‐induced genotoxicity in rats

Villarini

Caldini

Moretti

et al. 2008

Environ and Mol Mutagen

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“…This procarcinogen could thus provide an adequate model for studying colorectal cancer. However, mutiple treatments with DMH (20-40 mg/kg body mass) and a long-term experimental period are needed to induce large bowel neoplasms [15][16][17] . We present here a newly developed colitis-associated CRC mouse model in which dysplasia and cancer developed within 10 wk when mice were given a single, low dose of DMH followed by three repeated administrations of 30 g/L DSS in drinking water.…”

Section: Introductionmentioning

confidence: 99%

A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium

Wang

Wang²,

Lv³

et al. 2004

WJG

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AIM:To develop an efficient animal colitis-associated carcinogenesis model and to detect the expression of β-catenin and p53 in this new model. METHODS:Dysplasia and cancer were investigated in mice pretreated with a single intraperitoneal injection of 20 mg/kg body mass of 1,2-dimethylhydrazine prior to three repetitive oral administrations of 30 g/L dextran sulfate sodium to give conditions similar to the clinically observed active and remission phases. Immunohistochemical staining of β-catenin and p53 was performed on paraffin-imbedded specimens of animals with cancer and/or dysplasia, those without dysplasia and the normal control animals. RESULTS:At wk 11, four early-invasive adenocarcinomas and 36 dysplasia were found in 10 (90.9%) of the 11 mice that underwent 1,2-dimethylhydrazine-pretreatment with 3 cycles of 30 g/L dextran sulfate sodium-exposure. Dysplasia and/or cancer occurred as flat lesions or as dysplasia-associated lesion or mass (DALM) as observed in humans. Colorectal carcinogenesis occurred primarily on the distal portion of the large intestine. No dysplasia and/or cancer lesion was observed in the control groups with 1,2-dimethylhydrazine pretreatment or 3 cycles of 30 g/L dextran sulfate sodium exposure alone. Immunohistochemical investigation revealed that β-catenin was translocated from cell membrane to cytoplasm and/or nucleus in 100% of cases with dysplasia and neoplasm, while normal membrane staining was observed in cases without dysplasia and the normal control animals. Nuclear expression of p53 was not detected in specimens. CONCLUSION:A single dose of procarcinogen followed by induction of chronic ulcerative colitis results in a high incidence of colorectal dysplasia and cancer. Abnormal expression of β-catenin occurs frequently in dysplasia and cancer. This novel mouse model may provide an excellent vehicle for studying colitis-related colon carcinogenesis.Wang JG, Wang DF, Lv BJ, Si JM. A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium. World J Gastroenterol

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“…Several studies of humans and experimental animals suggested that the influence of diet was mediated by altering the metabolic activity of intestinal bacterial flora [1,2] . Some of these enteric bacteria are beneficial to the host and have been shown to exert antimutagenic and anticarcinogenic properties [3][4][5] .…”

Section: Introductionmentioning

confidence: 99%

“…The experimental carcinogen DMH has been used in the study of the effect of diet in experimental animals [1,11] . As the DMH model is known to closely parallel the human disease in term of disease presentation, gross and microscopic pathology [12] , it is anticipated that DMH-induced colon tumor in rats would respond to chemotherapeutic drugs used in man [13] .…”

Section: Introductionmentioning

confidence: 99%

Lack of inhibitory effects of Lactic acid bacteria on 1,2-dimethylhydrazine-induced colon tumors in rats

Li²

2003

WJG

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AIM:A myriad of healthful effects has been attributed to the probiotic lactic acid bacteria, perhaps the most controversial issue remains that of anticancer activity. This study was aimed at investigating the putative anti-cancer effects of lactic acid bacteria strains on the progression of colon tumor in 1,2-dimethylhydrazine (DMH)-treated animals. METHODS:The strain of lactic acid bacteria used in this study was lactic acid bacteria NZ9000 that conformed to the characteristics of plasmid free. Sixty male Wistar rats were given subcutaneous injections of DMH at a dose of 40 mg/kg body wt or saline once a week for 10 weeks. The rats were divided into 6 experimental groups. After the last DMH injection, animals in groups 1 and 4 were gavaged with 1 ml of lactic acid bacteria at a dose of 5×10 9 per day or vehicle until sacrifice at the end of week 22 or week 52. Animals in groups 1-3 were killed at the end of week 22 for histopathological examination. The whole period of experimental observation was 52 weeks. RESULTS:By the end of 22nd week, final average body weights of the rats treated with DMH alone and all animals receiving lactic acid bacteria were significantly decreased compared with the vehicle control (P<0.05). No differences in tumor incidence, multiplicity, dimensions and stage in the colonic mucosa were observed among the groups. At week 52, the survival rate of the rats administered lactic acid bacteria was lower than that of the rats treated with DMH that were fed on control fluids of non-lactococcus lactis. The mean survival time of lactic acid bacteria-treated animals was 39 weeks. CONCLUSION:These results indicate that lactic acid bacteria lacks inhibitory effects on the progression of colon tumor in DMH-treated animals, and does not support the hypothesis that alteration of colonic flora may exert an influence on the progression of colon tumor.Li W, Li CB. Lack of inhibitory effects of Lactic acid bacteria on 1,2-dimethylhydrazine-induced colon tumors in rats. World J Gastroenterol 2003; 9(11): 2469-2473

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Inhibitory effects of freeze-dried milk fermented by selected Lactobacillus bulgaricus strains on carcinogenesis induced by 1,2-dimethylhydrazine in rats and by diethylnitrosamine in hamsters

Cited by 29 publications

References 25 publications

Modulatory activity of a Lactobacillus casei strain on 1,2‐dimethylhydrazine‐induced genotoxicity in rats

Modulatory activity of a Lactobacillus casei strain on 1,2‐dimethylhydrazine‐induced genotoxicity in rats

A novel mouse model for colitis-associated colon carcinogenesis induced by 1,2-dimethylhydrazine and dextran sulfate sodium

Lack of inhibitory effects of Lactic acid bacteria on 1,2-dimethylhydrazine-induced colon tumors in rats

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