1887

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Volume 57, Issue 1

Oral administration of a catalase-producing can prevent a chemically induced colon cancer in mice Free

Abstract

Reactive oxygen species, such as hydrogen peroxide (HO), are involved in various aspects of tumour development. Decreasing their levels can therefore be a promising approach for colon cancer prevention. The objective of this study was to evaluate the effect of catalase-producing on the prevention of an experimental murine 1,2-dimethylhydrazine (DMH)-induced colon cancer. DMH-treated BALB/c mice received either a catalase-producing strain or the isogenic non-catalase-producing strain as a control, whereas other untreated mice did not receive bacterial supplementation. Catalase activity and HO levels in intestinal fluids and blood samples were measured, and changes in the histology of the large intestines during tumour progression were evaluated. The catalase-producing strain used in this study was able to slightly increase catalase activities in DMH-treated mice (1.19±0.08 U ml) and reduce HO levels (3.4±1.1 μM) compared to (i) animals that received the non-catalase-producing strain (1.00±0.09 U ml, 9.0±0.8 μM), and (ii) those that did not receive bacterial supplementation (1.06±0.07 U ml, 10.0±1.1 μM). Using the histopathological grading scale of chemically induced colorectal cancer, animals that received the catalase-producing had a significantly lesser extent of colonic damage and inflammation (2.0±0.4) compared to animals that received the non-catalase-producing (4.0±0.3) or those that did not receive bacterial supplementation (4.7±0.5). The catalase-producing strain used in this study was able to prevent tumour appearance in an experimental DMH-induced colon cancer model.

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Keyword(s): DMH, 1,2-dimethylhydrazine , LAB, lactic acid bacteria and ROS, reactive oxygen species
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2008-01-01
2024-04-19
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Oral administration of a catalase-producing Lactococcus lactis can prevent a chemically induced colon cancer in mice
J. Med. Microbiol. 57, 100 (2008); https://doi.org/10.1099/jmm.0.47403-0
/content/journal/jmm/10.1099/jmm.0.47403-0
/content/journal/jmm/10.1099/jmm.0.47403-0
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