The BuAc plays an important role in cell growth regulation, it is considered to be an inhibitor of cell proliferation and to strongly induce in vitro differentiation for a wide variety of neoplastic cells (6), including mammary gland, large bowel, rectum, liver, cervix and ovary (5, 12, 16).
Furthermore BuAc induces apoptosis by modulation of pro-apoptotic and anti-apoptotic gene expression as well as liberation of citochrome C, a pro-apoptotic enzyme, from the mitochondria (16).
Cyclins, cyclin-dependent kinases (cdk) and cdk inhibitor proteins are some of the molecular pathways through which BuAc causes cell cycle arrest and differentiation to prevent the cell proliferation (16).
Experimental works have used sodium butyrate as a BuAc source; it was administered by luminal instillation and oral consumption at high concentration.
In the present experience, using pure BuAc diluted in drinking water, without sodium and esterification, was observed an important decrease of dysplastic lesions, considered pre-neoplastic lesions and histological markers of colon cancer, compared with the twofold found in sub-groups DMH-treated without BuAc supplementation.
These observations agree with investigations which support the fact that the BuAc is an inhibitor of cell proliferation (6), as well as tumor cell proliferation in colon cancer (5).