Abstract
Colon cancer is the third most common malignant neoplasm in the world and it remains an important cause of death, especially in western countries. The toxic environmental pollutant, 1, 2-dimethylhydrazine (DMH), is also a colon-specific carcinogen. Tannic acid (TA) is reported to be effective against various types of chemically induced toxicity and also carcinogenesis. In the present study, we evaluated the chemopreventive efficacy of TA against DMH induced colon toxicity in a rat model. Efficacy of TA against the colon toxicity was evaluated in terms of biochemical estimation of antioxidant enzyme activities, lipid peroxidation, histopathological changes and expression of early molecular markers of inflammation and tumor promotion. DMH treatment induced oxidative stress enzymes (p<0.001) and an early inflammatory and tumor promotion response in the colons of Wistar rats. TA treatment prevented deteriorative effects induced by DMH through a protective mechanism that involved reduction of oxidative stress as well as COX-2, i-NOS, PCNA protein expression levels and TNF-α(p<0.001) release. It could be concluded from our results that TA markedly protects against chemically induced colon toxicity and acts plausibly by virtue of its antioxidant, anti-inflammatory and antiproliferative activities.
Highlights
Colorectal cancer is one of major cause of death in the world, the causes of this disease are not completely understood
DMH is metabolized in liver to form azoxymethane and methylazoxymethanol which is further transported to colon via bile or blood to generate its ultimate carcinogenic metabolite, diazonium ion which elicits an oxidative stress by methylating biomolecules of colonic epithelial cells and leads to promutagenic events as a result of inflammation and tumor promotion
Chemoprevention is the use of plant based nontoxic substance, including many dietary agents, to avert or reverse the process of cancer development
Summary
Colorectal cancer is one of major cause of death in the world, the causes of this disease are not completely understood. It is the third most common form of malignancy in both men and women (Jemal et al, 2010). DMH is metabolized in liver to form azoxymethane and methylazoxymethanol which is further transported to colon via bile or blood to generate its ultimate carcinogenic metabolite, diazonium ion which elicits an oxidative stress by methylating biomolecules of colonic epithelial cells and leads to promutagenic events as a result of inflammation and tumor promotion
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