Base excision repair, folate deficiency and cancer

<p>Folate, an essential water soluble vitamin has been implicated in the etiology of many types of cancer especially colorectal cancer. Folate deficiency has been reported to incapacitate DNA repair pathways and thereby affect the genomic stability. Our lab has reported previously and here again through this research that folate deficiency affects the DNA damage inducibility of base excision repair pathway. Our study shows the differential effect folate deficiency has on the expression of the genes involved in this pathway. Further, our study shows the increase in preneoplastic lesions in the colon of mice exposed to folate deficiency in response to dimethylhydrazine, a colon and liver carcinogen. This study further supports our findings from previous studies from our lab that folate deficiency increases the susceptibility to cancer by deregulating DNA repair pathways, base excision repair in this scenario. Similarly, methionine restriction also, increases accumulation of preneoplastic lesions and incapacitates base excision repair in mice exposed to dimethylhydrazine. Since methionine restriction has shown to produce beneficial effects in laboratory rodents when the animals are exposed to long term restrictions, it would be interesting to put our animal models on methionine restriction and folate deficient diets for longer periods to test whether long term adaptations would bring about any beneficial effects</p>

Name thesis:degree_name

Ph.D.

Level thesis:degree_level

Open Access Dissertation

Discipline thesis:degree_discipline

Nutrition and Food Science

Year dc:date.available

2011

Author dc:creator

• Unnikrishnan, Archana

Contributors dc:contributor

• Ahmad R. Heydari

• AP endonuclease, DNA polymerase Beta, DNA repair, Folate
• Nutrition

Repository record dc:identifier

https://digitalcommons.wayne.edu/oa_dissertations/399

OAI identifier oai:identifier

oai:digitalcommons.wayne.edu:oa_dissertations-1398