Rat colonic reactive oxygen species production and DNA damage are mediated by diet and age

Abstract

Colon cancer is the second leading cause of death from cancer in the United States. Studies suggest that oxidative damage to DNA caused by reactive oxygen species (ROS) is a critical initiating event in carcinogenesis. Rates of colon cancer increase with age, and it is possible that ROS and/or DNA damage accumulate in aged animals and lead to carcinogenic mutations. Dietary factors, particularly fat and fiber, are important risk modifiers of colon cancer. Differences in the production of ROS and the susceptibility of DNA to oxidative damage between young and old animals and those consuming certain types of fat and fiber could be key to age- and diet-related variation in colon cancer incidence. By examining levels of ROS and DNA damage in 28-day-old and 10-month-old rats consuming different types and combinations of dietary fat and fiber, we have determined that ROS and DNA damage are both affected by age and dietary fat and fiber. The roles of age and diet in colonic ROS and DNA damage have not been examined in connection with each other, and they may play important related roles in the development or prevention of colon cancer.