Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/6/1999
Publication Date: N/A
Interpretive Summary: Beta-carotene is widely distributed in the fruits and vegetables of a typical American diet. Vitamin A, an essential nutrient, is formed from beta carotene. How beta-carotene is changed to vitamin A and what other nutrients might affect this process are not well understood. Therefore, we carried out studies to determine if other nutrients such as minerals affect the conversion of beta-carotene to vitamin A. Rats were fed special diets varying widely in iron and copper, resulting in changes in the levels of these minerals in the intestinal tissue, the site where the beta-carotene conversion takes place. The data suggest that the enzyme responsible for the conversion of beta-carotene to vitamin A can be changed by dietary iron and copper. Thus, it may be possible to increase the conversion of beta-carotene to vitamin A by dietary means. This could benefit people who consume diets low in pre-formed vitamin A including young Hispanic American children, vegetarians, peoples in developing countries and others at risk for vitamin A deficiency. This information will be useful to nutritionists, dietitians, and health care professionals.
Technical Abstract: Previous in vitro studies have suggested that beta-carotene 15, 15'-dioxygenase is an iron-dependent enzyme. However, in vivo, it is very difficult to raise iron concentration in tissues by simply increasing dietary iron. Due to the iron/copper interaction that has been shown to exist in rats, we hypothesized that intestinal iron concentration could be modified by varying levels of dietary copper. Weanling male Sprague-Dawle rats (40-45g) were divided into four dietary groups: two copper-adequate groups (60 ug Cu/g diet) and two copper-deficient groups (0.6 ug Cu/g) combined with either normal iron (44 ug Fe/g) or high iron (87 ug Fe/g). Iron and copper concentrations were determined by atomic absorption spectrophotometry and dioxygenase activity by HPLC. Results showed that intestinal copper was significantly reduced (1.7-fold) by the consumption of the copper-deficient diets. Intestinal iron was not changed by doubling gdietary iron in either copper-adequate or copper-deficient rats. However, as hypothesized, the two copper-deficient groups exhibited higher (2.4-fold, P<0.001) intestinal iron that the copper-adequate controls. Copper-deficiency resulted in an increase (>1.4-fold, P<0.01) of the intestinal dioxygenase activity. In contrast, the enzyme activity was not affected by dietary iron. Finally, the enzyme activity was positively correlated with iron concentration and negatively correlated with copper concentration in small intestine. These results suggest that in vivo, intestinal beta-carotene 15,15'-dioxygenase may be an iron-dependent enzyme sensitive to copper status.