The influence of dietary copper, Cu2+ additions and Cu/Zn SOD additions on liver homogenate PGE2 and PGF2α production was examined in rats. Dietary copper deficiency significantly decreased both PGE2 and PGF2α synthesis in liver homogenates. Cu2+ additions to 10 μM or 100 μM (final) had no effect on PGE2 or PGF2α synthesis in either deficient or control liver homogenates. Addition of purified Cu/Zn SOD to a concentration approximately equal to that of control liver, significantly increased PGE2 and PGF2α synthesis in both control and copper deficient liver homogenates. Addition of purified Cu/Zn SOD to a concentration approximately three times that of control liver significantly depressed PGE2 and PGF2α synthesis in copper-deficient liver homogenates. In all cases addition of arachidonic acid (100 μM, final) had no influence on the above listed responses. Both PGE2 and PGF2α production by liver homogenates showed a significant correlation with SOD. Both dietary copper and added Cu/Zn SOD, but not added Cu2+, influence PGE2 and PGF2α production in liver homogenates.
- superoxide dismutase
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Nutrition and Dietetics