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Jae Rin Suh, A Katherine Herbig, Patrick J Stover

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▪ Abstract  Folate catabolism has been assumed to result from the nonenzymatic oxidative degradation of labile folate cofactors. Increased rates of folate catabolism and simultaneous folate deficiency occur in several physiological states, including pregnancy, cancer, and when anticonvulsant drugs are used. These studies have introduced the possibility that folate catabolism may be a regulated cellular process that influences intracellular folate concentrations. Recent studies have demonstrated that the iron storage protein ferritin can catabolize folate in vitro and in vivo, and increased heavy-chain ferritin synthesis decreases intracellular folate concentrations independent of exogenous folate levels in cell culture models. Ferritin levels are elevated in most physiological states associated with increased folate catabolism. Therefore, folate catabolism is emerging as an important component in the regulation of intracellular folate concentrations and whole-body folate status.