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Related Experiment Videos

New perspectives on folate catabolism.

J R Suh1, A K Herbig, P J Stover

  • 1Division of Nutritional Sciences, Cornell University, Ithaca, New York 14853, USA. JRS22@cornell.edu

Annual Review of Nutrition
|May 26, 2001
PubMed
Summary

Folate catabolism, previously thought nonenzymatic, may be regulated by ferritin. Elevated ferritin levels decrease intracellular folate, impacting folate status during pregnancy, cancer, and anticonvulsant drug use.

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Area of Science:

  • Biochemistry
  • Cellular Biology
  • Nutritional Science

Background:

  • Folate catabolism was traditionally attributed to nonenzymatic oxidative degradation of folate cofactors.
  • Increased folate catabolism and deficiency are observed in conditions like pregnancy, cancer, and during anticonvulsant drug therapy.
  • These associations suggest folate catabolism might be a regulated cellular process influencing intracellular folate levels.

Purpose of the Study:

  • To investigate the role of ferritin in folate catabolism.
  • To determine if ferritin influences intracellular folate concentrations.

Main Methods:

  • In vitro and in vivo studies examining ferritin's interaction with folate.
  • Cell culture models with manipulated heavy-chain ferritin synthesis.
  • Measurement of intracellular folate concentrations under varying ferritin levels.

Main Results:

  • Demonstrated that ferritin can catabolize folate both in vitro and in vivo.
  • Showed that increased heavy-chain ferritin synthesis reduces intracellular folate concentrations independently of external folate availability.
  • Observed elevated ferritin levels in physiological states linked to increased folate catabolism.

Conclusions:

  • Folate catabolism is likely a regulated cellular process, not solely nonenzymatic degradation.
  • Ferritin plays a significant role in catalyzing folate catabolism.
  • Ferritin emerges as a key factor in regulating intracellular folate concentrations and overall folate status.

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