Impact of Folic Acid Supplementation on Single- and Double-Stranded RNA Degradation in Human Colostrum and Mature Milk

Sufficient intake of folic acid is necessary for normal embryogenesis, fetal, and neonatal development. Folic acid facilitates nucleic acid internalization, and protects cellular DNA from nuclease degradation. Human milk contains enzymes, antimicrobial proteins, and antibodies, along with macrophage...

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Veröffentlicht in:Journal of medicinal food 2014, 17(7), , pp.804-809
Hauptverfasser: Kocic, Gordana, Bjelakovic, Ljiljana, Bjelakovic, Bojko, Jevtoci-Stoimenov, Tatjana, Sokolovic, Dusan, Cvetkovic, Tatjana, Kocic, Hristina, Stojanovic, Svetlana, Langerholc, Tomaz, Jonovic, Marina
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Sprache:eng
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Zusammenfassung:Sufficient intake of folic acid is necessary for normal embryogenesis, fetal, and neonatal development. Folic acid facilitates nucleic acid internalization, and protects cellular DNA from nuclease degradation. Human milk contains enzymes, antimicrobial proteins, and antibodies, along with macrophages, that protect against infections and allergies. However, little to no information is available on the effects of folic acid supplementation on degradation of nucleic acids in human milk. In the present study, we aimed to determine the RNase activity (free and inhibitor-bound) in colostrum and mature milk, following folic acid supplementation. The study design included a total of 59 women, 27 of whom received 400 μg of folic acid daily periconceptionally and after. Folic acid supplementation increased the free RNase and polyadenylase activity following lactation. However, the increased RNase activity was not due to de novo enzyme synthesis, as the inhibitor-bound (latent) RNase activity was significantly lower and disappeared after one month. Folic acid reduced RNase activity by using double-stranded RNA as substrate. Data suggests that folic acid supplementation may improve viral RNAs degradation and mRNA degradation, but not dsRNA degradation, preserving in this way the antiviral defense.
ISSN:1557-7600
1096-620X
1557-7600
DOI:10.1089/jmf.2013.0093