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• Sources of 8-OHdG in VLBW infants
  Josephine A Drury
  Published on: 22 March 2016

• Published on: 22 March 2016

  Sources of 8-OHdG in VLBW infants

  • Josephine A Drury, Research Assistant
  • Other Contributors:
    • Richard W. I. Cooke

  Dear Editor

  We read the paper by Shoji et al.[1] with interest but would like to offer an alternative explanation for their findings. They observed lower 8-OHdG at 14 and 28 days in preterm infants fed with breast-milk as compared with formula. This replicates their previous findings with term infants and tested at 28 days.[2] The levels reported here are lower than those reported in their term infants, r...

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  Dear Editor

  We read the paper by Shoji et al.[1] with interest but would like to offer an alternative explanation for their findings. They observed lower 8-OHdG at 14 and 28 days in preterm infants fed with breast-milk as compared with formula. This replicates their previous findings with term infants and tested at 28 days.[2] The levels reported here are lower than those reported in their term infants, raising questions about its usefulness as a marker of oxidative damage.

  Our data in neonates (24 weeks - term; 1 ng/mg creatinine = 2.5 micromol/mol creatinine) on a NICU during the first month of life showed lower levels during the first two weeks, but higher levels later as growth accelerated and increased enteral nutrition was supplied.[3] We suggested that urinary 8-OHdG was reflecting growth velocity rather than oxidative stress in these infants. Rapid growth produces a larger pool of free nucleotides more prone to oxidative damage than nucleotides incorporated into DNA. Breast-fed infants grow more slowly initially than formula-fed infants and we feel that this is the likely explanation for the differences seen by Shoji et al. No growth data is given in this paper, but previously published work showed an average weight increase in the first month of 33% in breast-fed infants compared with 46% in formula-fed infants.[2]

  8-OHdG levels in formula were significantly higher than in breast- milk [2] and given their physiological immaturity it is likely that exogenous intake may affect urinary excretion in these subjects to a greater extent than that reported in recovery experiments in rats.[4]

  Although we are quoted as saying that 8-OHdG "is considered to be a very sensitive biomarker of oxidative DNA damage in LBW infants" we actually concluded our paper with "8-OHdG levels are unlikely to be a useful marker of oxygen derived free radical activity in neonates".

  References

  1. Shoji H, Shimizu T, Shinohara K, Oguchi S, Shiga S, Yamashiro Y. Suppressive effects of breast milk on oxidative DNA damage in very low birthweight infants. Arch Dis Child Fetal Neonatal Ed 2004;89(2):F136-8.

  2. Shoji H, Oguchi S, Shimizu T, Yamashiro Y. Effect of human breast milk on urinary 8-hydroxy-2'-deoxyguanosine excretion in infants. Pediatr Res 2003;53(5):850-2.

  3. Drury JA, Jeffers G, Cooke RW. Urinary 8-hydroxydeoxyguanosine in infants and children. Free Radic Res 1998;28(4):423-8.

  4. Shigenaga MK, Gimeno CJ, Ames BN. Urinary 8-hydroxy-2'- deoxyguanosine as a biological marker of in vivo oxidative DNA damage. Proc Natl Acad Sci U S A 1989;86(24):9697-701.

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  Conflict of Interest:
  None declared.

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