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Developmental 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure of either parent
enhances the risk of necrotizing enterocolitis in neonatal mice.
Mokshagundam S, Ding T, Rumph JT, Dallas M, Stephens VR, Osteen KG, Bruner-Tran
Submitted Externally on 9/28/2020
Birth defects research, REFERENCES
Volume : Pages
Necrotizing enterocolitis (NEC) is a rare, but potentially fatal intestinal
inflammatory condition most often arising in premature infants. Infants provided
formula are also at greater risk of developing this disease. Although the
majority of formula-fed, preterm infants do not develop NEC, up to 30% of
infants with the disease do not survive. Thus, identifying additional, currently
unrecognized factors, which may predispose a specific infant to NEC development
would be a significant clinical advancement. In this regard, we have previously
reported that offspring of female or male mice with a history of developmental
exposure to the environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin
(TCDD) exhibit altered sensitivity to inflammatory challenges and are frequently
born premature. Herein, we examined the possibility that, compared to unexposed
mice (F1NONE ), developmental TCDD exposure of either parent (maternal, F1MTCDD
, or paternal, F1PTCDD ) would enhance the risk of NEC in offspring (F2TCDD
mice) in association with supplemental formula feeding., Beginning on postnatal
day 7, all neonates were randomized to maternal milk only or maternal milk with
up to 20 supplemental formula feedings. All pups remained with the Dams and were
additionally allowed to nurse ad libitum., Formula-fed F2NONE pups rarely
developed NEC while this disease was common in formula-fed F2MTCDD and F2PTCDD
mice. Unexpectedly, 50% of F2MTCDD pups that were not provided supplemental
formula also developed NEC., Our studies provide evidence that a history of
parental TCDD exposure enhances the risk of NEC in offspring and suggest
exposure to environmental immunotoxicants such as TCDD may also contribute to
this inflammatory disease in humans.
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Financial support for this work was provided by the NIDDK Mouse Metabolic Phenotyping Centers (National MMPC, RRID:SCR_008997,
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