Premium
Diethanolamine alters neurogenesis and induces apoptosis in fetal mouse hippocampus
Author(s) -
Craciunescu Corneliu N.,
Wu Renan,
Zeisel Steven H.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.06-5978com
Subject(s) - neurogenesis , hippocampus , offspring , apoptosis , fetus , endocrinology , medicine , neural stem cell , andrology , biology , chemistry , pregnancy , neuroscience , microbiology and biotechnology , biochemistry , stem cell , genetics
Diethanolamine (DEA) is present in many consumer products such as shampoo. Dermal administration of DEA diminishes hepatic stores of the essential nutrient choline, and we previously reported that dietary choline deficiency during pregnancy reduces neurogenesis and increases apoptosis in the hippocampus of fetal rats and mice. Therefore, DEA could also alter brain development. Timed‐pregnant C57BL/6 mice were dosed dermally from gestation day 7 through 17 with DEA at 0, 20, 80, 160, 320, and 640 mg/kg body/day. At doses of DEA > 80 mg/kg body/day, we observed decreased litter size. In fetuses (embryonic day 17) collected from dams treated dermally with 80 mg/kg body/day DEA, we observed decreased neural progenitor cell mitosis at the ventricular surface of the ventricular zone of the hippocampus [to 56 ±14% ( se ) histone 3 (H3) phosphorylation as compared to controls; P < 0.01]. We also observed increased apoptosis in fetal hippocampus (to 170 ± 10% of control measured using TUNEL and to 178 ± 7% of control measured using activated caspase 3; P < 0.01). Thus, maternal exposure to DEA reduces the number of neural progenitor cells in hippocampus by two mechanisms, and this could permanently alter memory function in offspring of mothers exposed to this common ingredient of shampoos and soaps.—Craciunescu, C. N., Wu, R., Zeisel, S. H. Diethanolamine alters neurogenesis and induces apoptosis in fetal mouse hippocampus. FASEB J. 20, 1635–1640 (2006)