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Effects of 13 developmentally toxic chemicals on the migration of rat cephalic neural crest cells in vitro
Author(s) -
Usami Makoto,
Mitsunaga Katsuyoshi,
Miyajima Atsuko,
Takamatu Mina,
Kazama Shugo,
Irie Tomohiko,
Doi Osamu,
Takizawa Tatsuya
Publication year - 2016
Publication title -
congenital anomalies
Language(s) - English
Resource type - Journals
eISSN - 1741-4520
pISSN - 0914-3505
DOI - 10.1111/cga.12121
Subject(s) - neural crest , chemistry , toxicity , in vitro , tributyltin , salicylic acid , developmental toxicity , cell migration , teratology , retinoic acid , pharmacology , biochemistry , biology , fetus , environmental chemistry , pregnancy , genetics , organic chemistry , gene
The inhibition of neural crest cell ( NCC ) migration has been considered as a possible pathogenic mechanism underlying chemical developmental toxicity. In this study, we examined the effects of 13 developmentally toxic chemicals on the migration of rat cephalic NCCs ( cNCCs ) by using a simple in vitro assay. cNCCs were cultured for 48 h as emigrants from rhombencephalic neural tubes explanted from rat embryos at day 10.5 of gestation. The chemicals were added to the culture medium at 24 h of culture. Migration of cNCCs was measured as the change in the radius (radius ratio) calculated from the circular spread of cNCCs between 24 and 48 h of culture. Of the chemicals examined, 13‐ cis ‐retinoic acid, ethanol, ibuprofen, lead acetate, salicylic acid, and selenate inhibited the migration of cNCCs at their embryotoxic concentrations; no effects were observed for acetaminophen, caffeine, indium, phenytoin, selenite, tributyltin, and valproic acid. In a cNCC proliferation assay, ethanol, ibuprofen, salicylic acid, selenate, and tributyltin inhibited cell proliferation, suggesting the contribution of the reduced cell number to the inhibited migration of cNCCs . It was determined that several developmentally toxic chemicals inhibited the migration of cNCCs , the effects of which were manifested as various craniofacial abnormalities.