Trichostatin A mitigates radiation-induced teratogenesis in C57Bl/6 mice

Abstract

Radiation exposure in utero is known to lead to serious concerns to both the mother and children, including developmental anomalies in the children. In the recent past trichostatn A, an HDAC inhibitor and epigenetic modifier, has been shown to mitigate radiation induced anomalies in the male reproductive system of C57BL/6 mice. Therefore, the current study was undertaken to evaluate the mitigating effects of trichostatin A against radiation induced developmental anomalies in mice. Fetuses of in utero whole body gamma irradiated mice during active organogenesis period were examined for developmental anomalies on 8.5 and 18.5 day of gestation. In utero radiation exposure caused developmental anomalies like microcephaly, microphthalamia, gastroschisis and kinky tail besides prenatal mortality. Trichostatin A administration post irradiation was observed to reduce 50% of prenatal mortality at E18.5 by reducing congenital and developmental anomalies. Observation of such results could be corroborated with the HDAC inhibitory potential of trichostatin A knowing that developmental anomalies may have epigenetic origin. Trichostatin A therefore can be considered as a potential radiomitigator.