The consequences of early-life exposure to chemicals in the environment are emerging concerns. Chronic exposure to naturally occurring inorganic arsenic has been known to cause various adverse health effects, including cancers, in humans. On the other hand, animal studies by Dr. M. Waalkes’ group reported that arsenite exposure of pregnant F0 females, only from gestational day 8 to 18, increased hepatic tumours in the F1 (arsenite-F1) males of C3H mice, whose males tend to develop spontaneous hepatic tumours later in life. Since this mice model illuminated novel unidentified consequences of arsenic exposure, the authors wished to further investigate the background mechanisms. In the same experimental model, a variety of factors that were affected by gestational arsenic exposure were identified, including epigenetic and genetic changes, as possible constituents of multiple steps of late-onset hepatic tumour augmentation in arsenite-F1 males. Furthermore, the study discovered that the F2 males born to arsenite-F1 males developed hepatic tumours at a significantly higher rate than the control F2 males. The results imply that the tumour augmenting effect is inherited by arsenite-F2 males through the sperm of arsenite-F1. This study summarised the investigation on the consequences of gestational arsenite exposure in F1 and F2 mice to discuss novel aspects of biological effects of gestational arsenic exposure.
Authors: Nohara K, Suzuki T, Okamura K, Matsushita J, Takumi S. ;Full Source: Genes Environ. 2017 Mar 1; 39:3. doi: 10.1186/s41021-016-0069-1. eCollection 2017. ;