Reproductive and neurobehavioral effects of maternal exposure to ethiprole in F1-generation mice

2017 ◽  
Vol 110 (3) ◽  
pp. 259-275 ◽  
Author(s):  
Toyohito Tanaka ◽  
Toshinari Suzuki ◽  
Akiko Inomata
2015 ◽  
Vol 2 ◽  
pp. 341-350 ◽  
Author(s):  
Xiugong Gao ◽  
Jeffrey J. Yourick ◽  
Vanessa D. Topping ◽  
Thomas Black ◽  
Nicholas Olejnik ◽  
...  

2017 ◽  
Vol 03 (01) ◽  
Author(s):  
Sumita Halder ◽  
Rajarshi Kar ◽  
Nilesh Chandra ◽  
Swapan K Bhattacharya ◽  
Pramod K Mediratta ◽  
...  

2000 ◽  
Vol 38 (4) ◽  
pp. 325-334 ◽  
Author(s):  
R.L. Sprando ◽  
T.F.X. Collins ◽  
T.N. Black ◽  
N. Olejnik ◽  
J.I. Rorie ◽  
...  

2021 ◽  
Author(s):  
Yukiko Tando ◽  
Hitoshi Hiura ◽  
Asuka Takehara ◽  
Yumi Ito-Matsuoka ◽  
Takahiro Arima ◽  
...  

Exposure to environmental factors during fetal development may lead to epigenomic modifications in fetal germ cells, altering gene expression and promoting diseases in successive generations. In mouse, maternal exposure to Di (2-ethylhexyl) phthalate (DEHP) is known to induce defects in spermatogenesis in successive generations, but the mechanism(s) of impaired spermatogenesis are unclear. Here, we showed that maternal DEHP exposure results in DNA hypermethylation of promoters of spermatogenesis-related genes in fetal testicular germ cells in F1 mice, and hypermethylation of Hist1h2ba, Sycp1 and Taf7l, which are crucial for spermatogenesis, persisted from fetal testicular cells to adult spermatogonia, resulting in the downregulation of expression of these genes. Forced methylation of these gene promoters silenced expression of these loci in a reporter assay. Expression and methylation of those genes tended to be downregulated and increased, respectively in F2 spermatogonia following maternal DEHP exposure. These results suggested that DEHP induced hypermethylation of Hist1h2ba, Sycp1 and Taf7l in fetal germ cells results in downregulation of these genes in spermatogonia and subsequent defects in spermatogenesis, at least in the F1 generation.


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Yukiko Tando ◽  
Hitoshi Hiura ◽  
Asuka Takehara ◽  
Yumi Ito-Matsuoka ◽  
Takahiro Arima ◽  
...  

Exposure to environmental factors during fetal development may lead to epigenomic modifications in fetal germ cells, altering gene expression and promoting diseases in successive generations. In mouse, maternal exposure to di(2-ethylhexyl) phthalate (DEHP) is known to induce defects in spermatogenesis in successive generations, but the mechanism(s) of impaired spermatogenesis are unclear. Here, we showed that maternal DEHP exposure results in DNA hypermethylation of promoters of spermatogenesis-related genes in fetal testicular germ cells in F1 mice, and hypermethylation of Hist1h2ba, Sycp1, and Taf7l, which are crucial for spermatogenesis, persisted from fetal testicular cells to adult spermatogonia, resulting in the downregulation of expression of these genes. Forced methylation of these gene promoters silenced expression of these loci in a reporter assay. These results suggested that maternal DEHP exposure-induced hypermethylation of Hist1h2ba, Sycp1, and Taf7l results in downregulation of these genes in spermatogonia and subsequent defects in spermatogenesis, at least in the F1 generation.


1993 ◽  
Vol 9 (6) ◽  
pp. 1027-1035 ◽  
Author(s):  
Toyohito Tanaka

The color additive amaranth was given in the drinking water at levels of 0 (control), 0.025, 0.075, and 0.225% from 5 weeks of age in F0 generation until F1 generation mice were weaned, with selected reproductive, developmental and behavioral parameters being measured. Amaranth had little adverse effect upon litter size, litter weight and sex ratio. Average body weight in both sexes of the F1 mice was significantly increased in the 0.025% group in both sexes. Survival index at postnatal day (PND) 21 was reduced in the 0.025% amaranth group. For the neurobehavioral parameters, surface righting at PND 4 in fernale offspring and olfactory orientation in both sexes were significantly affected by treatment. Several parameters of movement activity of male offspring at 3 weeks of age were affected in amaranth 0.075% group, but those of female offspring were similar in all groups. The dose levels of amaranth in this study produced a little adverse effect on behavioral development in mice.


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