Journal
JOURNAL OF APPLIED TOXICOLOGY
Volume 36, Issue 1, Pages 105-112Publisher
WILEY
DOI: 10.1002/jat.3149
Keywords
arsenic; gestational exposure; hepatic tumor; transgenerational; gene expression
Categories
Funding
- National Institute for Environmental Studies [1115AA082, 1315AT001]
- Ministry of Education, Culture, Sports, Science and Technology of Japan [23390166, 26293154]
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Gestational exposure can affect the F-2 generation through exposure of F-1 germline cells. Previous studies reported that arsenite exposure of only F-0 females during their pregnancy increases hepatic tumors in the F-1 males in C3H mice, whose males are predisposed spontaneously to develop hepatic tumors later in life. The present study addressed the effects of gestational arsenite exposure on tumorigenesis of the F-2 males in C3H mice. Expression analysis of several genes in the normal livers at 53 and 80weeks of age clearly showed significant changes in the F-2 males obtained by crossing gestational arsenite-exposed F-1 (arsenite-F-1) males and females compared to the control F-2 males. Some of the changes were shown to occur in a late-onset manner. Then the tumor incidence was assessed at 75-82 weeks of age in the F-2 males obtained by reciprocal crossing between the control and arsenite-F-1 males and females. The results demonstrated that the F-2 males born to arsenite-F-1 males developed tumors at a significantly higher rate than the F-2 males born to the control F-1 males, irrespective of exposure of F-1 females. Gene expressions of hepatocellular carcinoma markers -catenin (CTNNB1) and interleukin-1 receptor antagonist in the tumors were significantly upregulated in the F-2 males born to arsenite-F-1 males compared to those born to the control F-1 males. These results show that arsenite exposure of only F-0 pregnant mice causes late-onset changes and augments tumors in the livers of the F-2 males by affecting the F-1 male offspring. Copyright (c) 2015 John Wiley & Sons, Ltd. Gestational exposure can affect the F-2 generation through exposure of F-1 germ cells. We assessed tumor incidence in the F-2 males obtained by reciprocal crossing between the control and gestationally arsenite-exposed F-1 males and females in C3H mice. The results demonstrated that the F-2 males born to arsenite-F-1 males developed tumors at a significantly higher rate than the F-2 males born to the control F-1 males. We also characterized gene expression of several hepatocellular carcinoma markers in the F-2 tumors.
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