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PLoS One. 2017 Aug 24;12(8):e0183831. doi: 10.1371/journal.pone.0183831. eCollection 2017.

Combinatorial effects of zinc deficiency and arsenic exposure on zebrafish (Danio rerio) development.

Beaver LM1,2, Truong L3,4, Barton CL3,4, Chase TT1, Gonnerman GD3,4, Wong CP1,2, Tanguay RL2,3,4,5, Ho E1,2,4,5,6.

Author information

1
Biological and Population Health Sciences, Oregon State University, Corvallis, Oregon, United States of America.
2
Linus Pauling Institute, Oregon State University, Corvallis, Oregon, United States of America.
3
Department of Environmental and Molecular Toxicology, Sinnhuber Aquatic Research Laboratory, Oregon State University, Corvallis, Oregon, United States of America.
4
The Environmental Health Sciences Center, Oregon State University, Corvallis, Oregon, United States of America.
5
Center for Genome Research and Biocomputing, Oregon State University, Corvallis, Oregon, United States of America.
6
Moore Family Center for Whole Grain Foods, Nutrition and Preventive Health, Oregon State University, Corvallis, Oregon, United States of America.

Abstract

Zinc deficiency and chronic low level exposures to inorganic arsenic in drinking water are both significant public health concerns that affect millions of people including pregnant women. These two conditions can co-exist in the human population but little is known about their interaction, and in particular, whether zinc deficiency sensitizes individuals to arsenic exposure and toxicity, especially during critical windows of development. To address this, we utilized the Danio rerio (zebrafish) model to test the hypothesis that parental zinc deficiency sensitizes the developing embryo to low-concentration arsenic toxicity, leading to altered developmental outcomes. Adult zebrafish were fed defined zinc deficient and zinc adequate diets and were spawned resulting in zinc adequate and zinc deficient embryos. The embryos were treated with environmentally relevant concentrations of 0, 50, and 500 ppb arsenic. Arsenic exposure significantly reduced the amount of zinc in the developing embryo by ~7%. The combination of zinc deficiency and low-level arsenic exposures did not sensitize the developing embryo to increased developmental malformations or mortality. The combination did cause a 40% decline in physical activity of the embryos, and this decline was significantly greater than what was observed with zinc deficiency or arsenic exposure alone. Significant changes in RNA expression of genes that regulate zinc homeostasis, response to oxidative stress and insulin production (including zip1, znt7, nrf2, ogg1, pax4, and insa) were found in zinc deficient, or zinc deficiency and arsenic exposed embryos. Overall, the data suggests that the combination of zinc deficiency and arsenic exposure has harmful effects on the developing embryo and may increase the risk for developing chronic diseases like diabetes.

PMID:
28837703
PMCID:
PMC5570330
DOI:
10.1371/journal.pone.0183831
[Indexed for MEDLINE]
Free PMC Article

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