Molecular evidence of offspring liver dysfunction after maternal exposure to zinc oxide nanoparticles

Journal Article · Tue Aug 15 04:00:00 EDT 2017 · Toxicology and Applied Pharmacology

DOI:https://doi.org/10.1016/J.TAAP.2017.06.021· OSTI ID:22722907

Hao, Yanan ^[1]; Liu, Jing ^[2]; Feng, Yanni; Yu, Shuai; Zhang, Weidong; Li, Lan; Min, Lingjiang ^[1]; Zhang, Hongfu ^[3]; Shen, Wei ^[1]; Zhao, Yong ^[1]

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1. College of Animal Science and Technology, Qingdao Agricultural University, Qingdao 266109 (China)
2. Core Laboratories of Qingdao Agricultural University, Qingdao 266109 (China)
3. State Key Laboratory of Animal Nutrition, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing 100193 (China)

Recently, reproductive, embryonic and developmental toxicity have been considered as one important sector of nanoparticle (NP) toxicology, with some studies already suggesting varying levels of toxicity and possible transgenerational toxic effects. Even though many studies have investigated the toxic effects of zinc oxide nanoparticles (ZnO NPs), little is known of their impact on overall reproductive outcome and transgenerational effects. Previously we found ZnO NPs caused liver dysfunction in lipid synthesis. This investigation, for the first time, explored the liver dysfunction at the molecular level of gene and protein expression in offspring after maternal exposure to ZnO NPs. Three pathways were investigated: lipid synthesis, growth related factors and cell toxic biomarkers/apoptosis at 5 different time points from embryonic day-18 to postnatal day-20. It was found that the expression of 15, 16, and 16 genes in lipid synthesis, growth related factors and cell toxic biomarkers/apoptosis signalling pathway respectively in F1 animal liver were altered by ZnO NPs compared to ZnSO{sub 4}. The proteins in these signalling pathways (five in each pathways analyzed) in F1 animal liver were also changed by ZnO NPs compared to ZnSO{sub 4}. The results suggest that ZnO NPs caused maternal liver defects can also be detected in offspring that might result in problems on offspring liver development, mainly on lipid synthesis, growth, and lesions or apoptosis. Along with others, this study suggests that ZnO NPs may pose reproductive, embryonic and developmental toxicity; therefore, precautions should be taken with regard to human exposure during daily life. - Highlights: • Oral ZnO NPs exposure caused abnormal gene and protein expression in offspring liver. • Oral ZnO NPs exposure could induce inheritance impacts on liver development. • Oral ZnO NPs exposure could be considered as developmental hazardous material.

• OSTI ID: 22722907
• Journal Information: Toxicology and Applied Pharmacology, Journal Name: Toxicology and Applied Pharmacology Vol. 329; ISSN TXAPA9; ISSN 0041-008X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
APOPTOSIS
BIOLOGICAL MARKERS
GENES
LIPIDS
LIVER
NANOPARTICLES
PLANT GROWTH
PROGENY
SYNTHESIS
TOXICITY
ZINC OXIDES
ZINC SULFATES