Exposure to zinc oxide nanoparticles affects reproductive development and biodistribution in offspring rats

Jo, Eunhye; Seo, Gyounbaek; Kwon, Jung-Taek; Lee, Mimi; Lee, Byoung Cheun; Eom, Ig-Chun; Kim, Philje; Choi, Kyunghee

doi:10.2131/jts.38.525

Cited by 87 publications

(42 citation statements)

References 16 publications

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“…It results from an imbalance between ROS generation and the antioxidant system (enzymatic and not-enzymatic antioxidant). Previous studies have shown that exposure to Nano-ZnO caused oxidative stress in vitro and in vivo (Chen et al, 2014; Huang et al, 2010; Jo et al, 2013; Sharma et al, 2012a; Sharma et al, 2012b). In our study, although exposure to Nano-ZnO only caused a slight, but not significant increase in MDA contents, Nano-ZnO resulted in a significant decrease in GSH contents in liver tissues.…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress and oxidative stress are involved in ZnO nanoparticle-induced hepatotoxicity

et al. 2015

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Zinc oxide nanoparticles (Nano-ZnO) are widely used in sunscreens, clothes, medicine and electronic devices. However, the potential risks of human exposure and the potential for adverse health impacts are not well understood. Previous studies have demonstrated that exposure to Nano-ZnO caused liver damage and hepatocyte apoptosis through oxidative stress, but the molecular mechanisms that are involved in Nano-ZnO-induced hepatotoxicity are still unclear. Endoplasmic reticulum (ER) is sensitive to oxidative stress, and also plays a crucial role in oxidative stress-induced damage. Previous studies showed that ER stress was involved in many chemical-induced liver injuries. We hypothesized that exposure to Nano-ZnO caused oxidative stress and ER stress that were involved in Nano-ZnO-induced liver injury. To test our hypothesis, mice were gavaged with 200 mg/kg or 400 mg/kg of Nano-ZnO once a day for a period of 90 days, and blood and liver tissues were obtained for study. Our results showed that exposure to Nano-ZnO caused liver injury that was reflected by focal hepatocellular necrosis, congestive dilation of central veins, and significantly increased alanine transaminase (ALT) and aspartate transaminase (AST) levels. Exposure to Nano-ZnO also caused depletion of glutathione (GSH) the liver tissues. In addition, our electron microscope results showed that ER swelling and ribosomal degranulation were observed in the liver tissues from mice treated with Nano-ZnO. The mRNA expression levels of ER stress-associated genes (grp78, grp94, pdi-3, xbp-1) were also up-regulated in Nano-ZnO-treated mice. Nano-ZnO caused increased phosphorylation of RNA-dependent protein kinase-like ER kinase (PERK) and eukaryotic initiation factor 2α (eIF2α). Finally, we found that exposure to Nano-ZnO caused increased ER stress-associated apoptotic protein levels, such as caspase-3, caspase-9, caspase-12, phosphorylation of JNK, and CHOP/GADD153, and up-regulation of pro-apoptotic genes (chop and bax). These results suggest that oxidative stress and ER stress-induced apoptosis are involved in Nano-ZnO-induced hepatotoxicity in mice.

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Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress and oxidative stress are involved in ZnO nanoparticle-induced hepatotoxicity

et al. 2015

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“…Also, other studies of gold nanoparticles demonstrated no toxicological responses in the maternal or fetal organs (Rattanapinyopituk, et al 2014, Yang, et al 2012). The reproductive development and distribution of silver nanoparticles and zinc oxide nanoparticles were studied in rats, and both materials showed transfer from mother to offspring (Jo, et al 2013, Melnik, et al 2013). Zinc oxide nanoparticles exposure started at 2 weeks before mating and was continued until PND 4, resulting in reduced number of born/live pups, decreased body weights of pups and increase fatal resorption; nanoparticles were detected in the liver and kidneys of pups (Jo, et al 2013).…”

Section: Discussionmentioning

confidence: 99%

“…The reproductive development and distribution of silver nanoparticles and zinc oxide nanoparticles were studied in rats, and both materials showed transfer from mother to offspring (Jo, et al 2013, Melnik, et al 2013). Zinc oxide nanoparticles exposure started at 2 weeks before mating and was continued until PND 4, resulting in reduced number of born/live pups, decreased body weights of pups and increase fatal resorption; nanoparticles were detected in the liver and kidneys of pups (Jo, et al 2013). Carbon nanotubes (CNT), like C 60 , are composed entirely of carbon, and can either be single walled or multi walled (SWCNT or MWCNT, respectively).…”

Section: Discussionmentioning

confidence: 99%

Distribution and biomarker of carbon‐14 labeled fullerene C₆₀ ([¹⁴C(U)]C₆₀) in pregnant and lactating rats and their offspring after maternal intravenous exposure

Snyder

Fennell

Wingard

et al. 2015

J of Applied Toxicology

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A comprehensive distribution study was conducted in pregnant and lactating rats exposed to a suspension of uniformly carbon-14 labeled C60 ([14C(U)]C60). Rats were administered [14C(U)]C60 (~0.2 mg [14C(U)]C60/kg body weight) or 5% polyvinylpyrrolidone (PVP)-saline vehicle via a single tail vein injection. Pregnant rats were injected on gestation day (GD) 11 (terminated with fetuses after either 24h or 8d), GD15 (terminated after 24h or 4d), or GD18 (terminated after 24h). Lactating rats were injected on postnatal day 8 and terminated after 24h, 3d or 11d. The distribution of radioactivity in pregnant dams was influenced by both the state of pregnancy and time of termination after exposure. The percentage of recovered radioactivity in pregnant and lactating rats was highest in liver and lungs. Radioactivity was quantitated in over 20 tissues. Radioactivity was found in placenta and in fetuses of pregnant dams, and in the milk of lactating rats and in pups. Elimination of radioactivity was <2% in urine and feces at each time point. Radioactivity remained in blood circulation up to 11 days after [14C(U)]C60 exposure. Biomarkers of inflammation, cardiovascular injury and oxidative stress were measured to study the biological impacts of [14C(U)]C60 exposure. Oxidative stress were elevated in female pups of exposed dams. Metabolomics analysis of urine showed that [14C(U)]C60 exposure to pregnant rats impacted the pathways of vitamin B, regulation of lipid and sugar metabolism and aminoacyl-tRNA biosynthesis. This study demonstrated that [14C(U)]C60 crosses the placenta at all stages of pregnancy examined, and is transferred to pups via milk.

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“…Recently, groups have recently demonstrated translocation of PEG-SWCNTs to the tissues supporting fetal development (placenta and yolk sac) after IV injection and zinc oxide nanomaterials were distributed to the liver and kidney within the fetal tissues after maternal ingestion 44, 45 . These materials have also been measured in the mammary tissue or milk of lactating dams 45, 46 .…”

Section: Alternate Modelsmentioning

confidence: 99%

“…These materials have also been measured in the mammary tissue or milk of lactating dams 45, 46 . Some groups have also initiated investigations of female fertility after MWCNT exposure 45, 47 however these studies are in their infancy. We have reported that, ENM exposures during gestation can lead to significant microvascular dysfunction in maternal and fetal vessels 48 .…”

Section: Alternate Modelsmentioning

confidence: 99%

Vascular distribution of nanomaterials

Stapleton

Nurkiewicz

2014

WIREs Nanomed Nanobiotechnol

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Once considered primarily occupational, novel nanotechnology innovation and application has led to widespread domestic use and intentional biomedical exposures. With these exciting advances, the breadth and depth of toxicological considerations must also be expanded. The vascular system interacts with every tissue in the body, striving to homeostasis. Engineered nanomaterials (ENM) have been reported to distribute in many different organs and tissues. However, these observations have tended to use approaches requiring tissue homogenization and/or gross organ analyses. These techniques, while effective in establishing presence, preclude an exact determination of where ENM are deposited within a tissue. It is necessary to identify this exact distribution and deposition of ENM throughout the cardiovascular system, with respect to vascular hemodynamics and in vivo/ in vitro ENM modifications taken into account if nanotechnology is to achieve its full potential. Distinct levels of the vasculature will first be described as individual compartments. Then the vasculature will be considered as a whole. These unique compartments and biophysical conditions will be discussed in terms of their propensity to favor ENM deposition. Understanding levels of the vasculature will also be discussed. Ultimately, future studies must verify the mechanisms speculated on and presented herein.

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Exposure to zinc oxide nanoparticles affects reproductive development and biodistribution in offspring rats

Cited by 87 publications

References 16 publications

Endoplasmic reticulum stress and oxidative stress are involved in ZnO nanoparticle-induced hepatotoxicity

Endoplasmic reticulum stress and oxidative stress are involved in ZnO nanoparticle-induced hepatotoxicity

Distribution and biomarker of carbon‐14 labeled fullerene C₆₀ ([¹⁴C(U)]C₆₀) in pregnant and lactating rats and their offspring after maternal intravenous exposure

Vascular distribution of nanomaterials

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Exposure to zinc oxide nanoparticles affects reproductive development and biodistribution in offspring rats

Cited by 87 publications

References 16 publications

Endoplasmic reticulum stress and oxidative stress are involved in ZnO nanoparticle-induced hepatotoxicity

Endoplasmic reticulum stress and oxidative stress are involved in ZnO nanoparticle-induced hepatotoxicity

Distribution and biomarker of carbon‐14 labeled fullerene C60 ([14C(U)]C60) in pregnant and lactating rats and their offspring after maternal intravenous exposure

Vascular distribution of nanomaterials

Contact Info

Product

Resources

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Distribution and biomarker of carbon‐14 labeled fullerene C₆₀ ([¹⁴C(U)]C₆₀) in pregnant and lactating rats and their offspring after maternal intravenous exposure