{"title":"The effects of indirect exposure of nanosilver on caspase-8 and caspase-9 levels in liver and brain of suckling rats","authors":"M. Fatemi","doi":"10.22038/NMJ.2019.06.00004","DOIUrl":null,"url":null,"abstract":"Objective(s): The adverse health effects of nanosilver (AgNp) on adult animal models have been well documented. However, data is scarce regarding the toxic effects of AgNp on sensitive developmental stages. The present study aimed to investigate the effects of maternal milk exposure to AgNp on apoptosis induction in the liver and brain of the offspring of rats. Materials and Methods: Lactating Wistar rats were intragastrically exposed to the vehicle (deionized water) or two doses of AgNp (25 and 100 mg/kg) for 21 days. Liver and brain samples were collected from the male pups of the mothers on postnatal day 21. The silver content and levels of caspase-8 and caspase-9 in the tissues were measured using the ICP-MS analysis and ELISA assay, respectively. For histopathological examinations, the tissue sections were stained using the hematoxylin-eosin (H&E) stain and examined by light microscopy.Results: A significant, dose-dependent increase was observed in the silver content of the liver and brain of the pups and maternal milk exposed to AgNp. In addition, the level of caspase-9 significantly increased in the liver and brain in the pups exposed to the high dose of AgNp (100 mg/kg-1), while no significant changes were observed in the level of caspase-8 in the experimental groups compared to the controls. Histopathological studies also demonstrated tissue damage in the liver and brain of the pups exposed to the high dose of AgNp. Conclusion: According to the results, lactational exposure to AgNp may induce apoptosis via the intrinsic pathway in the offspring tissues of rats. However, further investigation is required in order to document these findings.","PeriodicalId":18933,"journal":{"name":"Nanomedicine Journal","volume":"6 1","pages":"176-182"},"PeriodicalIF":1.4000,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nanomedicine Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22038/NMJ.2019.06.00004","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"NANOSCIENCE & NANOTECHNOLOGY","Score":null,"Total":0}
引用次数: 1
Abstract
Objective(s): The adverse health effects of nanosilver (AgNp) on adult animal models have been well documented. However, data is scarce regarding the toxic effects of AgNp on sensitive developmental stages. The present study aimed to investigate the effects of maternal milk exposure to AgNp on apoptosis induction in the liver and brain of the offspring of rats. Materials and Methods: Lactating Wistar rats were intragastrically exposed to the vehicle (deionized water) or two doses of AgNp (25 and 100 mg/kg) for 21 days. Liver and brain samples were collected from the male pups of the mothers on postnatal day 21. The silver content and levels of caspase-8 and caspase-9 in the tissues were measured using the ICP-MS analysis and ELISA assay, respectively. For histopathological examinations, the tissue sections were stained using the hematoxylin-eosin (H&E) stain and examined by light microscopy.Results: A significant, dose-dependent increase was observed in the silver content of the liver and brain of the pups and maternal milk exposed to AgNp. In addition, the level of caspase-9 significantly increased in the liver and brain in the pups exposed to the high dose of AgNp (100 mg/kg-1), while no significant changes were observed in the level of caspase-8 in the experimental groups compared to the controls. Histopathological studies also demonstrated tissue damage in the liver and brain of the pups exposed to the high dose of AgNp. Conclusion: According to the results, lactational exposure to AgNp may induce apoptosis via the intrinsic pathway in the offspring tissues of rats. However, further investigation is required in order to document these findings.