ZnO-NPs alleviate aflatoxin B1-induced hepatoxicity in ducklings by promoting hepatic metallothionein expression

Aflatoxin B1 (AFB1) is a mycotoxin widely present in animal feed and human food, posing a serious threat to animal and human health. This study was aim to illustrate the mechanism of the protective role of MT against AFB1-induced hepatotoxicity, as well as to explore the feasibility of enhancing the...

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Main Authors: Beiyu Zhang, Meiling Li, Guangteng Zhou, Xin Gu, Longqiang Xie, Man Zhao, Qingbiao Xu, Gaoming Tan, Niya Zhang
Format: Article
Language:English
Published: Elsevier 2023-05-01
Series:Ecotoxicology and Environmental Safety
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0147651323003305
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author Beiyu Zhang
Meiling Li
Guangteng Zhou
Xin Gu
Longqiang Xie
Man Zhao
Qingbiao Xu
Gaoming Tan
Niya Zhang
author_facet Beiyu Zhang
Meiling Li
Guangteng Zhou
Xin Gu
Longqiang Xie
Man Zhao
Qingbiao Xu
Gaoming Tan
Niya Zhang
author_sort Beiyu Zhang
collection DOAJ
description Aflatoxin B1 (AFB1) is a mycotoxin widely present in animal feed and human food, posing a serious threat to animal and human health. This study was aim to illustrate the mechanism of the protective role of MT against AFB1-induced hepatotoxicity, as well as to explore the feasibility of enhancing the tolerance of poultry to AFB1 by upregulating the expression of hepatic MT. After being exposed to AFB1 (50 ng/kg) primary duckling hepatocytes, the cell viability, the antioxidant index (SOD and GPx) and the mRNA levels of MT downstream genes (PTGR, p53, TrxR, AR and Bcl-2) significantly (p < 0.05) decreased, while the intracellular formation of (AFBO)-DNA adduct content, apoptosis, and MDA content significantly (p < 0.05) increased. Interestingly, overexpression of MT in primary duckling hepatocytes markedly (p < 0.05) reversed the detrimental impact of AFB1 and increased the expression of MT downstream genes. HepG2 cells were applied to study the mechanism how MT works to relieve the hepatic toxicity of AFB1. The ZnO-NPs (20 μg/mL) + AFB1 (20 μg/mL) group significantly (p < 0.05) increased the cell viability, the expression of NRF2, NQO1 and SOD, and expression of MT and MTF-1, as well as significantly (p < 0.05) decreased LDH, ROS and apoptotic rate, comparing with the AFB1 group. While joint treatment with AFB1 and ZnO-NPs, the hepatic toxicity exerted by AFB1 alone was reversed, along with the translocation of MTF-1 from the cytoplasm to the nucleus and upregulated its expression. Duckling trails were further carried out. A total number of 96 1-day-old healthy Cherry Valley commercial ducklings were randomly allocated according to a 2 by 2 factorial arrangement of treatments with the main factors including oral administration of AFB1 (0 vs. 40 μg/kg) and dietary supplementation of ZnO-NPs (0 vs. 60 mg/kg) for 7 days. It showed that AFB1 exposure caused body weight loss (p < 0.05), impaired liver structure and failure in hepatic function (activity of ALT, AST and concentration of TP and GLU) (p < 0.05), and decreases in antioxidant capacity(activity of SOD, CAT and concentration of GSH) (p < 0.05), along with the decrease in hepatic concentration of Zn, increase in expression of apoptosis-related genes and protein CAS3 and mRNA Bcl-2 expression (p < 0.05), and suppressed mRNA levels of antioxidant-related genes MT, SOD1, NRF2, and NQO1 (p < 0.05). In accordance with the cell test, dietary supplementation with ZnO-NPs mitigated the toxicity exerted by AFB1. In conclusion, ZnO-NPs has the protective effects against AFB1-induced hepatocyte injury by activating the expression of MTF-1 and the ectopic induction of MT expression, providing detailed information on the detoxification ability of MT on AFB1.
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spelling doaj.art-9d4d81d4536b4084a9157f18f29bbe402023-04-24T04:36:43ZengElsevierEcotoxicology and Environmental Safety0147-65132023-05-01256114826ZnO-NPs alleviate aflatoxin B1-induced hepatoxicity in ducklings by promoting hepatic metallothionein expressionBeiyu Zhang0Meiling Li1Guangteng Zhou2Xin Gu3Longqiang Xie4Man Zhao5Qingbiao Xu6Gaoming Tan7Niya Zhang8Department of Animal Nutrition and Feed Science, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaCorrespondence to: Department of Animal Nutrition and Feed Science, Huazhong Agricultural University, Wuhan 430070, China.; Department of Animal Nutrition and Feed Science, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaAflatoxin B1 (AFB1) is a mycotoxin widely present in animal feed and human food, posing a serious threat to animal and human health. This study was aim to illustrate the mechanism of the protective role of MT against AFB1-induced hepatotoxicity, as well as to explore the feasibility of enhancing the tolerance of poultry to AFB1 by upregulating the expression of hepatic MT. After being exposed to AFB1 (50 ng/kg) primary duckling hepatocytes, the cell viability, the antioxidant index (SOD and GPx) and the mRNA levels of MT downstream genes (PTGR, p53, TrxR, AR and Bcl-2) significantly (p < 0.05) decreased, while the intracellular formation of (AFBO)-DNA adduct content, apoptosis, and MDA content significantly (p < 0.05) increased. Interestingly, overexpression of MT in primary duckling hepatocytes markedly (p < 0.05) reversed the detrimental impact of AFB1 and increased the expression of MT downstream genes. HepG2 cells were applied to study the mechanism how MT works to relieve the hepatic toxicity of AFB1. The ZnO-NPs (20 μg/mL) + AFB1 (20 μg/mL) group significantly (p < 0.05) increased the cell viability, the expression of NRF2, NQO1 and SOD, and expression of MT and MTF-1, as well as significantly (p < 0.05) decreased LDH, ROS and apoptotic rate, comparing with the AFB1 group. While joint treatment with AFB1 and ZnO-NPs, the hepatic toxicity exerted by AFB1 alone was reversed, along with the translocation of MTF-1 from the cytoplasm to the nucleus and upregulated its expression. Duckling trails were further carried out. A total number of 96 1-day-old healthy Cherry Valley commercial ducklings were randomly allocated according to a 2 by 2 factorial arrangement of treatments with the main factors including oral administration of AFB1 (0 vs. 40 μg/kg) and dietary supplementation of ZnO-NPs (0 vs. 60 mg/kg) for 7 days. It showed that AFB1 exposure caused body weight loss (p < 0.05), impaired liver structure and failure in hepatic function (activity of ALT, AST and concentration of TP and GLU) (p < 0.05), and decreases in antioxidant capacity(activity of SOD, CAT and concentration of GSH) (p < 0.05), along with the decrease in hepatic concentration of Zn, increase in expression of apoptosis-related genes and protein CAS3 and mRNA Bcl-2 expression (p < 0.05), and suppressed mRNA levels of antioxidant-related genes MT, SOD1, NRF2, and NQO1 (p < 0.05). In accordance with the cell test, dietary supplementation with ZnO-NPs mitigated the toxicity exerted by AFB1. In conclusion, ZnO-NPs has the protective effects against AFB1-induced hepatocyte injury by activating the expression of MTF-1 and the ectopic induction of MT expression, providing detailed information on the detoxification ability of MT on AFB1.http://www.sciencedirect.com/science/article/pii/S0147651323003305Aflatoxin B1DucklingsLiverMetallothioneinMetal-regulatory transcription factor-1ZnO-NPs
spellingShingle Beiyu Zhang
Meiling Li
Guangteng Zhou
Xin Gu
Longqiang Xie
Man Zhao
Qingbiao Xu
Gaoming Tan
Niya Zhang
ZnO-NPs alleviate aflatoxin B1-induced hepatoxicity in ducklings by promoting hepatic metallothionein expression
Ecotoxicology and Environmental Safety
Aflatoxin B1
Ducklings
Liver
Metallothionein
Metal-regulatory transcription factor-1
ZnO-NPs
title ZnO-NPs alleviate aflatoxin B1-induced hepatoxicity in ducklings by promoting hepatic metallothionein expression
title_full ZnO-NPs alleviate aflatoxin B1-induced hepatoxicity in ducklings by promoting hepatic metallothionein expression
title_fullStr ZnO-NPs alleviate aflatoxin B1-induced hepatoxicity in ducklings by promoting hepatic metallothionein expression
title_full_unstemmed ZnO-NPs alleviate aflatoxin B1-induced hepatoxicity in ducklings by promoting hepatic metallothionein expression
title_short ZnO-NPs alleviate aflatoxin B1-induced hepatoxicity in ducklings by promoting hepatic metallothionein expression
title_sort zno nps alleviate aflatoxin b1 induced hepatoxicity in ducklings by promoting hepatic metallothionein expression
topic Aflatoxin B1
Ducklings
Liver
Metallothionein
Metal-regulatory transcription factor-1
ZnO-NPs
url http://www.sciencedirect.com/science/article/pii/S0147651323003305
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