Dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) induces oxidative damage promoting cell apoptosis primarily via mitochondrial pathway in the hepatopancreas of carp, Cyprinus carpio

To investigate the mechanisms of BDE-47 on hepatotoxicity in fish, this study examined the effects of dietary exposure to BDE-47 (40 and 4000 ng/g) on carp for 42 days. The results showed that BDE-47 significantly increased carp’s condition factor and hepatosomatic index. Pathological results reveal...

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Main Authors: Xin Zhang, Yujie Huang, Lei Yang, Shuhuang Chen, Youlian Liu, Ni Tang, Zhiqiong Li, Xiaoli Zhang, Liangyu Li, Defang Chen
Format: Article
Language:English
Published: Elsevier 2024-04-01
Series:Ecotoxicology and Environmental Safety
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0147651324002689
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author Xin Zhang
Yujie Huang
Lei Yang
Shuhuang Chen
Youlian Liu
Ni Tang
Zhiqiong Li
Xiaoli Zhang
Liangyu Li
Defang Chen
author_facet Xin Zhang
Yujie Huang
Lei Yang
Shuhuang Chen
Youlian Liu
Ni Tang
Zhiqiong Li
Xiaoli Zhang
Liangyu Li
Defang Chen
author_sort Xin Zhang
collection DOAJ
description To investigate the mechanisms of BDE-47 on hepatotoxicity in fish, this study examined the effects of dietary exposure to BDE-47 (40 and 4000 ng/g) on carp for 42 days. The results showed that BDE-47 significantly increased carp’s condition factor and hepatosomatic index. Pathological results revealed unclear hepatic cord structure, hepatocytes swelling, cellular vacuolization, and inflammatory cell infiltration in the hepatopancreas of carp. Further investigation showed that ROS levels significantly increased on days 7, 14, and 42. Moreover, the activities of antioxidant enzymes SOD, GSH, CAT, and GST increased significantly from 1 to 7 days, and the transcription levels of antioxidant enzymes CAT, Cu-Zn SOD, Mn-SOD, GST, and GPX, and antioxidant pathway genes Keap1, Nrf2, and HO-1 changed significantly at multiple time-points during the 42 days. The results of apoptosis pathway genes showed that the mitochondrial pathway genes Bax, Casp3, and Casp9 were significantly upregulated and Bcl2 was significantly downregulated, while the transcription levels of FADD and PERK were significantly enhanced. These results indicate that BDE-47 induced oxidative damage in hepatopancreas, then it promoted cell apoptosis mainly through the mitochondrial pathway. This study provides a foundation for analyzing the mechanism of hepatotoxicity induced by BDE-47 on fish.
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spelling doaj.art-60e85102cff6438ca8e886c825ad73e62024-03-27T04:51:15ZengElsevierEcotoxicology and Environmental Safety0147-65132024-04-01274116192Dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) induces oxidative damage promoting cell apoptosis primarily via mitochondrial pathway in the hepatopancreas of carp, Cyprinus carpioXin Zhang0Yujie Huang1Lei Yang2Shuhuang Chen3Youlian Liu4Ni Tang5Zhiqiong Li6Xiaoli Zhang7Liangyu Li8Defang Chen9Department of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, 211 Huimin Road, Chengdu, Sichuan, ChinaDepartment of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, 211 Huimin Road, Chengdu, Sichuan, ChinaDepartment of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, 211 Huimin Road, Chengdu, Sichuan, China; Yuxi Agriculture Vocation-Technical College, 41 Xiangjiazhuang Road, Yuxi, Yunnan, ChinaDepartment of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, 211 Huimin Road, Chengdu, Sichuan, ChinaDepartment of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, 211 Huimin Road, Chengdu, Sichuan, ChinaDepartment of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, 211 Huimin Road, Chengdu, Sichuan, ChinaDepartment of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, 211 Huimin Road, Chengdu, Sichuan, ChinaInstitute of Fisheries Research, Chengdu Academy of Agricultural and Forestry Sciences, 200 Nongke Road, Chengdu, Sichuan, ChinaInstitute of Fisheries Research, Chengdu Academy of Agricultural and Forestry Sciences, 200 Nongke Road, Chengdu, Sichuan, China; Correspondence to: Institute of Fisheries Research, Chengdu Academy of Agricultural and Forestry Sciences, China.Department of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, 211 Huimin Road, Chengdu, Sichuan, China; Correspondence to: Department of Aquaculture, College of Animal Science and Technology, Sichuan Agricultural University, China.To investigate the mechanisms of BDE-47 on hepatotoxicity in fish, this study examined the effects of dietary exposure to BDE-47 (40 and 4000 ng/g) on carp for 42 days. The results showed that BDE-47 significantly increased carp’s condition factor and hepatosomatic index. Pathological results revealed unclear hepatic cord structure, hepatocytes swelling, cellular vacuolization, and inflammatory cell infiltration in the hepatopancreas of carp. Further investigation showed that ROS levels significantly increased on days 7, 14, and 42. Moreover, the activities of antioxidant enzymes SOD, GSH, CAT, and GST increased significantly from 1 to 7 days, and the transcription levels of antioxidant enzymes CAT, Cu-Zn SOD, Mn-SOD, GST, and GPX, and antioxidant pathway genes Keap1, Nrf2, and HO-1 changed significantly at multiple time-points during the 42 days. The results of apoptosis pathway genes showed that the mitochondrial pathway genes Bax, Casp3, and Casp9 were significantly upregulated and Bcl2 was significantly downregulated, while the transcription levels of FADD and PERK were significantly enhanced. These results indicate that BDE-47 induced oxidative damage in hepatopancreas, then it promoted cell apoptosis mainly through the mitochondrial pathway. This study provides a foundation for analyzing the mechanism of hepatotoxicity induced by BDE-47 on fish.http://www.sciencedirect.com/science/article/pii/S01476513240026892,2′,4,4′-tetrabromodiphenyl ether (BDE-47)Cyprinus carpioDietary exposureAntioxidant systemApoptotic pathway
spellingShingle Xin Zhang
Yujie Huang
Lei Yang
Shuhuang Chen
Youlian Liu
Ni Tang
Zhiqiong Li
Xiaoli Zhang
Liangyu Li
Defang Chen
Dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) induces oxidative damage promoting cell apoptosis primarily via mitochondrial pathway in the hepatopancreas of carp, Cyprinus carpio
Ecotoxicology and Environmental Safety
2,2′,4,4′-tetrabromodiphenyl ether (BDE-47)
Cyprinus carpio
Dietary exposure
Antioxidant system
Apoptotic pathway
title Dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) induces oxidative damage promoting cell apoptosis primarily via mitochondrial pathway in the hepatopancreas of carp, Cyprinus carpio
title_full Dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) induces oxidative damage promoting cell apoptosis primarily via mitochondrial pathway in the hepatopancreas of carp, Cyprinus carpio
title_fullStr Dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) induces oxidative damage promoting cell apoptosis primarily via mitochondrial pathway in the hepatopancreas of carp, Cyprinus carpio
title_full_unstemmed Dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) induces oxidative damage promoting cell apoptosis primarily via mitochondrial pathway in the hepatopancreas of carp, Cyprinus carpio
title_short Dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) induces oxidative damage promoting cell apoptosis primarily via mitochondrial pathway in the hepatopancreas of carp, Cyprinus carpio
title_sort dietary exposure to 2 2 4 4 tetrabromodiphenyl ether bde 47 induces oxidative damage promoting cell apoptosis primarily via mitochondrial pathway in the hepatopancreas of carp cyprinus carpio
topic 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47)
Cyprinus carpio
Dietary exposure
Antioxidant system
Apoptotic pathway
url http://www.sciencedirect.com/science/article/pii/S0147651324002689
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