Effects and mechanism of perinatal nonylphenol exposure on cardiac function and myocardial mitochondria in neonatal rats
Background: Nonylphenol (NP) is a common environmental endocrine disruptor that is associated with the development of cardiovascular disease. However, the toxic effect of NP on mitochondria in the heart of offspring to exposed individuals remains exclusive. Objective: To investigate whether perinata...
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Elsevier
2023-06-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651323004815 |
| _version_ | 1797823393941159936 |
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| author | Chengyu Ni Kai Pan Jie Xu Xianping Long FangMei Lin Yanling Nie Yu Yang Jie Yu |
| author_facet | Chengyu Ni Kai Pan Jie Xu Xianping Long FangMei Lin Yanling Nie Yu Yang Jie Yu |
| author_sort | Chengyu Ni |
| collection | DOAJ |
| description | Background: Nonylphenol (NP) is a common environmental endocrine disruptor that is associated with the development of cardiovascular disease. However, the toxic effect of NP on mitochondria in the heart of offspring to exposed individuals remains exclusive. Objective: To investigate whether perinatal NP exposure causes mitochondrial damage in the hearts of offspring of exposed individuals and determine its mechanism of action through both animal and cell experiments. Methods and results: For the in vivo experiment, pregnant rats were randomly divided into four groups: the control group (corn oil, C), low dose group (2.5 mg/kg/day, L-NP group), medium dose group (50 mg/kg/day, M-NP group), and high dose group (100 mg/kg/day, H-NP group), with 12 rats in each group. The NP concentration in the hearts of offspring at PND21 and PND90 increased with the increase of the NP dose. Perinatal NP exposure induced a gradual increase in systolic blood pressure in offspring at PND90. In the H-NP group, there was a high degree of inflammatory cell infiltration, myofibril breaks, inconspicuous or absent nuclei, and pink collagen deposition. At PND90, the membrane integrity of mitochondria in the H-NP group was disrupted, the cristae disorder was aggravated, and there was internal lysis with vacuolation. Compared to the control group, the mitochondrial membrane potential of offspring at PND21 and PND90 was decreased in each of the NP exposure groups. NP exposure decreased the activity of mitochondrial respiratory enzyme complex I (CI) and increased the activity of mitochondrial respiratory enzyme complex IV (CIV) in the offspring. At PND21 and PND90, the mRNA and protein expression levels of cardiac mitochondrial PGC-1α, NRF-1, and TFAM decreased with increasing NP dose in a dose-dependent manner. In the in vitro experiment, H9C2 cells were divided into the following four groups: the blank group, RSV group (15 μg/ml), RSV + NP group (15 μg/ml RSV + 120 mmol/L NP), and NP group (120 mmol/L). With increasing NP concentration, the cell survival rate gradually decreased. Compared to the control, the membrane potential was significantly decreased in the NP group; the protein expression levels of SIRT1, PGC-1α, NRF-1, and TFAM in the NP group were significantly lower. Conclusion: Perinatal NP exposure caused mitochondrial damage and dysfunction in the offspring of exposed individuals in a dose-dependent manner. This toxic effect may be related to NP-induced mitochondrial pathology in the offspring and the inhibition of both gene and protein expression involved in the PGC-1α/NRF-1/TFAM mitochondrial biogenesis signaling pathway following NP exposure. |
| first_indexed | 2024-03-13T10:23:21Z |
| format | Article |
| id | doaj.art-f52eaaa9ca054cd28fca6fe6bbc9c223 |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-03-13T10:23:21Z |
| publishDate | 2023-06-01 |
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| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-f52eaaa9ca054cd28fca6fe6bbc9c2232023-05-20T04:29:05ZengElsevierEcotoxicology and Environmental Safety0147-65132023-06-01258114977Effects and mechanism of perinatal nonylphenol exposure on cardiac function and myocardial mitochondria in neonatal ratsChengyu Ni0Kai Pan1Jie Xu2Xianping Long3FangMei Lin4Yanling Nie5Yu Yang6Jie Yu7School of Public Health, Zunyi Medical University, Zunyi, Guizhou 563000, PR China; Department of Medicine, Hubei College of Chinese Medicine, Jingzhou, Hubei 434020, PR ChinaSchool of Public Health, Zunyi Medical University, Zunyi, Guizhou 563000, PR ChinaSchool of Public Health, Zunyi Medical University, Zunyi, Guizhou 563000, PR ChinaDepartment of Cardiology, Affiliated Hospital of Zunyi Medical University, Guizhou, PR ChinaSchool of Public Health, Zunyi Medical University, Zunyi, Guizhou 563000, PR ChinaSchool of Public Health, Zunyi Medical University, Zunyi, Guizhou 563000, PR ChinaSchool of Public Health, Zunyi Medical University, Zunyi, Guizhou 563000, PR ChinaSchool of Public Health, Zunyi Medical University, Zunyi, Guizhou 563000, PR China; Corresponding author.Background: Nonylphenol (NP) is a common environmental endocrine disruptor that is associated with the development of cardiovascular disease. However, the toxic effect of NP on mitochondria in the heart of offspring to exposed individuals remains exclusive. Objective: To investigate whether perinatal NP exposure causes mitochondrial damage in the hearts of offspring of exposed individuals and determine its mechanism of action through both animal and cell experiments. Methods and results: For the in vivo experiment, pregnant rats were randomly divided into four groups: the control group (corn oil, C), low dose group (2.5 mg/kg/day, L-NP group), medium dose group (50 mg/kg/day, M-NP group), and high dose group (100 mg/kg/day, H-NP group), with 12 rats in each group. The NP concentration in the hearts of offspring at PND21 and PND90 increased with the increase of the NP dose. Perinatal NP exposure induced a gradual increase in systolic blood pressure in offspring at PND90. In the H-NP group, there was a high degree of inflammatory cell infiltration, myofibril breaks, inconspicuous or absent nuclei, and pink collagen deposition. At PND90, the membrane integrity of mitochondria in the H-NP group was disrupted, the cristae disorder was aggravated, and there was internal lysis with vacuolation. Compared to the control group, the mitochondrial membrane potential of offspring at PND21 and PND90 was decreased in each of the NP exposure groups. NP exposure decreased the activity of mitochondrial respiratory enzyme complex I (CI) and increased the activity of mitochondrial respiratory enzyme complex IV (CIV) in the offspring. At PND21 and PND90, the mRNA and protein expression levels of cardiac mitochondrial PGC-1α, NRF-1, and TFAM decreased with increasing NP dose in a dose-dependent manner. In the in vitro experiment, H9C2 cells were divided into the following four groups: the blank group, RSV group (15 μg/ml), RSV + NP group (15 μg/ml RSV + 120 mmol/L NP), and NP group (120 mmol/L). With increasing NP concentration, the cell survival rate gradually decreased. Compared to the control, the membrane potential was significantly decreased in the NP group; the protein expression levels of SIRT1, PGC-1α, NRF-1, and TFAM in the NP group were significantly lower. Conclusion: Perinatal NP exposure caused mitochondrial damage and dysfunction in the offspring of exposed individuals in a dose-dependent manner. This toxic effect may be related to NP-induced mitochondrial pathology in the offspring and the inhibition of both gene and protein expression involved in the PGC-1α/NRF-1/TFAM mitochondrial biogenesis signaling pathway following NP exposure.http://www.sciencedirect.com/science/article/pii/S0147651323004815NonylphenolHeartMitochondriaH9C2 cellsPGC-1α/NRF-1/TFAM signaling pathway |
| spellingShingle | Chengyu Ni Kai Pan Jie Xu Xianping Long FangMei Lin Yanling Nie Yu Yang Jie Yu Effects and mechanism of perinatal nonylphenol exposure on cardiac function and myocardial mitochondria in neonatal rats Ecotoxicology and Environmental Safety Nonylphenol Heart Mitochondria H9C2 cells PGC-1α/NRF-1/TFAM signaling pathway |
| title | Effects and mechanism of perinatal nonylphenol exposure on cardiac function and myocardial mitochondria in neonatal rats |
| title_full | Effects and mechanism of perinatal nonylphenol exposure on cardiac function and myocardial mitochondria in neonatal rats |
| title_fullStr | Effects and mechanism of perinatal nonylphenol exposure on cardiac function and myocardial mitochondria in neonatal rats |
| title_full_unstemmed | Effects and mechanism of perinatal nonylphenol exposure on cardiac function and myocardial mitochondria in neonatal rats |
| title_short | Effects and mechanism of perinatal nonylphenol exposure on cardiac function and myocardial mitochondria in neonatal rats |
| title_sort | effects and mechanism of perinatal nonylphenol exposure on cardiac function and myocardial mitochondria in neonatal rats |
| topic | Nonylphenol Heart Mitochondria H9C2 cells PGC-1α/NRF-1/TFAM signaling pathway |
| url | http://www.sciencedirect.com/science/article/pii/S0147651323004815 |
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