Abstract |
Cadmium (Cd), a toxic heavy metal pollutant, is a threat to human and eatable fish health. Common carps are widely cultivated and eaten by humans. However, there are no reports about Cd-damaged common carp hearts. Our experiment attempted to investigate the cardiotoxicity of Cd to common carps by establishing a common carp Cd exposure model. Our results showed that Cd injured hearts. Moreover, Cd treatment induced autophagy via miR-9-5p/ Sirt1/mTOR/ULK1 pathway. Cd exposure caused oxidant/ antioxidant imbalance and oxidative stress; and led to energetic impairment. Energetic impairment partook in oxidative stress-mediated autophagy through AMPK/mTOR/ULK1 pathway. Furthermore, Cd caused mitochondrial division/fusion imbalance and resulted in inflammatory injury via NF-κB-COX-2-PTGEs and NF-κB-COX-2-TNF-α pathways. Oxidative stress mediated mitochondrial division/fusion imbalance, further induced inflammation and autophagy via OPA1/NF-κB-COX-2-TNF-α- Beclin1 and OPA1/NF-κB-COX-2-TNF-α/P62 pathways under Cd treatment. Taken together, miR-9-5p, oxidative stress, energetic impairment, mitochondrial division/fusion imbalance, inflammation, and autophagy participated in the mechanism of Cd- cardiotoxicity to common carps. Our study revealed harmful effect of Cd on hearts, and provided new information for researches of environmental pollutant toxicity.
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Authors | Yuhao Liu, Xu Lin, Zhiyu Hao, Meijin Yu, You Tang, Xiaohua Teng, Wei Sun, Lu Kang |
Journal | Fish & shellfish immunology
(Fish Shellfish Immunol)
Vol. 138
Pg. 108853
(Jul 2023)
ISSN: 1095-9947 [Electronic] England |
PMID | 37245677
(Publication Type: Journal Article)
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Copyright | Copyright © 2023 Elsevier Ltd. All rights reserved. |
Chemical References |
- Cadmium
- NF-kappa B
- Tumor Necrosis Factor-alpha
- Cyclooxygenase 2
- MicroRNAs
- TOR Serine-Threonine Kinases
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Topics |
- Humans
- Animals
- Carps
(metabolism)
- Cadmium
(toxicity)
- NF-kappa B
(metabolism)
- Cardiotoxicity
- Tumor Necrosis Factor-alpha
(metabolism)
- Cyclooxygenase 2
- Oxidative Stress
- MicroRNAs
(metabolism)
- Inflammation
(chemically induced, veterinary)
- TOR Serine-Threonine Kinases
(metabolism)
- Autophagy
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