1. Academic Validation
  2. Benzophenone induces cardiac developmental toxicity in zebrafish embryos by upregulating Wnt signaling

Benzophenone induces cardiac developmental toxicity in zebrafish embryos by upregulating Wnt signaling

  • Chemosphere. 2023 Sep 27:140283. doi: 10.1016/j.chemosphere.2023.140283.
Yuhua Zuo 1 Chao Chen 2 Fasheng Liu 3 Hongmei Hu 2 Chao Wen 3 Si Dong 3 Xinjun Liao 3 Zigang Cao 3 Xiaoyun Shi 3 Zilin Zhong 2 Jianjun Chen 4 Huiqiang Lu 5
Affiliations

Affiliations

  • 1 School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, 325003, Zhejiang, China.
  • 2 Shanghai Key Laboratory of Anesthesiology and Brain Functional Modulation, Clinical Research Center for Anesthesiology and Perioperative Medicine, Translational Research Institute of Brain and Brain-Like Intelligence, Department of Pediatrics, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, Shanghai, 200434, China; Department of Medical Genetics, School of Medicine, Tongji University, Shanghai, 200092, China.
  • 3 Affiliated Hospital of Jinggangshan University, Center for Clinical Medicine Research of Jinggangshan University, Ji'an, 343009, Jiangxi, China.
  • 4 Shanghai Key Laboratory of Anesthesiology and Brain Functional Modulation, Clinical Research Center for Anesthesiology and Perioperative Medicine, Translational Research Institute of Brain and Brain-Like Intelligence, Department of Pediatrics, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, Shanghai, 200434, China; Department of Medical Genetics, School of Medicine, Tongji University, Shanghai, 200092, China. Electronic address: [email protected].
  • 5 Affiliated Hospital of Jinggangshan University, Center for Clinical Medicine Research of Jinggangshan University, Ji'an, 343009, Jiangxi, China. Electronic address: [email protected].
Abstract

Benzophenone (BP) is a vital ingredient in many popular consumer products, such as cosmetics. BP potential toxicity to humans and aquatic organisms has emerged as an increased concern. In current study, we utilized a zebrafish model to assess BP-induced developmental cardiotoxicity. Following BP exposure, zebrafish embryos exhibited developmental toxicity, including increased mortality, reduced hatchability, delayed yolk sac absorption, and shortened body length. Besides, BP exposure induced cardiac defects in zebrafish embryos, comprising pericardial edema, reduced myocardial contractility and rhythm disturbances, and altered expression levels of cardiac developmental marker genes. Mechanistically, BP exposure disturbed the redox state and increased the level of Apoptosis in zebrafish cardiomyocytes. Transcriptional expression levels of Wnt signaling genes, involving lef1, axin2, and β-catenin, were upregulated after BP treatment. Inhibition of Wnt signaling with IWR-1 could rescue the BP-induced cardiotoxicity in zebrafish. In summary, BP exposure causes cardiotoxicity via upregulation of the Wnt signaling pathway in zebrafish embryos.

Keywords

Aquatic contamination; Benzophenone; Cardiotoxicity; Cosmetics; Wnt signaling.

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