2. Academic Validation
  3. Benoxacor caused developmental and cardiac toxicity in zebrafish larvae

Benoxacor caused developmental and cardiac toxicity in zebrafish larvae

  • Ecotoxicol Environ Saf. 2021 Nov:224:112696. doi: 10.1016/j.ecoenv.2021.112696.
Weixin Zhang 1,  Jiajie Yan 1,  Yong Huang 2,  Ziqin Wang 1,  Bo Cheng 1,  Jinze Ma 1,  You Wei 2,  Yunlong Meng 2,  Huiqiang Lu 3
Affiliations

Affiliations

  • 1 Ganzhou Key Laboratory for Drug Screening and Discovery, School of Geography and Environmental Engineering, Gannan Normal University, Ganzhou 341000, Jiangxi, China.
  • 2 Ganzhou Key Laboratory for Drug Screening and Discovery, School of Geography and Environmental Engineering, Gannan Normal University, Ganzhou 341000, Jiangxi, China; College of Chemistry and Chemical Engineering, Gannan Normal University, Ganzhou 341000 Jiangxi, China.
  • 3 Ganzhou Key Laboratory for Drug Screening and Discovery, School of Geography and Environmental Engineering, Gannan Normal University, Ganzhou 341000, Jiangxi, China; College of Chemistry and Chemical Engineering, Gannan Normal University, Ganzhou 341000 Jiangxi, China; Jiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Jiangxi Key Laboratory of Developmental Biology of Organs, Affiliated Hospital of Jinggangshan University, Ji'an 343009, China. Electronic address: [email protected].
PMID: 34455182 DOI: 10.1016/j.ecoenv.2021.112696
Abstract

Benoxacor (BN) is a highly effective antidote of dichloroacetamide herbicides generally used to protect crops from herbicidal damage. As a commonly used agrochemical, this Herbicide antidote is continuously discharged in watercourses thus causing toxicity to aquatic organisms, and ultimately leading to contamination of the food chain. To date, its potential toxicity to the cardiac development of aquatic organisms has not been evaluated. In the present study, we have selected the zebrafish as a model to study the impact of BN on embryonic developmental and cardiac toxicity. The zebrafish embryos were exposed in 0.5, 1.0 and 2.0 mg/L BN from 5.5 to 72 h post-fertilization (hpf). The results indicated that the exposure to BN led to increased mortality and diminished heart and hatching rates in the embryos. BN exposure also brought pericardial edema (PE) and linear stretching of heart. Besides, exposure to BN induced an excessive accumulation of Reactive Oxygen Species (ROS) in the zebrafish embryos and abnormal activities of the antioxidant Enzymes, including catalase (CAT) and malondialdehyde (MDA). Moreover, exposure to BN caused serious cardiac toxicity of the embryos, accompanied by abnormality of heart development- and apoptosis-related genes. Surprisingly, astaxanthin (ASTA), as a common antioxidant, was found to be able to partially rescue the cardiac toxicity caused by BN, which indicated that ROS are probably the major reason for the resulting cardiotoxicity in zebrafish embryos. Our results suggest the need for a comprehensive safety evaluation of the regular consumption of benoxacor, which provides scientific basis for the development of health standards and assessment of potential risk in aquatic organisms or even human.

Keywords

Benoxacor; Cardiotoxicity; Herbicide safeners; Oxidative stress; Zebrafish.

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