Parental exposure to 1,2-benzisothiazol-3(2 H)-one induces intergenerational cardiac and ocular development toxicity in F
5 affiliations
- 1Department of Obstetrics and Gynaecology, Xiangyang No. 1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, China
- 2Department of Obstetrics and Gynecology, Xiangyang No. 1 People's Hospital, Wuhan University of Science and Technology, Xiangyang, 441000, China
- 3Department of Reproductive Medicine, Key Laboratory of Zebrafsh Modeling and Drug Screening for Human Diseases of Xiangyang City, Xiangyang No. 1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, China
- 4Department of Obstetrics and Gynaecology, Xiangyang No. 1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, China; Corresponding authors.
- 5Department of Reproductive Medicine, Key Laboratory of Zebrafsh Modeling and Drug Screening for Human Diseases of Xiangyang City, Xiangyang No. 1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, China; Corresponding authors.
Abstract
1,2-Benzisothiazol-3(2 H)-one (BIT) is a widely utilised preservative in industrial applications and has been frequently detected in aquatic environments. The widespread occurrence and potential bioaccumulation of BIT in the environment raise significant ecological concerns. Although previous studies have addressed the embryonic toxicity of BIT, the intergenerational toxicity stemming from parental exposure to BIT remain inadequately understood. This study exposed parental zebrafish to BIT (300 ng/L and 300 μg/L) for 120 days to investigate its impact on the F 1 generation, focusing on embryonic development, histopathology, and transcriptomic profiling through comprehensive phenotypic and molecular assessments. Our results demonstrated that parental BIT exposure did not significantly affect hatchability or mortality in the F 1 offspring. However, it resulted in significant developmental impairments in F 1 larvae, manifested as increased deformity rates (yolk sac edema, shortened body length), cardiovascular developmental disorders (pericardial edema, increased Bulbus Arteriosus-Sinus Venosus distance, and decreased heart rate, blood flow velocity, and blood pressure), and ocular and visual developmental disorders (decreased ocular area, reduced movement velocity, and reduced total movement distance). RNA-sequencing analysis revealed a significant enrichment of pathways associated with cardiac muscle contraction, cardiac morphogenesis, and ocular development. Transcriptomic analysis identified organ-specific transcriptional alterations in F 1 larvae, including the dysregulation of genes essential for heart development ( vmhcl , cox4i1l , bag3 , brk1 ) and ocular development ( opn1mw2 , arr3a , arr3b ). Our findings indicate that parental BIT exposure can lead to embryonic developmental defects in F 1 larvae, thereby providing novel insights into the intergenerational toxicity of BIT.
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BibTeX
@article{haiqinmao2026parental,
title = {{Parental exposure to 1,2-benzisothiazol-3(2 H)-one induces intergenerational cardiac and ocular development toxicity in F}},
author = {Haiqin-Mao and Qi Xie and Guiying-Wei and Mengjie-Shi and Chao Zhong and Jiaolong-Huang and Pengxia-Yu and Chunhui-Hu and Jie Deng and Peng Duan},
journal = {Ecotoxicology and Environmental Safety},
year = {2026},
month = oct,
doi = {10.1016/j.ecoenv.2026.120938},
url = {https://doi.org/10.1016/j.ecoenv.2026.120938},
note = {CC BY},
}
RIS
TY - JOUR
TI - Parental exposure to 1,2-benzisothiazol-3(2 H)-one induces intergenerational cardiac and ocular development toxicity in F
AU - Haiqin-Mao
AU - Qi Xie
AU - Guiying-Wei
AU - Mengjie-Shi
AU - Chao Zhong
AU - Jiaolong-Huang
AU - Pengxia-Yu
AU - Chunhui-Hu
AU - Jie Deng
AU - Peng Duan
PY - 2026
DA - 2026/10/25
JO - Ecotoxicology and Environmental Safety
DO - 10.1016/j.ecoenv.2026.120938
UR - https://doi.org/10.1016/j.ecoenv.2026.120938
AB - 1,2-Benzisothiazol-3(2 H)-one (BIT) is a widely utilised preservative in industrial applications and has been frequently detected in aquatic environments. The widespread occurrence and potential bioaccumulation of BIT in the environment raise significant ecological concerns. Although previous studies have addressed the embryonic toxicity of BIT, the intergenerational toxicity stemming from parental exposure to BIT remain inadequately understood. This study exposed parental zebrafish to BIT (300 ng/L and 300 μg/L) for 120 days to investigate its impact on the F 1 generation, focusing on embryonic development, histopathology, and transcriptomic profiling through comprehensive phenotypic and molecular assessments. Our results demonstrated that parental BIT exposure did not significantly affect hatchability or mortality in the F 1 offspring. However, it resulted in significant developmental impairments in F 1 larvae, manifested as increased deformity rates (yolk sac edema, shortened body length), cardiovascular developmental disorders (pericardial edema, increased Bulbus Arteriosus-Sinus Venosus distance, and decreased heart rate, blood flow velocity, and blood pressure), and ocular and visual developmental disorders (decreased ocular area, reduced movement velocity, and reduced total movement distance). RNA-sequencing analysis revealed a significant enrichment of pathways associated with cardiac muscle contraction, cardiac morphogenesis, and ocular development. Transcriptomic analysis identified organ-specific transcriptional alterations in F 1 larvae, including the dysregulation of genes essential for heart development ( vmhcl , cox4i1l , bag3 , brk1 ) and ocular development ( opn1mw2 , arr3a , arr3b ). Our findings indicate that parental BIT exposure can lead to embryonic developmental defects in F 1 larvae, thereby providing novel insights into the intergenerational toxicity of BIT.
SN - 0147-6513
SN - 1090-2414
ER -