2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent organic pollutant (POP) known for pronounced developmental and reproductive toxicity in humans, rodents, and fish. We previously determined that sublethal juvenile exposure in zebrafish (50 parts per trillion; 3- and 7-weeks post fertilization) resulted in transgenerational male-mediated infertility. Here, we used the same exposure paradigm to investigate potential effects on sperm motility and whole-body steroid and thyroid hormone levels contributing to infertility. In progressive sperm collected from developmentally exposed fish, velocity measures (VCL, VSL, VAP) were significantly decreased, while remaining kinematic parameters (LIN, STR, WOB, ALH, and BCF) were unaffected. Temporal analysis over four ten-second intervals revealed differential kinematics in exposed sperm. All three velocity metrics at both early (1) and late (4) timepoints were significantly decreased in progressive sperm of exposed fish, while kinematic parameters LIN, STR, and WOB were decreased at the final timepoint (4) only. Corresponding with motility outcomes, sperm structural genes were downregulated in spermatozoa cell clusters. Vitellogenin was significantly increased in whole-body homogenates of exposed adult males, while cortisol, 11-ketotestosterone (11-KT), testosterone, triiodothyronine (T3), and thyroxine (T4) levels were unaffected. While adverse reproductive outcomes of TCDD exposure are well-studied in fish, ours is the first to use CASA (computer-aided sperm analysis) to characterize impacts of TCDD exposure in fish. Vitellogenin induction and deficits in progressive sperm motility in male fish over 10 months after the initial exposure highlight the persistence of endocrine and reproductive dysregulation in these developmentally exposed fish, with concerning implications for sensitive populations in contaminated environments.
Keywords: CASA; Reproductive toxicology; Sperm motility; TCDD; Vitellogenin; Zebrafish; scRNAseq.
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