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Developmental toxicity and thyroid hormone-disrupting effects of acetyl tributyl citrate in zebrafish and Japanese medaka
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Researchers found that the non-phthalate plasticizer acetyl tributyl citrate (ATBC) caused developmental toxicity and disrupted thyroid hormone signaling in zebrafish and Japanese medaka embryos, suggesting it may not be a safe alternative to conventional phthalate plasticizers.
Chemical pollution from plasticizers in water environments is a serious environmental problem worldwide. Phthalate plasticizers have potential endocrine-disrupting effects in vertebrates. In this study, the effects of a non-phthalate acetyl tributyl citrate (ATBC) plasticizer on endocrine hormone activity (according to thyroid-related gene expression) and the developmental toxicity of ATBC were determined in zebrafish (Danio rerio) and Japanese medaka (Oryzias latipes) embryos. ATBC exposure increased the mortality of zebrafish and Japanese medaka at concentrations of 443.05 and 1,937.41 μg/L, respectively. Body curvature, edema, and growth inhibition were also observed after ATBC exposure in both species. Importantly, both species exhibited suppressed thyroid-related gene mRNA expression after ATBC exposure. ATBC exposure significantly suppressed the expression of thyroid-stimulating hormone beta subunit (tshβ), iodothyronine deiodinase 1 (dio1), dio2, and thyroid hormone receptor alpha (trα) in zebrafish. In Japanese medaka, ATBC exposure suppressed the mRNA expression of dio2, trα, and trβ but not tshβ and dio1. In summary, ATBC exposure inhibited thyroid-related gene expression and led to improper swim bladder inflation in the test species. This is the first report of a non-phthalate ATBC plasticizer inducing abnormal embryo development and disrupting thyroid hormone activity in fish.
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Tiny plastic particles (nanoplastics) fed to developing zebrafish embryos got absorbed into their bodies, disrupted thyroid hormone levels, and interfered with brain development—leading to problems like impaired eyesight, heart issues, and abnormal behavior. Even at very low doses (far below what you might expect matters), these effects showed up, and the researchers couldn't find a "safe" level where no harm occurred. Since zebrafish are a common stand-in for studying how chemicals affect early human development, this raises real concerns about whether the nanoplastics we're increasingly exposed to in food, water
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Researchers studied how polystyrene microplastics affect the toxicity of BHA, a synthetic antioxidant commonly used in plastics, on developing zebrafish. The study found that co-exposure to microplastics and BHA enhanced developmental toxicity by disrupting thyroid function and metabolism, suggesting that microplastics can amplify the harmful effects of their own chemical additives on aquatic organisms.
Combined Toxicities of Di-Butyl Phthalate and Polyethylene Terephthalate to Zebrafish Embryos
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Researchers exposed zebrafish embryos to polyethylene terephthalate microplastics and the plasticizer di-butyl phthalate, both alone and in combination. While the microplastics alone mainly delayed hatching, the plasticizer caused severe developmental abnormalities and death. The study found that the microplastics actually reduced the toxicity of the plasticizer by adsorbing it, though they also slowed its breakdown, creating a more persistent exposure risk.
Early-life exposure to five biodegradable plastics impairs eye development and visually-mediated behavior through disturbing hypothalamus-pituitary-thyroid (HPT) axis in zebrafish larvae
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Zebrafish exposed to five types of biodegradable plastic microplastics during early development showed impaired eye growth, damaged retinas, and disrupted thyroid hormone signaling. Some plastics also caused abnormal visual behavior, suggesting actual vision loss. These findings are important because biodegradable plastics are marketed as safer alternatives, yet they may still harm developing organisms, including potentially affecting human fetal development.
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