2026-10-02 九州大学
短鎖PFASの一種PFBSは、ゼブラフィッシュにおいて代謝異常と細胞ストレスを引き起こし、発生に影響を及ぼす可能性が示唆された。 ※本画像は、謝准教授のアイデアをもとにChatGPTで作成しています。
＜関連情報＞
- https://www.kyushu-u.ac.jp/ja/researches/view/1589
- https://www.sciencedirect.com/science/article/pii/S2772416626005875
ペルフルオロブタンスルホン酸は代謝ストレスを誘発し、ゼブラフィッシュ胚の細胞ストレスおよび発生異常を引き起こす Perfluorobutane sulfonate induces metabolic stress leading to cellular stress and developmental defects in zebrafish embryos
Zulvikar Syambani Ulhaq, Delbert Almerick T. Boncan, Da-Wei Liu, Chen Hsu, Jingru Qin, Jen‐Kun Chen, May-Su You, Ting Fung Chan, Yukiko Ogino, Yun-Jin Jiang, Keng Po Lai, William Ka Fai Tse
Journal of Hazardous Materials Advances Available online: 23 September 2026
DOI:https://doi.org/10.1016/j.hazadv.2026.101596
Highlights
- PFBS exposure disrupts metabolic homeostasis in developing embryos.
- Metabolic stress occurs before cellular dysfunction and developmental toxicity.
- Early developmental stages are highly sensitive to short-chain PFAS.
- Toxicity occurs despite the presumed safety of PFBS alternatives.
- Findings support pathway-based risk assessment of emerging PFAS.
Abstract
Perfluorobutane sulfonate (PFBS) is a short-chain per- and polyfluoroalkyl substance (PFAS) widely adopted as a substitute for restricted long-chain homologs. Despite its increasing prevalence, the mechanisms underlying PFBS-induced developmental toxicity remain incompletely understood. Using an integrated zebrafish model, we demonstrate that PFBS bioaccumulates and disrupts metabolic homeostasis, including hyperglycemia associated with impaired insulin signaling and dysregulated lipid metabolism. Alterations in metabolic pathways, together with disturbances in the tricarboxylic acid (TCA) cycle, were accompanied by increased cytosolic oxidative stress, lipid peroxidation, and apoptosis. These metabolic and oxidative alterations were associated with impaired organ development and function. Major outcomes included cardiac contractile deficits with reduced cardiac output, craniofacial abnormalities associated with collagen suppression, neurodevelopmental defects involving altered neural patterning and axonal integrity, and selective rod photoreceptor loss accompanied by visual dysfunction. Collectively, these findings support a mechanistic framework in which PFBS-induced metabolic dysregulation contributes to oxidative stress and multi-organ developmental toxicity, highlighting the need for continued toxicological evaluation of short-chain PFAS alternatives.
