Chlorphoxim

wild-type AB; Tg (sox10: GFP) transgenic (6 hours post-fertilization embryos)^[1]

2.5 mg/L, 5 mg/L, 7.5 mg/L, 10 mg/L, 12.5 mg/L

aqueous immersion; continuous; 6 hpf to 96 hpf (most assays); 6 hpf to 6 dpf (motion analysis)

Determined 96 hpf 50% lethal concentration (LC₅₀) as 8.4 mg/L, with mortality increasing in a dose-dependent manner.
Reduced hatchability rate to 76.7%, decreased average heart rate to 50 beats/20 s, and induced pericardium edema in 33.3% of embryos at 7.5 mg/L at 96 hpf.
Reduced sox10-GFP fluorescence intensity, caused enlarged cerebral ventricles, increased intercellular spaces, and decreased neonatal neurons in the brain of Tg (sox10: GFP) embryos at 2.5-7.5 mg/L at 96 hpf.
Reduced total distance traveled, movement time, average speed, motion frequency, and maximum acceleration in a dose-dependent manner at 2.5-7.5 mg/L at 6 dpf; measured acetylcholinesterase (AChE) activity as 1.0 U/mgprot at 7.5 mg/L at 6 dpf.
Altered neurodevelopmental gene expression at 7.5 mg/L: syn2a (0.33-fold of control), gfap (0.32-fold), elavl3 (3.2-fold), neurog (0.59-fold), gap43 (0.64-fold), sox19b (1.41-fold).
Significantly increased reactive oxygen species (ROS) fluorescence intensity at 7.5 mg/L; reduced superoxide dismutase (SOD), malondialdehyde (MDA), and catalase (CAT) activities to 0.68-fold, 0.55-fold, and 0.64-fold of control, respectively, at 7.5 mg/L.
Increased p53 protein level, elevated Bax expression, and increased Bax/Bcl2 ratio at 7.5 mg/L; showed increased apoptotic brain cells via acridine orange (AO) staining at 7.5 mg/L.