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  3. Chlorphoxim

Chlorphoxim is a broad-spectrum and highly efficient insecticide. Chlorphoxim kills pests by inhibiting AChE. Chlorphoxim inhibits the activities of SOD and CAT in zebrafish embryos. Chlorphoxim induces oxidative stress in zebrafish embryos by activating ROS. Chlorphoxim induces apoptosis by upregulating the expression levels of Bax, Bcl2 and p53 in zebrafish embryos. Chlorphoxim exhibits neurotoxicity and developmental toxicity. Chlorphoxim is used in agricultural research for the control of various pests.

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Chlorphoxim

Chlorphoxim Chemical Structure

CAS No. : 14816-20-7

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Description

Chlorphoxim is a broad-spectrum and highly efficient insecticide. Chlorphoxim kills pests by inhibiting AChE. Chlorphoxim inhibits the activities of SOD and CAT in zebrafish embryos. Chlorphoxim induces oxidative stress in zebrafish embryos by activating ROS. Chlorphoxim induces apoptosis by upregulating the expression levels of Bax, Bcl2 and p53 in zebrafish embryos. Chlorphoxim exhibits neurotoxicity and developmental toxicity. Chlorphoxim is used in agricultural research for the control of various pests[1].

In Vivo

Chlorphoxim (2.5-12.5 mg/L; water immersion; 6 hpf to 96 hpf/6 dpf) induces dose-dependent developmental toxicity, neurotoxicity, oxidative stress and apoptosis in zebrafish embryos, with an LC50 of 8.4 mg/L[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: wild-type AB; Tg (sox10: GFP) transgenic (6 hours post-fertilization embryos)[1]
Dosage: 2.5 mg/L, 5 mg/L, 7.5 mg/L, 10 mg/L, 12.5 mg/L
Administration: aqueous immersion; continuous; 6 hpf to 96 hpf (most assays); 6 hpf to 6 dpf (motion analysis)
Result: 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.
Molecular Weight

332.74

Formula

C12H14ClN2O3PS

CAS No.
SMILES

N#CC(=NOP(=S)(OCC)OCC)C=1C=CC=CC1Cl

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