Temephos

Temephos (Temefos) is an orally active, blood-brain barrier-permeable organophosphate insecticide and AChE inhibitor. By irreversibly inhibiting AChE to induce cholinergic overactivation, Temephos effectively blocks larval development of Aedes aegypti (yellow fever mosquito) and Aedes albopictus (Asian tiger mosquito), and is commonly used in studies related to Dengue Virus, Zika Virus and other relevant pathogens. Temephos exhibits genotoxicity and neurodevelopmental toxicity, and may also cause liver injury, reproductive system abnormalities and cholinergic poisoning symptoms in mammals. Temephos tends to accumulate in adipose tissues and aquatic organisms, and is excreted via feces after metabolism through oxidation and hydrolysis. Note that CYP-mediated metabolic detoxification may reduce the actual larvicidal efficacy of Temephos against some mosquito species. Temephos can be used in research related to dengue fever, Zika virus disease, chikungunya and dracunculiasis^[1][2][3][4].
In Vitro:Temephos (10 μM) exerts extremely weak genotoxic effects on human lymphocytes and HepG2 cells, and induces DNA fragmentation in blood cells; however, such toxicity is weaker than that of 0.05% DMSO (HY-Y0320C)^[1].
Temephos (0.01-0.15 ppm; 24 h) exhibits an LC₅₀ value 15-fold higher and an LC₉₅ value 14-fold higher in temephos-resistant Aedes aegypti (Cucuta strain) than in the susceptible New Orleans strain, with an LC₅₀ of 0.066 ppm and an LC₉₅ of 0.18 ppm^[3].
Co-incubation with temephos (0.05-0.15 ppm; 24 h) and 0.5 ppm DEF increases the sensitivity of temephos-resistant Aedes aegypti (Cucuta strain) to temephos by 36-fold, reducing the LC₅₀ of temephos to 0.0019 ppm^[3].
When applied in the field, Temephos (1 ppm; 24 h) maintains 100% mortality of temephos-resistant Aedes aegypti (Cucuta strain) for 8 weeks without water change, but the mortality decreases with two water changes per week^[3].
Temephos (LC₆₀; 24 h) induces overexpression of CYP6N12, CYP6M11 and CYP6F3 in temephos-resistant Aedes aegypti (Cucuta strain) larvae^[3]. In Vivo:Temephos (0.0043 mg/kg; daily; 18 consecutive days during gestation) exhibits a low-level, concentration-dependent genotoxic effect in pregnant Swiss mice during mid-gestation without causing fetal physiological malformations^[1].
Temephos (50 mg/kg; days 6-13 of gestation) causes hyperactivity and impaired social interaction in offspring of pregnant Swiss mice, indicating neurodevelopmental toxicity^[1].
Temephos (100 ppm; dietary; continuous exposure via feed) reduces offspring duckling weight and increases liver damage indicators in mallard hens without causing miscarriage or fetal deformities^[1].
Temephos (10-100 ppm; via drinking water) at 100 ppm is toxic to mallard ducklings, increasing mortality and inhibiting AChE activity, while 10 ppm does not increase mortality^[1].
Temephos (LC₅₀ concentration; egg exposure) causes general growth reduction in mallard embryos without inducing organ-specific defects or deformities^[1].
Temephos (2.3-100 mg/kg/day; up to 44-90 days) exhibits a no-observed adverse effect level of 2.3 mg/kg/day over 90 days and a lowest observable adverse effect level of 100 mg/kg/day over 44 days in rats, with additional low-dose toxic effects including genotoxicity, reproductive harm, and liver damage^[2].
Temephos (300 mg/kg; p.o.; single dose) is well absorbed, extensively metabolized into reactive metabolites including Tem-oxons and Tem-dioxons, widely distributed across rat tissues with preferential accumulation in fat, eliminated with an 8.6-hour elimination half-life, and produces temephos-sulfone-monohydrolyzed, which remains stable in blood until 36 hours, accumulates in the kidney, and may serve as an exposure biomarker^[4].