Carbosulfan exposure during embryonic period can cause developmental disability in rats

• Carbosulfan forms toxic metabolites which are harmful.
• Exposure during pregnancy can affect neurodevelopment.
• Oxidative damage induced by carbosulfan can alter behavior.
• Sensorimotor changes, anxiety and oxidative damage to cerebellum was observed.
• Embryonic period is sensitive to carbosulfan.

Carbosulfan, a wide spectrum pesticide is used to improve crop productivity. During their application, they disperse in the environment exerting harmful consequences on human health. We speculated that exposure to carbosulfan, a carbamate insecticide during early development can affect neurogenesis and synaptic development. In order to test this, pregnant dams were exposed to carbosulfan in four doses (0.5, 1, 2, and 4 mg/kg) during the embryonic period (ED 1–15). Offspring were evaluated for neurobehavioral changes, oxidative markers, acetylcholinesterase levels, and formation of carbonylated proteins. Histopathology of the cerebellum was carried out. Carbosulfan exposure produced alteration in sensorimotor tasks, motor function and elevated anxiety in pups. Carbosulfan affected growth rate of pups in a dose dependent manner. A significant increase in malondialdehyde, a lipid peroxide marker, carbonylated proteins and a dose dependent decrease in the levels of glutathione and glutathione peroxidase were observed. Carbosulfan produced a decline in acetylcholinesterase levels which might contribute to poor exploratory behavior. Distinct changes in the Purkinje cells were observed as the dose of carbosulfan increased. Largely, alteration in behavior can be due to oxidative damage, thereby, affecting neurogenesis, synaptogenesis and myelination. Therefore the propensity of carbosulfan to induce developmental disability is high and should be cautiously avoided during embryonic development.