Endosulfan increases IL-1β, IL-6, IL-17, and TNF-α production in pregnant rats and causes fetal brain cell apoptosis

Endosulfan is a persistent organic pollutant commonly used as an insecticide in Indonesia. It has been reported to cause teratogenic effects, i.e., to decrease humoral activity, produce inflammation, and induce apoptosis in various type of cells. This study investigated the effect of endosulfan on the expression of IL-1β, IL-6, IL-17, and TNF-α in rats (Rattus norvegicus), as well as the incidence of fetal brain cell apoptosis. This experiment was carried out on pregnant rats divided into 4 groups: negative control (I), endosulfan: 1 mg/kg (II), 10 mg/kg (III), and 50 mg/kg (IV). The solution of endosulfan was given daily during the 20-day test period. Rat serum was collected for the measurement of IL-1β, IL-6, IL-17, and TNF-α using the ELISA kit. Fetal rat brains were taken and stained with Annexin V for apoptosis detection. The proinflammatory cytokine levels in Groups II, III, and IV were higher than in Group I, with significant increases of IL-1β (p = 0.016), IL-6 (p = 0.009), IL-17 (p < 0.001), and TNF-α (p < 0.001). The intensity of Annexin V in 4 groups of rats showed that the incidence of apoptosis increased with increasing endosulfan doses. In conclusion, the administration of endosulfan in pregnant rats increased the expression of IL-1β, IL-6, IL-17, and TNF-α and triggered apoptosis in fetal brain cells.