Impaired development of female mouse offspring maternally exposed to simazine

• Maternal exposure to simazinae impairs normal development of female offspring.
• Body, ovarian, and uterine weights were decreased in female offspring.
• Their ovaries have increased apoptotic granulosa cells.
• Genes that regulate apoptosis and proliferation were downregulated in their ovaries.
• Simazine-induced suppression of viability and proliferation was confirmed in vitro.

Simazine is a suspected endocrine disruptor and the second most commonly detected pesticide in surface and groundwater worldwide. We evaluated the toxicity of simazine in female mouse offspring with in utero and lactational exposure to the agent. Pregnant mice were exposed to environmentally relevant doses (from 5 to 500 μg/kg) of simazine via oral administration, and their female offspring were then analyzed. The female offspring showed shortened anogenital distance and decreased whole body, ovarian, and uterine weights. Their ovaries showed increased apoptotic granulosa cells. In addition, expression of critical genes involved in regulation of cellular apoptosis and proliferation was significantly downregulated in the ovaries of simazine-exposed mice. Moreover, in vitro exposure of human granulosa cell-derived KGN cells to simazine (0.003–1 nM) resulted in decreased viability and proliferation. Thus, the present study demonstrates that maternal exposure to low doses of simazine impairs normal development of female offspring via disturbance of cellular apoptosis and proliferation.