Delayed in sensorimotor reflex ontogeny, slow physical growth, and impairments in behaviour as well as dopaminergic neuronal death in mice offspring following prenatally rotenone administration.

Abstract

The environment is varying day by day with the introduction of chemicals such as pesticides, most of which have not been effectively studied for their influence on a susceptible group of population involving infants and pregnant females. Rotenone is an organic pesticide used to prepare Parkinson's disease models. A lot of literature is available on the toxicity of rotenone on the adult brain, but to the best of our knowledge, effect of rotenone on prenatally exposed mice has never been investigated yet. Therefore, the recent work aims to evaluate the toxic effect of rotenone on mice, exposed prenatally. We exposed female mice to rotenone at the dose of 5mg/Kg b.w. throughout the gestational period with oral gavage. We then investigated the effects of rotenone on neonate's central nervous systems as well as on postnatal day (PD) 35 offspring. In the rotenone group, we observed slow physical growth, delays in physical milestones and sensorimotor reflex in neonates and induction of anxiety and impairment in cognitive performances of offspring at PD-35. Additionally, immunohistochemical analysis revealed a marked reduction in TH-positive neurons in substantia nigra. Histological examination of the cerebellum revealed a decrease in Purkinje neurons in the rotenone exposed group as compared to the control. The data from the study showed that prenatally exposure to rotenone affects growth, physical milestones, neuronal population and behaviour of mice when indirectly exposed to the offspring through their mother. This study could provide a great contribution to researchers to find out the molecular mechanism and participating signalling pathway behind these outcomes.