The effect of Gallic acid on prenatal entorhinal cortex and CA1/CA3 hippocampal areas in trimethyltin intoxication rat

Prenatal intoxication with trimethyletin (TMT) induces widespread neuronal death in the central nervous system by inducing oxidative stress. The aim of this study was to evaluate the antioxidant effect of gallic acid (GA) on the neuronal density of the entorhinal cortex, hippocampal pyramidal cells and oxidative stress parameters in the fetal forebrain following TMT intoxication.

25 pregnant Wistar female rats were randomly divided into 5 groups, including control, TMT+Saline, TMT+GA100, TMT+GA200 and TMT+GA400. To induce TMT intoxication, TMT (9 mg/kg body weight) was injected intraperitoneally into pregnant rats on embryonic day (ED) 14. From the ED12 to ED18, the treatment groups received orally GA at different doses. After fetal cesarean section on the ED21, neuronal density assessment of the entorhinal cortex, CA1 and CA3 regions of the hippocampus and forebrain level of catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) was performed by ELISA.

The results showed a significant increase in the activity of CAT and SOD enzymes and a significant decrease in MDA in the forebrain of GA-receiving groups compared to the TMT + Saline group. In addition, increased neuronal density was observed in the entorhinal cortex and CA1/CA3 regions of the hippocampus in the GA treated rats compared to the TMT + Saline group.

Prenatal TMT intoxication induced oxidative stress in the fetal forebrain, causing damage to the entorhinal cortex and hippocampus of rat fetal brain. On the other hand, GA prevented and improved neuronal damage in these areas of the fetal brain.