Trimethyltin can induce cell death in the entorhinal cortex of rat brain: a histological architecture and neuronal density evaluation of the neuroprotective role of lithium chloride.

Trimethyltin as a methylated organotin can induce selective neuronal death in the central nervous system of humans and rodents. On the other hand, lithium has neuroprotective and neurotrophic effects. Therefore, the aim of this study was to evaluate the neuroprotective effects of lithium chloride on neuronal density in the entorhinal cortex of rat brain after trimethyltin intoxication. Thirty male Sprague-Dawley rats were divided into three equal groups: control, trimethyltin (8 mg/kg, single dose, intraperitoneally), and trimethyltin + lithium chloride (single dose of 8 mg/kg of trimethyltin + 20 mg/kg lithium chloride for 14 consecutive days, intraperitoneally). At the end of the experiment, the entorhinal cortex histopathological examination was performed in all rats of each group. Our results showed that the neural density of the entorhinal cortex in trimethyltin and trimethyltin + lithium chloride groups was significantly decreased in comparison to control group in the levels of P < 0.01 and P < 0.05, respectively. Also, there was a significant increase in the neural density of the entorhinal cortex in trimethyltin + lithium chloride group against trimethyltin group ( P < 0.05). These results demonstrated that chronic administration of lithium chloride had significant effects in amelioration of trimethyltin-induced cell death in the entorhinal cortex of rat brain. [ABSTRACT FROM AUTHOR]