Galbanic acid mitigates hippocampal cell death and memory impairment in lead-exposed prepubertal rats via antioxidant mechanisms.

The developmental neurotoxicity of lead, a result of its adverse effects on the developing nervous system, is associated with various mechanisms. One such mechanism involves the disturbance of the equilibrium between pro-oxidants and antioxidants within the developing brain which can be ameliorated with natural antioxidants. The aim of this study was to investigate the potential protective effects of Galbanic acid (GA) on lead acetate-induced developmental neurotoxicity in pre-pubertal rats. In this experimental study, 32 prepubertal immature male rats divided into 4 groups (n = 8); group 1 (control): rats received deionized drinking water, group 2 (Pb acetate): rat received deionized drinking water containing 0.3% lead acetate, group 3 (Pb acetate + GA): rats received deionized drinking water containing 0.3% lead acetate with 1 mg/kg of GA by gavage every other day, group 4 (GA): rats received deionized drinking water with a dose of 1 mg/kg of GA. Lead acetate exposure resulted in spatial memory deficits (p < 0.01), increase in lead concentration (p < 0.001), ROS levels by 150% (p < 0.001) and MDA levels by 200% (p < 0.001). Lead acetate also caused histopathological changes in the Cornu Ammonis 1 and 3 (CA1 and CA3) regions of hippocampus (p < 0.001), while also impairing mitochondrial function and inducing 15% mitochondrial membrane potential (MMP) collapse (p < 0.001). However, co-administration of GA alongside lead acetate significantly ameliorated these effects, demonstrating improvements in spatial memory (p < 0.01), ROS generation (p < 0.001), MDA levels (p < 0.001), and histological changes (p < 0.001). These findings highlight the antioxidant properties of GA and suggest its therapeutic potential in mitigating oxidative stress related damage.