RESUMEN
H2S plays vital roles in modulation brain function. It is associated with antioxidant and anti-inflammatory properties. We assessed the H2S impact on spatial learning and memory deficit and cell death due to lead exposure, and probable mechanisms of action. The 36 male Wistar rats that (200-220 g), were in random assigned to 3 groups, control group (12 rats), lead acetate group (12 rats), and lead acetate +H2S groups (NaHS as a H2S donor; 5/6 mg/kg; 12 rats). Administration of lead to rats was performed through acute lead poisoning (25 mg/kg of lead acetate, IP through 3 days). Using male Morris water maze, their spatial learning and memory function were measured. We carried out ELISA method to calculate TNF-α and antioxidant enzymes level. Immunohistochemical staining was applied for evaluating the caspase-3 expression levels. Treatment with H2S improved learning and memory impairment in Pb-exposed rats (P<0.05). H2S treatment suppressed Pb-related apoptosis in the hippocampal CA1 subfield (P<0.01). Also, the TNF-α over-expression in the CA1 region of hippocampus due to lead exposure showed a significant reduction (P<0.05) after administrating H2S. Simultaneously, H2S treatment reduced the MDA levels, enhanced SOD, GSH level than the Pb-exposed group in hippocampus (P<0.05). H2S was able to significantly improve Pb-related spatial learning and memory deficit, and neuronal cell death in the CA1 region of hippocampus in the male rats at least partly by reducing oxidative stress and TNF.