The effect of aluminium on NTPDase and 5′-nucleotidase activities from rat synaptosomes and platelets

Aluminium (Al), a neurotoxic compound, has been investigated in a large number of studies both in vivo and in vitro. In this study, we investigated the effect in vivo of long-term exposure to Al on NTPDase (nucleoside triphosphate diphosphohydrolase) and 5′-nucleotidase activities in the synaptosomes (obtained from the cerebral cortex and hippocampus) and platelets of rats. Here, we investigated a possible role of platelets as peripheral markers in rats. Rats were loaded by gavage with AlCl3 50 mg/(kg day), 5 days per week, totalizing 60 administrations. The animals were divided into four groups: (1) control (C), (2) 50 mg/kg of citrate solution (Ci), (3) 50 mg/kg of Al plus citrate (Al + Ci) solution and (4) 50 mg/kg of Al (Al). ATP hydrolysis was increased in the synaptosomes from the cerebral cortex by 42.9% for Al + Ci and 39.39% for Al, when compared to their respective control (p < 0.05). ADP hydrolysis was increased by 13.15% for both Al and Al + Ci, and AMP hydrolysis increased by 32.7% for Al and 27.25% for Al + Ci (p < 0.05). In hippocampal synaptosomes, the hydrolysis of ATP, ADP and AMP, was increased by 58.5%, 28.5% and 25.92%, respectively, for Al (p < 0.05) and 36.7%, 22.5% and 37.64% for Al + Ci, both when compared to their respective controls. ATP, ADP and AMP hydrolysis, in platelets, was increased by 172.3%, 188.52% and 92.1%, respectively in Al + Ci, and 317.9%, 342.8% and 177.9%, respectively, for Al, when compared to their respective controls (p < 0.05). Together, these results indicate that Al increases NTPDase and 5′-nucleotidase activities, in synaptosomal fractions and platelets. Thus, we suggest that platelets could be sensitive peripheral markers of Al toxicity of the central nervous system.