Efeitos da rutina sobre a atividade da aceticolinesterase e sobre o comportamento em ratos expostos ao cádmio

Abstract

This study investigated the effect of administration of cadmium (Cd), Rutin (Rut), or both, on lipid peroxidation in different brain structures, memory, anxiety and activity of the enzyme acetylcholinesterase (AChE) (ex vivo, in vitro and kinetic). The rats received Cd (2 mg / kg) and Rut (40 and 80 mg / kg) by gavage for 21 administrations on alternate days. To the ex vivo study, the animals were divided into six groups (n = 10): saline/saline, saline/Rut40, saline/Rut80, Cd/saline, Cd/Rut40 and Cd/Rut80. The trials of AChE in vitro were performed at concentrations of 1, 5, 10, 25 and 50 mM of Rut in rat brain homogenate controls. The same concentrations were used for kinetic analysis of Electroforus electricus (E.e.AChE). Cd increased lipid peroxidation in all structures analyzed except in the striatum. Rut reversed this effect only in the hypothalamus and hippocampus. Cd caused a decrease in test step-down latency and administration of Rut (40 and 80 mg/kg) reversed this effect of Cd. Cd increased the number and the percent of entries in enclosed arms of plus-maze, suggesting an anxiogenic effect of Cd. Rut (40 and 80 mg/kg) reversed the anxiogenic effect of Cd. Rats that were exposed to Cd and/or treated with Rut showed no altered sensitivity to shock, nor the locomotor activity. The ex vivo activity of the enzyme AChE increased in the cortex and hypothalamus of rats that received only Cd. Rut reversed this increase in both doses. In vitro activity of the enzyme AChE was inhibited at all concentrations of synaptosome cortex, cerebellum, striatum, hippocampus and hypothalamus. The kinetic analysis of the interaction between the Rut and E.e.AChE showed a competitive inhibition. The findings show that treatment with Rut decreased oxidative damage to the membrane, prevented the increase in AChE activity, reversed the memory deficit and anxiety caused by Cd. Moreover, characterized Rut as an inhibitor of AChE, showing that this flavonoid may modulate cholinergic neurotransmission and, consequently, improve cognition.