RESUMEN
In the title compound, [RuCl(C(10)H(14))(C(14)H(16)N(2))]PF(6), the aromatic ring of the isopropyl-methyl-benzene fragment shows an η(6)-arene coordination to the ruthenium atom. Its coordination sphere is completed by a chloride ligand and 2-(sec-butyl-imino-meth-yl)quinoline. The dihedral angle between the η(6)-arene ring and the quinoline Schiff base is 45.64â (9)°. The sec-butyl substituent and the PF(6) (-) anion are disordered over two positions with ratios of 0.595â (11):0.405â (11) and 0.752â (8):0.248â (8), respectively.
RESUMEN
Acute and subacute administration of zinc exert neuroprotective effects in hypoxia-ischemia animal models; yet the effect of chronic administration of zinc still remains unknown. We addressed this issue by injecting zinc at a tolerable dose (0.5 mg/kg weight, i.p.) for 14 days before common carotid artery occlusion (CCAO) in a rat. After CCAO, the level of zinc was measured by atomic absorption spectrophotometry, nitrites were determined by Griess method, lipoperoxidation was measured by Gerard-Monnier assay, and mRNA expression of 84 genes coding for cytokines, chemokines, and their receptors was measured by qRT-PCR, whereas nitrotyrosine, chemokines, and their receptors were assessed by ELISA and histopathological changes in the temporoparietal cortex-hippocampus at different time points. Long-term memory was evaluated using Morris water maze. Following CCAO, a significant increase in nitrosative stress, inflammatory chemokines/receptors, and cell death was observed after 8 h, and a 2.5-fold increase in zinc levels was detected after 7 days. Although CXCL12 and FGF2 protein levels were significantly increased, the long-term memory was impaired 12 days after reperfusion in the Zn+CCAO group. Our data suggest that the chronic administration of zinc at tolerable doses causes nitrosative stress, toxic zinc accumulation, and neuroinflammation, which might account for the neuronal death and cerebral dysfunction after CCAO.