Abstract
Chlorhexidine (CHX) is a bis-bis-guanide with anphipatic and antiseptic properties and is largely used in dentistry, mainly for management of periodontal problems and in oral pre-operatory procedures. The present study concerns the effect of CHX on lipid peroxidation, mitochondrial permeability transition (MPT), and the interaction of CHX with ferritin (HoSF). CHX (100 μM) increased iron release from HoSF by ∼13-fold when compared to control values. CHX also increased iron-dependent lipid peroxidation. MPT induced by CHX was protected by ethylene glycol-bis(β-aminoethyl-ether)- N, N, N′, N′-tetraacetic acid (EGTA), dithiothreitol (DTT), and cyclosporin A (CsA), showing a Ca 2+-dependent effect, in which oxidation of thiol groups is involved, as well as the involvement of the transmembrane proteinaceous pore. BHT, catalase or o-phenanthroline did not protect MPT induced by CHX. This suggests that a ROS-independent mechanism is involved in the induction of MPT.
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