Abstract: The cerebral tissue injury induced by ischemia and reperfusion or trauma has been considered to be due to over production of oxygen free radicals (OFRs). The aim of this study was to evaluate the effects of schisanhenol (Sal) on Fe²⁺-cysteine (Cys) induced injury of rat cerebral mitochondria and synaptosomes in vitro. Incubation of cerebral mitochondria or synaptosomes with Fe²⁺-Cys at 37℃ resulted in an increase of malondiadehyde (MDA) formation and decrease of ATPase activity. Sal(10^-4 mol·L^-1) completely inhibited Fe²⁺-Cys induced increase of MDA formation of mitochondria and synaptosomes as well as the loss of ATPase activity of mitochondria. The swelling of mitochondria and reduction of membrane fluidity of mitochondria and synaptosomes induced by Fe²⁺-Cys were also prevented by Sal. Sal(10^-5mol·L^-1) was shown to siganificantly inhibit the decrease of synaptosomal GSH content induced by H₂O₂. The electron micrographs also showed that Sal markedly reduced the pathological damage of mitochondria and synaptosomes induced by Fe²⁺-Cys. The results suggest that Sal has protetive action against Fe²⁺-Cys induced injury of rat cerebral mitochondria and synaptosomes.