Ferroptosis,a newly defined programmed cell death,is different from classic apoptosis and necrosis.It is charac-terized by intracellular iron accumulation,severe lipid peroxidation,and typical mitochondrial morphological and functional chan-ges.Mitochondrial cascade reactions inducing oxidative stress and neuronal death are important events during the pathogenesis of Alzheimer's disease(AD).This review mainly summarized research advances of the role and mechanism of intracellular iron metabolism,mitochondrial lipid metabolism and amino acid metabolism abnormalities in neuron ferroptosis during progress of AD.

The effects of manganese on selenium content and glutathione peroxidaseactivity in blood and myocardium, and on selenium excretion in growing ratswere studied to ferret out the interaction of the two essential trace elements.Manganese dichloride (40mg/kg of MnCl2.4H2O) was administered daily to a group of 17 rats for 35 days intraperitoneally. An obvious increase in manganese content in serum and myocardium was induced. However, selenium levels in the two tissues of manganese-treated rats were significantly lower than the controls. From the 14th day on, glutathione peroxidase activities in whole blood of manganese-treated rats were below the controls, and on the 35th day, the activities of the selenium-containing enzyme in blood and myocardium were reduced by 29.33% (P

In this study, the effects of overvitamin D on cardiac lesions and the protective effects of zinc on them were studied. The results showed that cardiac MDA and calcium were significantly increased and cardiac lesions were characterized by nonspecial focal necrosis, accompaning with myofib-eral and interstitial calcification. Zinc could remarkably decrease cardiac MDA and calcium and the cardiac lesions were also much milder. It suggested that cardiac lesions induced by overvitamin D related to both cardiac lipid peroxide and calcium overload. It might be concluded that zinc could protect heart from overvitamin D intoxication.