Objectives To investigate the effect of Subchronic Aluminum-MaltolateAl(mal)3 exposure on neuron ferroptosis in rats and its possible mechanism.
Methods 18 healthy male Specific Pathogen Free (SPF) Sprague-Dawley (SD) rats were chosen and randomly divided into three groups according to their body weights: the control (saline) group and the 9 and 18 μmol/kg Al(mal)3 treated groups with 6 rats in each group. Rats in the control group received intraperitoneal (ip.) injections of 0.9 % normal saline and rats in 9 and 18 μmol/kg Al(mal)3 treated groups received ip. administrations of these two doses respectively once a day for 90 days. The learning and memory abilities as well as the general activities of rats were tested with Morris Watermaze (MWM) and Open Field Test (OFT). The changes of mitochondria ultrastructure in neurons of rats were observed by Transmission Electron Microscopy (TEM). The contents of GSH and Fe in animal brain tissue were detected using glutathione (GSH) test kit and tissue iron test kit.
Results Compared with the control group, the time of finding platform site of each exposed group was significantly and gradually prolonged. In the OFT, compared with the control group, the retention time in the center of the arena in the exposed groups was significantly prolonged and the number of erect times decreased obviously(P < 0.05).The neuron of rats in the exposed groups showed specific characteristic changes of ferroptosis with shrinkage of mitochondria, increase of mitochondrial membrane density and disappearance of mitochondrial ridge under the TEM. With the increase of dose, the content of GSH in neurons decreased gradually, while the content of Fe increased gradually compared with the control group (P < 0.05).
Conclusions Subchronic exposure to Al(mal)3 can lead to ferroptosis in neurons of rats, and the decrease of GSH content and the increase of Fe content in brain tissue maybe important mechanisms of neuron ferroptosis induced by exposure to aluminum.
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