Selenium forms and dosages determined their biological actions in mouse models of Parkinson’s disease

Abstract

Selenium (Se), an essential antioxidant trace element, is reported to play a role in Parkinson’s disease (PD). However, there is a lack of systematic studies on different Se forms against PD. Our study is designed to compare the neuroprotective effects of inorganic and organic Se in two classical PD mice models and investigate the underlying mechanisms for their potentially differential actions against PD. In this study, different dosages of inorganic sodium selenite (Se-Na) or organic seleno-L-methionine (Se-Met) were fed to either acute or chronic PD mice models, and their neuroprotective effects and mechanisms were explored and compared. Se-Na provided better neuroprotective effects in PD mice than Se-Met administered at the same but at a relatively low Se dosage. Se-Na treatment could influence GPX activities but not their mRNA expressions in the midbrains of PD mice. The enhanced GPX activities caused by Se-Na, but not Se-Met, in PD mice could be the major reason for the positive actions of inorganic Se to prevent dopaminergic neuronal loss in this study. In vivo bio-distribution experiments found MPTP injection greatly changed Se bio-distribution in mice, which led to reversed alterations in the bioavailability of Se-Met and Se-Na. Se-Na had higher bioavailability than Se-Met in PD mice, which could explain its better neuroprotective effects compared to Se-Met. Our results proved that Se forms and dosages determined their biological actions in mouse models of PD. Our study will provide valuable scientific evidence to researchers and/or medical professionals in using Se for PD prevention or therapy.