Multi-omics reveals the hepatic metabolic mechanism of neurological symptoms caused by selenium exposure in Przewalski's gazelle (Procapra przewalskii).

Neurological symptoms resulting from selenium(Se) exposure significantly impact the health and conservation of Przewalski's gazelle. In this study, we performed proteomic and metabolomic analyses of the liver in Przewalski's gazelle for the first time, aiming to reveal the hepatic metabolic mechanisms underlying the neurological symptoms caused by Se exposure. We identified 89 differentially expressed proteins and 30 metabolites with altered regulation. Using multi-omics integrated analysis, we identified a neurofunctional regulation network composed of three metabolic pathways, with (S)-3-amino-2-methylpropionate transaminase being the key enzyme in the regulatory network. Molecular docking revealed that the binding of selenocysteine to (S)-3-amino-2-methylpropionate transaminase may act as a key factor in activating this regulatory network. Consequently, these findings provide important insights into the molecular mechanisms of neurological symptoms caused by Se exposure and have significant implications for the conservation in Przewalski's gazelle.