Fig. 5.

Se deficiency induced a hepatic redox imbalance via the regulation of selenoproteins at both the mRNA and protein level and blocks the GSH system. (A–F) A Se deficiency induced a hepatic redox imbalance by decreasing the anti-oxidant capacity and increasing ROS levels (n = 12). (G–I) The mRNA expression of 14 selenoprotein genes were significantly decreased in response to a Se deficiency, while one was significantly increased (SEPHS2) (n = 9). (J) Global proteomics identified five selenoproteins, which were all significantly decreased and in line with the transcription (n = 5). (K, L, M, and N) Targeted metabolomics and RNA sequencing showed that the metabolites and mRNA of the genes involved in the GSH system and related pathways were substantially changed, indicating a blocked GSH system (n = 10 and n = 3 for metabolites and mRNA, respectively). (O) The integrated redox parameters, targeted metabolome, global proteome, and transcriptome revealed that a Se deficiency induced a redox imbalance via regulation of selenoproteins at both the mRNA and protein level and their post-transcriptional regulations, which then blocked the GSH system and increased ROS. The green and red color represents the decreased and increased metabolites or transcripts in the Se-D group, compared with that in the Se-A group. Data are represented as mean ± SEM. The white and black bar represents the Se adequate (Se-A) and deficient (Se-D) group, respectively. *P < 0.05; **P < 0.01; ***P < 0.001). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)