Dietary selenium insufficiency induces cardiac inflammatory injury in chicks1-3

Background Laying hens undergo intensive metabolism and are vulnerable to cardiac insults. Past research demonstrated overt heart disorders of broiler chickens induced by dietary Se deficiency. Objective This study was to reveal effects and mechanism of dietary Se insufficiency on cardiac injuries of egg-type chicks in their early life. Methods White Leghorn chicks (0-day-old, female) were fed a corn-soy, Se-insufficient basal diet (BD, 0.05 mg Se/kg, n = 11) or the BD supplemented with 0.3 mg Se/kg (as sodium selenite, n = 8) for 35 days. Cardiac tissues were collected at the end of study for histology and to determine its relationship with heart Se contents, selenoprotein expression profiles, antioxidant and inflammatory status, and the Toll-like receptor 4/extracellular signal-regulated kinases/p38 map kinase/ C-Jun N-terminal kinase (TLR4/ERK/P38/JNK) pathway. Results Compared with those fed 0.35 mg Se/kg, chicks fed BD had significantly lower body weights and average daily gain, and 28% lower heart Se than Se-supplemented chicks, and developed cardiac mononuclear inflammatory cell infiltration, along with elevated (P < 0.05) serum levels of creatine kinase, aldolase, and interleukin-1. The BD decreased (P < 0.05) body weight and heart glutathione contents and expression of selenoproteins, but increased (P < 0.05) heart levels of malondialdehyde and reactive oxygen species. These changes were associated with increased (P < 0.05) mRNA and (or) protein levels of cyclooxygenases, lipoxygenase-12, cytokines (IL-1β), nuclear factor kappa B subunit (NF-κB), chemokines, and receptors (CCL20, CXCR1, CXCLI2), and increased (P < 0.1) TLR4/ERK /P38/JNK in the heart of Se-insufficient chicks. Conclusion Dietary Se insufficiency induced infiltration of mononuclear inflammatory cells in the heart of egg-type chicks. This cardiac injury was mediated by decreased functional expressions of selenoproteins which resulted in apparent elevated oxidative stress and subsequent activations of the TLR4 pathway and NF-κB.