ABSTRACT
The current NRC dietary selenium (Se) requirement (0.15 mg/kg) of broilers from 22 to 42 d of age is primarily based on a previous study reported in 1986, which might not be applicable to modern classes of rapidly growing broilers. The present experiment was conducted to determine the optimal dietary Se level for meeting metabolic and functional Se requirements of broilers fed a corn-soybean meal diet from 22 to 42 d of age. A total of 336 Arbor Acres male broilers at 22 d old were randomly assigned to 1 of 6 treatments with 7 replicates and fed a basal corn-soybean meal diet (control, containing 0.014 mg Se/kg) and the basal diet supplemented with 0.10, 0.20, 0.30, 0.40, or 0.50 mg Se/kg from Na2SeO3 for 21 d. The results showed that the Se concentrations in plasma, liver, kidney, pancreas, breast and thigh muscles, the activity of glutathione peroxidase (GPX) in plasma, liver and kidney, the mRNA expression levels of Gpx4, selenoprotein (Seleno) h and Selenou in liver, S elenop and Selenoh in kidney, and the protein expression levels of GPX4 in the liver and kidney of broilers were affected (P < 0.05) by supplemental Se level, and increased quadratically (P < 0.05) with the increase of supplemental Se level. The estimates of optimal dietary Se levels were 0.10 to 0.49 mg/kg based on the fitted broken-line or asymptotic models (P < 0.0001) of the above Se concentration indices, and 0.08 to 0.37 mg/kg based on the fitted broken-line, quadratic or asymptotic models (P < 0.007) of the above selenoprotein expression indices. These results indicate that the optimal dietary Se levels would be 0.49 mg/kg to support the maximum Se concentrations and 0.37 mg/kg to support the full expression of selenoproteins in plasma and various tissues of broilers fed a corn-soybean meal diet from 22 to 42 d of age.
ABSTRACT
Acyl carrier proteins (ACPs) are a group of small acidic proteins functioning as important cofactors in the de novo synthesis of fatty acids. In Arabidopsis, ACPs are encoded by a small gene family comprising five plastid members, AtACP1 to AtACP5, and three mitochondrial members. The biological functions and the transcriptional responses to abiotic stresses of most AtACPs have yet to be elucidated. The present study extends previous findings and provides new knowledge on the function of ACPs by examining the responses of AtACP-encoding genes to several abiotic stresses and, in particular, the role of AtACP5 in the adaptation to salt stress. Phylogenetic analysis showed that AtACP1, AtACP2, AtACP3, and AtACP5 can be classified into one group and separated from a group comprising AtACP4 and ACP homologs from related species. Quantitative RT-PCR analysis revealed that the expression of AtACP1, AtACP2, and AtACP3 was induced by drought. Both iron deficiency and nitrogen starvation resulted in down-regulation of AtACP4. The most pronounced response was observed for AtACP5, the expression of which was dramatically decreased by salt stress. Knock-out of AtACP5 showed increased sensitivity to NaCl stress, whereas transgenic lines overexpressing AtACP5 displayed increased salt tolerance relative to the wild-type. Overexpression of AtACP5 further led to an altered composition of fatty acids, mainly a decrease of oleic acid (C18:1) and an increase of palmitic acid (C16:0), and to a lower Na+/K+ ratio when compared to the salt stressed wild-type. The comprehensive transcriptional information on the small plastid AtACP gene family in response to various abiotic stresses and the further investigation of the AtACP5 indicate that AtACP5 might be critical for salt tolerance through alterations of the composition of fatty acids and, subsequently, the Na+/K+ ratio.
