PSXIII-5 Effects of B vitamins and hydroxy trace minerals supplementation on hepatic metabolism of beef cattle at finishing phase in pasture

Abstract

Abstract Vitamin B and trace minerals are crucial molecular signals involved in many biological pathways of energy metabolism and their bioavailability is compromised in high-producing ruminant animals. Despite the current knowledge of the effects of vitamin B complex and trace minerals on animal performance, their use as a rumen-protected form and its impact on liver metabolism in finishing beef cattle is poorly known. The present study aimed to assess the effects of ruminally protected B-vitamin blend (Trouw Nutrition, Italy) and hydroxy trace minerals (Cu and Zn; Micronutrients Inc., Indianapolis, IN) on hepatic proteome. A total of 20 non-castrated Nellore males with 353 ± 43 kg of initial BW were submitted in a high supplementation (1.7% of BW) in pasture and randomly assigned to one of the following treatments: CTRL – inorganic trace minerals without supplementation of vitamin B blend; SUP – supplementation of hydroxy trace minerals (Cu and Zn) and vitamin B blend (B5, B6, B7, B9, and B12). All animals were fed the same level of the experimental diet for 106 days and liver biopsy was performed at the end of the experimental period. We use shotgun proteomics combined with biological and network analyses of the protein differentially abundant between treatments, showing 37 proteins differentially abundant (P < 0.10) between treatment groups, where all proteins were up-regulated in the SUP treatment. These proteins were related to protein folding (P = 0.0456), oxidoreductase complex (P = 0.0155), mitochondrial respiratory chain complex IV (P = 0.0132), chaperonin-containing T-complex 2 (P = 0.0132), glutathione metabolism (P = 0.00026) and other linked to oxidative stress regulation. These results indicate that ruminal-protected vitamin B and hydroxy trace minerals supplementation during the finishing phase cause positive changes in the abundance of proteins related to oxidative metabolism and response to oxidative damage.