Enhancement of Copper Uptake of Yeast Through Systematic Optimization of Medium and the Cultivation Process of Saccharomyces cerevisiae.

Copper is an essential trace element for living organisms. Copper enriched by yeast of Saccharomyces cerevisiae is regarded as the biologically available organic copper supplement with great potentiality for application. However, the lower uptake ratio of copper ions makes the production of copper enriched by yeast uneconomically and environmentally unfriendly. In this study, S. cerevisiae Cu-5 with higher copper tolerance and intracellular copper accumulation was obtained by screening of our yeast strains collection. To increase the uptake ratio of copper ions, the medium composition and cultivation conditions for strain Cu-5 were optimized systematically. A medium comprised of glucose, yeast extract, (NH4)2SO4, and inorganic salts was determined, then a novel cultivation strategy including pH control at 5.5 and increasing amounts of yeast extract for a higher concentration of copper ion in the medium was developed. The uptake ratios of copper ions were more than 90% after combining 50 to 100 mg/L copper ions with 3.5 to 5.0 g/L yeast extract, which is the highest until now and is conducive to the cost-effective and environmentally friendly production of bioactive copper in yeast-enriched form.

Effects of pre-slaughter stressor and feeding preventative Chinese medicinal herbs on glycolysis and oxidative stability in pigs.

A total of 64 5-month-old Pietrain pigs were randomly allocated to four treatments with four replicates per treatment according to body weight. The pigs were fed either a standard corn-soybean meal based control diet (treatments 1 and 2), the standard diet with 1% Lycium barbarum (LB) (treatment 3), or the standard diet with 1% Polygala tenuifolia Willd (PT) (treatment 4). Serum lactic acid and glucose concentrations were increased in stressed pigs (P < 0.05). Addition of the herbs in the diet had no effect on the serum lactic acid concentration, but 1% LB decreased (P < 0.05) serum glucose concentration in the stressed pigs. Pre-slaughter stress also decreased (P < 0.01) liver glycogen concentration and the decrease could be inhibited by addition of 1% LB in the diet (P > 0.05). Pre-slaughter stress increased the concentration of maleic dialdehyde (MDA) (P < 0.05) and decreased glutathione peroxidase (GSH-Px) activity in serum, while dietary 1% LB increased (P < 0.05) the activity of GSH-Px and decreased the concentration of MDA in the serum. In conclusion, pre-slaughter stress induces oxidative stress in pigs and dietary supplementation with 1% LB improves antioxidant capacity in stressed pigs before slaughtering.

Clofibrate increases long-chain fatty acid oxidation by neonatal pigs.

BACKGROUND: Utilization of energy-dense lipid fuels is critical to the rapid development and growth of neonates. OBJECTIVE: To increase efficiency of milk fat utilization by newborn pigs, the effect of clofibrate on in vivo and in vitro long-chain fatty acid (LCFA) oxidation was evaluated. METHODS: Newborn male pigs were administered 5 mL of vehicle (2% Tween 80) with or without clofibrate (75 mg/kg body weight) once daily via i.g. gavage for 4 d. Total LCFA oxidative capacity was measured in respiration chambers after gastric infusion (n = 5 per treatment) with isoenergetic amounts of [1-(14)C]triglycerides (TGs), either oleic acid (18:1n-9) TG [3.02 mmol/kg body weight (BW)(0.75)] or erucic acid (22:1n-9) TG (2.46 mmol/kg BW(0.75)). Total expired (14)CO2 was collected and quantified at 20-min intervals over 24 h. Hepatic in vitro LCFA oxidation was determined simultaneously using [1-(14)C]oleic acid and erucic acid substrates. RESULTS: The in vivo 24-h accumulative [1-(14)C]TG oxidation (percentage of energy intake/kg BW(0.75)) tended to increase with clofibrate supplementation (P = 0.10), although there was no difference in the peak or mean utilization rate. The maximal extent of oleic acid TG oxidation was 1.6-fold that of erucic acid TG (P < 0.006). Hepatic in vitro LCFA oxidation increased 61% with clofibrate (P < 0.0008). The increase in mitochondria was 4-fold greater than in peroxisomes. The relative abundance of mRNA increased 2- to 3-fold for hepatic peroxisome proliferator-activated receptor α and its target genes (fatty acyl-coenzyme A oxidase and carnitine palmitoyltransferase) in the pigs that were administered clofibrate (P < 0.04). CONCLUSION: Clofibrate may improve in vivo LCFA oxidative utilization in neonatal pigs.