Effects of dietary protein-energy interrelationships on Holstein steer performance and ruminal bacterial fermentation in continuous culture.

In vivo and in vitro 3 x 2 factorial experiments were conducted concurrently to evaluate the incorporation of 0, 15, or 30% sugar beet pulp (SBP) as an energy source in diets fed to growing Holstein steers with either soybean meal (SBM) or alcohol-treated, defatted soybean flakes (ATSBF) as primary supplemental protein sources. Three groups of 42 Holstein steers each were fed six different diets from 54 kg initial BW to 320 kg in three experimental periods. There were no overall SBP level x protein source interactions (P greater than .05). Beet pulp level tended to decrease ADG (linear, P = .05) and increase feed/gain (linear, P less than .05) and DMI (quadratic, P less than .05). Each grower diet was used in a substrate for ruminal microbial metabolism in six dual-flow, continuous-culture fermenters. Organic matter and carbohydrate digestion were similar (P greater than .05) among diets. Increasing dietary levels of SBP caused a concomitant increase (P less than .05) in acetate and decrease (P less than .05) in butyrate and isobutyrate concentrations. Beet pulp level x protein source interactions (P less than .05) were observed for CP degradation, ammonia and nonammonia N, and dietary N flow. Crude protein degradation was higher (P less than .05) for the 0% SBP with SBM diet (81.3%) than for the 30% SBP with ATSBF diet (64.4%). Efficiency of bacterial synthesis was similar (P greater than .05) among diets. Results indicated that SBP is an effective dietary energy source for high-energy grower diets at 15 or 30% of the DM but may cause a decrease in some performance traits. There were no nutritional benefits of using ATSBF vs SBM as the supplemental N source.

Studies on the biliary efflux of GSH from rat liver due to the metabolism of aminopyrine.

The biliary efflux of GSH and GSSG due to aminopyrine was studied using perfused rat livers. The infusion of 0.8 mM aminopyrine led to a rapid rise in the amount of GSH released into the bile with only a small increase in the amount of GSSG released; caval GSH + GSSG efflux was unaffected. N-Benzylimidazole, an inhibitor of cytochrome P-450, completely blocked the response while phenobarbital pretreatment of the rats doubled the rate of GSH efflux. H2O2 and selenium-containing glutathione peroxidase were not involved since livers from selenium-deficient rats perfused with aminopyrine released GSH at the same rate as control livers. Aminopyrine injected i.p. into conscious rats also stimulated biliary GSH efflux to the same extent as with perfused livers. Biliary release of GSH in the perfused livers could be duplicated by infusing formaldehyde. It is proposed that formaldehyde produced during the N-demethylation of aminopyrine by cytochrome P-450 combines reversibly with GSH to form S-hydroxymethylglutathione which is oxidized by formaldehyde dehydrogenase to S-formylglutathione. Formaldehyde formed in excess of its capacity to be metabolized enzymatically is released into the bile as S-hydroxymethylglutathione which then dissociates to its initial reactants.