The effect of thermal processing and enzyme treatments of soybean meal on growth performance, ileal nutrient digestibilities, and chyme characteristics in broiler chicks.

Effects of thermal processing (toasting or extrusion) of untoasted soybean meal on growth performance, apparent ileal nutrient digestibilities, and chyme characteristics were studied in broiler chicks fed diets with soybean meal as the main protein source. Effects of increasing shear forces during extrusion as well as enzyme treatments (protease and carbohydrase) were also studied. When compared with toasting, extrusion significantly improved feed conversion ratio (1.56 vs 1.62) and apparent ileal digestibilities of CP and nonstarch polysaccharides (87.5 vs 82.2% and 26.7 vs 11.4%, respectively). Enzyme treatment improved apparent ileal digestibility of CP and nonstarch polysaccharide compared with no enzyme treatment (85.2 vs 83.7% and 20.6 vs 14.5%, respectively); however, enzyme treatments did not result in a better growth performance of the chicks. Among the enzyme treatments, no differences were found in growth performance and apparent ileal CP digestibility, whereas the carbohydrase significantly improved apparent ileal nonstarch polysaccharide digestibility compared with the other enzyme treatments. Extrusion of SBM at the highest shear level caused a significant increase in the water-holding capacity, chyme viscosity, and concentration of soluble nonstarch polysaccharides in the chyme compared with extrusion of SBM at lower shear levels. The increase in chyme viscosity did not affect growth performance, nor did it influence apparent ileal nutrient digestibilities.

Toxicity of methyl linoleate ozonide in the rat.

The in vivo toxicity of ozonides, possible intermediates in ozone-induced toxicity, was investigated. Methyl linoleate ozonide (MLO) (0.07 mmol/100 g body wt.), a model fatty acid ozonide, was administered to female Wistar rats either intravenously or intraperitoneally. After 24 h the rats were killed and the effects were examined. MLO was found to be toxic only after intravenous administration. The major effects were observed in the lungs. The lungs became enlarged from edema and showed severe hemorrhages. Further, total thiol was depleted in serum and lung tissue, accompanied with a significant decrease in activity of glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, and glutathione S-transferase. The vitamin E levels in serum and lung tissue were reduced. The malondialdehyde (MDA) concentrations in serum and lung tissue were elevated suggesting that in vivo oxidation had occurred. On intraperitoneal administration of MLO, no effects on enzyme activities, thiol and vitamin E content in lung tissue were observed. In serum, however, as on intravenous administration, an increase of the MDA levels and decreases of total thiol and vitamin E levels were found. In view of the route of administration it is to be expected that the ozonide is partly cleared by the liver, and the ozonide and its potentially toxic products are further detoxicated by vitamin E and thiols in serum before they reach the lung. The above data show that the main target organ for ozonides is the lung, and that the effects caused by MLO in vivo are in many respects similar to the effects found after acute ozone exposure. This supports the working hypothesis that ozonides may play a role in ozone-induced lung toxicity.

Vitamin D, within its range of fluctuation in commercial rat diets, does not influence nephrocalcinogenesis in female rats.

Massive, toxic doses of vitamin D have been shown to cause nephrocalcinosis in rats, but the effect of this vitamin within its range of fluctuation in commercial rat diets was unknown. Therefore, in two experiments with young female rats, the effect on nephrocalcinosis of a moderately increased level of vitamin D in the diet was studied, that is 5000 IU/kg versus the recommended concentration of 1000 IU/kg. This was done using purified diets with 0.5% (w/w) calcium and 0.04% magnesium containing either 0.2 or 0.6% phosphorus (P). Rats fed the diets containing 0.6% P showed severe kidney calcification compared to those fed the 0.2%-P diets. The level of vitamin D in the 0.2 and 0.6%-P diets did not affect kidney calcification. Bone density was increased after feeding diets containing 5000 instead of 1000 IU of vitamin D/kg. This study suggests that, within 28 days, a moderate increase of the amount of vitamin D in the diet has no influence on the development of kidney calcification. This in turn suggests that the variation in nephrocalcinosis severity and incidence seen in practice in rats fed different commercial diets is unlikely to be related to the different vitamin D concentrations in these diets. However, in rats fed such diets bone metabolism may be influenced differently.