Feeding broiler chicks diets containing keto- and hydroxy-acids: performance and carcass weight.

This study evaluated reduced dietary CP and supplementing amino acid analogs to sustain growth and carcass weight in 0- to 21-day-old Cobb × Avian-48 male broiler chicks. A total of 6 diets with 3 levels of CP (22.5, 19.5, and 16.5%) and 2 sources of AA analogs, either synthetic amino acids (SA) or keto-/hydroxy-acids (KA), were assigned randomly to 36 cages (8 chicks/cage) in a 3 × 2 factorial design. For SA diets, DL-Met, DL-Met + L-Ile, and D-Met + L-Ile + L-Val were used to supplement 22.5, 19.5, and 16.5% CP diets, respectively, and for corresponding KA diets, DL-Met was replaced with methionine hydroxy analog (MHA), L-Ile was replaced with keto-Ile, and L-Val was replaced with keto-Val. Water and all isocaloric diets (3,050 kcal ME/kg) were given ad libitum. Lowering dietary CP to 16.5% reduced BW at 7, 14, and 21 D (P ≤ 0.0001) and feed intake at 8 to 14, 15 to 21, and 0 to 21 D (P ≤ 0.001). Body weight gain (BWG) was reduced and feed-to-gain ratio (FGR) was increased (P ≤ 0.003 to 0.0001) at all times for chicks fed 16.5% CP; however, chicks fed 22.5 and 19.5% CP had comparable performance. Differences in 0 to 7 D BWG (SA, 122.9 vs. KA, 113.9 g/bird; P ≤ 0.04), a 0 to 21 D FGR cumulative effect (1.45 vs. 1.51; P ≤ 0.02), and a 15 to 21 D (P ≤ 0.04) and 0 to 21 D (P ≤ 0.05) CP × AA interaction were also observed. Greater liver weight among 16.5 vs. 19.5 or 22.5% CP fed chicks was found at 14 and 21 D (P ≤ 0.0001 and P = 0.06, respectively). Lower dietary CP reduced spleen weight on day 21 birds (P ≤ 0.0005) with lighter spleens among 16.5 and 19.5% vs. the 22.5% CP fed group (0.090, 0.095, 0.119 g/100 g BW, respectively). Breast weight at 21 D was significantly less for 16.5 vs. 22.5% CP fed chicks. Fat pad weight on day 21 was heaviest among 16.5% chicks (P ≤ 0.0004). Overall, lowering dietary CP to 16.5% had a negative effect, but keto-acid supplementation supported 0 to 21 D broiler growth compared to SA; however, transamination efficiency of KA may be lower for 0 to 7D old chicks compared to older birds.

Liver and colon oxidant status in growing rats fed increasing levels of dietary iron.

A study with four groups, each with 9 individually-housed, male albino rats (clinical average weight = 65 g), was undertaken to examine the effect of increasing dietary iron levels on the oxidant status in liver and colon of growing rats. The basal maize/soya diet contained 70 mg iron per kg and was supplemented with 200 (group II), 500 (group III) and 2000 (group IV) mg Fe/kg from iron (II) fumarate. Liver-Fe was closely correlated (r = 0.997) with dietary Fe intake. Feeding diets supplemented with 500 and 2000 mg Fe/kg over 28 days resulted in significantly elevated TBA-RS in liver homogenates. Vitamin E in the liver was about 20% lower in group IV compared to the controls. Liver SOD, G6PDH and CAT activities were not influenced by dietary iron, whereas liver GSHPx was decreased in groups III and IV. TBA-RS in the colon mucosa significantly increased only at a dietary iron supply of 2000 mg per kg. Iron-enriched diets caused a moderate dose-dependent enhancement in the concentration of methane sulfinic acid in feces samples, which was formed by the reaction of hydroxyl radicals and dimethyl sulfoxide. Liver was more sensitive than the colon mucosa to iron-induced lipid peroxidation. Compared with the recommended iron requirements of growing rats very high dietary iron levels were necessary to induce oxidative stress.

Metallothionein and zinc as potential antioxidants in radical-induced lipid peroxidation in cultured hepatocytes.

Rat hepatocytes were isolated by a two-step collagenase perfusion technique and introduced to the hydroxyl radical (OH)-generating xanthine-xanthine oxidase-iron (X/XO/Fe) system. The amount of thiobarbituric acid reactive substances (TBA) and thiobarbituric acid bound malondialdehyde (TBA-MDA) were assayed in homogenates after different phases of cultivation. The effects on lipid peroxidation of supplemented metallothionein (MT) ranging from 25 to 75 microM and zinc ranging from 14.5 to 77.8 microM, as well as the effect of a Zn-pretreatment for 18 h were investigated. The addition of X/XO/Fe resulted in a 3 to 4-fold increase in the levels of TBA and TBA-MDA. These results show that X/XO/Fe initiated the lipid peroxidation in the hepatocyte cell system. High doses of supplemented MT inhibited the production of TBA and TBA-MDA. Neither Zn nor the Zn-pretreatment, which resulted in an increase of intracellular MT, had any effect on TBA and TBA-MDA levels. This study suggests that MT can act as an antioxidant in high concentrations via the cysteinyl groups of the protein. The postulated protective effects of Zn via its release from the oxidized MT can be ruled out.

[Zinc--update of an essential trace element]. / Zink--Update eines essentiellen Spurenelements.

Since the recognition of zinc as an essential trace element in man and animals there has been a remarkable progress in our knowledge of the role of zinc in nutritional physiology, biology and medicine during the last few decades. Highlights in zinc research, mechanisms and homeostatic regulation of zinc absorption, sources of zinc intake, dietary factors and mineral interactions affecting zinc bioavailability are reviewed in the present paper. This is followed by an overview of the biochemical functions of zinc in enzymes, gene expression, endocrinology, immunology and oxidative stress. General signs and metabolic consequences of zinc deficiency as well as excessive intake and toxicity of zinc are summarized. Furthermore, national and international dietary zinc recommendations and different methods to determine the zinc status are discussed.