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The effect of insulin on the ascorbate recycling system in the chicken liver was examined. First, insulin was injected subcutaneously into the chicken, and liver glutathione-dependent dehydroascorbate reductase (GSH-DHAR) activity was determined. Insulin increased liver GSH-DHAR activity, but did not affect plasma and liver ascorbate concentration. Dehydroascorbate increased plasma and liver ascorbate levels, and liver GSH-DHAR activity. However, distinct changes in plasma insulin level were not observed by dehydroascorbate injection. In addition, reduction of external dehydroascorbate in cultured chicken hepatocytes could not be observed in an insulin-deprived culture, although the cells reduced external dehydroascorbate in a serum-free culture with insulin. We concluded that insulin affects the ascorbate recycling system as an essential factor in the chicken liver.

The process of the first-order solid-to-solid phase transition of 1-ethyl-3-(4-methylpentanoyl)urea (1) was observed by means of a detailed temperature-resolved single-crystal diffraction method, which resembles watching a series of stop-motion photographs. The transition consists of two elementary processes, one supramolecular and the other molecular. Crystal structures from before and after the phase transition are isostructural. The straight-ribbon-like one-dimensional hydrogen-bonding structure is formed and stacked to form a molecular layer. The geometry of the layer is retained during the phase transition. The relative position of the layer with its neighbours, on the other hand, changes gradually with increasing temperature. The change is accelerated at the temperature representing the start of the endotherm seen in the DSC curves of (1). The structural variation yields void space between the neighbouring layers. When the void space grows enough that the crystal is unstable, the 3-methylbutyl group on the last of the molecules turns into a disordered structure with drastic conformational changes to fill up the void space. The phase transition process is well supported with simple force-field calculations. A crystal of 1-(4-methylpentanoyl)-3-propylurea (2), which shows no solid-to-solid phase transitions, was also analysed by the same method for comparison.

ラジカルイニシエーターである2,2'ーアゾビスアミジノプロパン二塩酸塩(AAPH)およびL-アスコルビン酸-2-リン酸マグネシウム(APM)の投与が単冠白色レグホーン種雄ヒナの成長およびアスコルビン酸濃度に及ぼす影響について調査した。5mg/100g体重/1日のAAPHを14日間の投与すると,ヒナの体重増加量,飼料摂取量および飼料効率(体重増加量/飼料摂取量)は対照区のヒナに比べ有意に低下したが,APMを1.5%飼料に添加するとAAPHを投与したヒナの成長低下は緩和された。また,AAPHを投与するとヒナで血漿のアスコルビン酸量の有意な低下と血漿および肝臓のチオバルビツール酸反応物(TBRS)濃度の有意な増加がみられた。このTBARS濃度の増加は,APMの飼料添加により減少した。以上の結果より,AAPHを投与したヒナが,ラジカル傷害のモデル動物となり得ること,およびAAPH由来のラジカルによる酸化ストレスに,飼料へのAPMの添加が有効であることが示唆された。

Dehydroascorbic acid, the oxidized form of ascorbic acid, is rapidly reduced to ascorbate in living organs (ascorbate recycling). We examined the GSH-dependent dehydroascorbate reductase activity in several tissues of the chicken. The activity was highest in the liver, and second highest in the brain. The activity was localized in the cytosol fraction of the liver. We subsequently examined the dehydroascorbate reduction in separated chicken hepatocytes. The cellular ascorbate concentration was elevated in dehydroascorbate-treated cells. It is thought that hepatocytes incorporated external dehydroascorbate and converted it into ascorbate. These findings suggest that the liver plays an important role in ascorbate recycling by the chicken.

The present study was conducted to investigate the efficiency of utilization of L-ascorbic acid-2-phosphate magnesium (APM) in Single Comb White Leghorn male chicks and the effect of APM-supplemented diets on their growth.The efficiency of utilization of APM was determined, taking as its indicators the change in plasma ascorbic acid (AA) at 1, 2, 3, 4, 6, and 8 hours after administration by gavage into the crop and the percentage hydrolysis of APM to AA in jejunum tissue homogenates. It was shown that APM was converted to AA after ingestion and utilized in the bodies of chicks.Chick diets containing 0, 0.5, 1.0 and 1.5% of APM were offered to chicks at 7 days for ad libitum consumption for 14 days. The supplementation of diets with APM had no adverse effect on growth rate and feed efficiency in chicks.

40°Cの高温下に24および26日齢のニワトリヒナを7日間連続暴露させた場合におけるアスコルビン酸(AA:150ppm,1500ppm)投与の効果を検討した。1)40°C暴露ヒナの体重,増体量,飼料摂取量および飼料効率は20°Cで飼育したヒナに比べ有意に低下したが,AAの投与により高温暴露ヒナの成長低下は緩和された。2)40°C暴露により血漿,肝臓および腎臓のAA濃度は20°Cで飼育したヒナの値に比べ低下したものの,AA投与により緩和された。また,血漿および腎臓のAA濃度と腎臓のL-グロノラクトンオキシダーゼ活性との間にそれぞれ有意な負の相関(r=-0.681, P

The contribution of whole-body protein synthesis to diet-induced thermogenesis was estimated in refed chicks. After refeeding a single meal of a experimental diet, reduced whole-body protein synthesis by fasting was rapidly restored. It was considered that the rapid recovery of whole-body protein synthesis was brought about not by an increase in the amount of RNA but by an increase in protein-synthetic efficiency of each RNA. The contribution of whole-body protein synthesis to diet-induced thermogenesis estimated from differences in heat production and in whole-body protein synthesis of fasted and refed chicks was found to be 13% at 2 hours after refeeding, and 27% at 6 hours after refeeding.

Chicken liver is lack of ascorbic acid biosynthesis system, different from mammals and highly evoluted birds. Chicken hepatocytes cultured without ascorbate was expected to have lower ascorbate amounts than physiological levels. Intracellular was decreased as compared with intact liver by cell preparation performed with in situ collagenase perfusion. We added ascorbate to a primary culture of chicken hepatocytes in order to restore the amount of ascorbate. Serum-free Leivobitz's L-15 medium which do not contain ascorbate was used for control medium. Cells were cultured with several concentrations of ascorbate for 24 or 48 h. After ascorbate supplementation for 24 to 48 h, cellular ascorbate concentration increased depending on the dose of medium ascorbate. Medium lactate dehydrogenase activity derived from hepatocytes, an index of cell injury, decreased upon 5–100 mg/l of ascorbate supplementation for 48 h. Tyrosine aminotransferase activity, an index of liver function, increased following culture with 50 and 100 mg/l ascorbate for 48 h. The activities, however, decreased by supplementation with 1000 mg/l of ascorbate. In conclusion hepatocytes lost intracellular ascorbate during preparation by in situ collagenase perfusion. Supplementation of ascorbate restored cellular ascorbate concentration, lowered cell injury and raised tyrosine aminotransferase activitv in primary cultured chicken hepatocytes. Ascorbate treatment for 48 h at 50 mg/l was the best combination in this study for primary culture of chicken hepatpcyte with non-serum L-15 medium

The effect of administration of clenbuterol, a beta-adrenergic agonist, on live weight gain and protein synthesis of liver and breast muscle was investigated in 32 White Leghorn chicks. Protein synthesis was measured by injection of [3H]phenylalanine in a wing vein using the flooding dose method. No significant changes in body weight gain were caused by dietary administration of the beta-agonist at .25 mg/kg of diet from 3 to 6 wk of age, but fat retention in the liver and breast muscle was significantly reduced by the drug treatment. No stimulating effect on protein synthesis of the beta-agonist administration was found either in the breast muscle or in the liver. Protein synthesis in the breast muscle was unchanged whereas that in the liver was reduced significantly by feeding clenbuterol.

1. Energy cost of whole-body protein synthesis was measured in vivo in chicks by comparing the changes in protein synthesis and heat production after the administration of cycloheximide, an inhibitor of protein synthesis. 2. Incorporation of phenylalanine into whole-body protein fraction was promptly inhibited after the intravenous injection of cycloheximide, and the effect was sustained for at least 3 hr. 3. Both whole-body protein synthesis and total heat production were significantly reduced by the cycloheximide administration. 4. The energy cost of whole-body protein synthesis was calculated to be 5.35 kJ per g protein synthesis, and hence on a molar basis 7.52 ATPs are required per peptide bond synthesis.

1. Spleen immunoglobulin (IgG) synthesis was measured in vivo in chicks at 3 weeks of age by a large dose injection of labelled phenylalanine in combination with the isolation of IgG by immunological precipitation against anti-chicken IgG. 2. No appreciable amount of radioactivity was detected in serum IgG for the first 60 min of the isotope injection via the wing vein, indicating a minimum time lag necessary for the secretion of newly synthesized IgG into the circulation. 3. Synthesis rates of total spleen protein and spleen IgG were found to be 17.5 and 4.8 mg/day, respectively, suggesting that IgG synthesis would contribute to 27% of the total protein synthesis in the spleen of young chicks.

1. 1. Effect of low ambient temperature on protein turnover in the liver and whole body was investigated in chicks together with the contribution of protein synthesis to the total heat production. 2. 2. Both protein synthesis and degradation in the whole body were increased, the latter to a larger extent, at low ambient temperature (LT, 22°C) compared with adequate temperature (AT, 30°C). Liver protein synthesis was not significantly altered by the temperature treatment. 3. 3. The total heat production of LT group was as high as 160% of the AT group. 4. 4. The increased heat production due to enhanced whole-body protein synthesis accounted for only 1.4% of the heat increment in thermogenesis at low ambient temperature, suggesting that protein synthesis would contribute little, if any, to cold-induced thermogenesis in chicks.

1. The effect of starvation on whole-body protein synthesis and on the contribution of protein synthesis to basal metabolic rate was investigated in young chickens (Expt 1). Strain differences between layer and broiler chickens in whole-body protein synthesis and degradation rates were examined when the birds were starved (Expt 2).2. In Expt 1, 15-d-old White Leghorn male chickens were used, while in Expt 2 Hubbard (broiler) and White Leghorn (layer) male chickens at 14 d of age were used. They were starved for 4 d, and heat production was determined by carcass analysis after 2 and 4 d of starvation. Whole-body protein synthesis rates were measured on 0, 2 and 4 d of starvation (Expt 1), and on 0 and 4 d of starvation (Expt 2).3. The results showed that starving reduced whole-body protein synthesis in terms of fractional synthesis rate and the amount synthesized. Whole-body protein degradation was increased by starvation both in terms of fractional synthesis rate and the amount degraded on a per kg body-weight basis.4. Reduced fractional synthesis rate of protein in the whole body was accounted for by reductions in both protein synthesis per unit RNA and RNA:protein ratio.5. In the fed state, whole-body protein synthesis and degradation rates, whether expressed as fractional rates or amounts per unit body-weight, tended to be higher in layer than in broiler chickens. In the starved state, the difference in the rate of protein synthesis between the two strains virtually disappeared, while the degradation rates were higher in layer than in broiler birds.6. Based on the assumed value of 3.56 kJ/g protein synthesized (Waterlow et al. 1978), the heat associated with whole-body protein synthesis in the starved state was calculated to range from 14 to 17% of the basal metabolic rate with no strain difference between layer and broiler chickens.