The effect of biotin supplementation on ascorbic acid metabolism in chickens

The objective of the paper was to show the effect of supplementation of biotin (vitamin H) on vitamin C synthesis in chickens. A significant vitamin C increase was observed in kidneys, adrenal glands, liver, glandular stomach, jejunum wall, caecum wall and in blood plasma. A clear increase in the level of D-glucuronic acid was observed in adrenal glands, jejunum wall, and caecum wall. The activity of L-gulono-gamma-oxidase enzyme clearly increased in adrenal glands, jejunum wall and in stomach. The increase in vitamin C synthesis was found in adrenal glands, jejunum, caecum wall and stomach, but accumulation of vitamin C took place in liver and kidneys. The data imply that the supplementation of biotin accelerates vitamin C synthesis in chickens. Biotin, increasing vitamin C level in the organism, indirectly affects all the processes taking place with the participation of vitamin C.     

Effect of ascorbic acid on tumour growth

The growth of tumours in guinea-pigs was observed for 20 weeks after placing them on various doses of vitamin C. Complete tumour regression occurred in 55% of those animals receiving 0-3 mg/kg/day ascorbic acid, whereas animals given 10 mg/kg/day showed tumour inhibition but no regression. In contrast, tumours in animals maintained on 1 g/kg/day ascorbic acid grew without sign of retardation. When increased amounts of ascorbic acid were restored to the diet of scorbutic tumour-bearing animals, tumours which had not regressed responded with enhanced growth. Likewise, animals previously maintained on 10 mg/kg ascorbic acid responded in turn to the additional vitamin with enhanced tumour growth. In contrast, all tumour-bearing animals maintained on 1 g/kh ascorbic acid died within 3 weeks when this dose was replaced with 0-3 mg/kg.     

Stability of ascorbic acid in orange juice exposed to light and air during storage

Single-strength orange juice prepared from three nationally available brands of frozen orange juice concentrate was analyzed for ascorbic acid after exposure to light and air for varying periods up to eighteen days. For two of the brands, brown, foil-covered bottles offered no greater protection against ascorbic acid loss than clear glass bottles. Storage time appeared to be a greater contributor to ascorbic acid loss than type of container in two brands. One brand showed both the effect of storage time and type of container, since the juice stored in the brown bottle lost significantly less ascorbic acid after the same period than juice stored in the clear bottle.     

Tissue ascorbic acid and polyol pathway metabolism in experimental diabetes

Previous studies demonstrating reduced plasma concentrations of ascorbic acid (AA) in diabetes and interactions between this vitamin and biochemical mechanisms such as synthesis of structural proteins, oxidative stress, polyol pathway and nonenzymatic glycation of proteins suggest that disturbed AA metabolism may be important in the pathogenesis of diabetic microangiopathy. However, limited information is available on the concentration of AA in tissues which develop diabetic complications. This study demonstrates reduced renal but not sciatic nerve or plasma AA concentration in two animal models of insulin-dependent diabetes mellitus, namely the STZ-diabetic rat and the spontaneously diabetic BB rat. Decreased lens AA concentration was also observed in STZ-diabetic rats. Improvement of glycaemic control by insulin treatment (albeit insufficient to achieve normoglycaemia) partially corrected lens and renal AA concentration in STZ-diabetic rats. AA treatment increased kidney and lens AA concentrations of STZ-diabetic and non-diabetic rats and corrected the abnormalities observed for untreated diabetic rats. Sciatic nerve AA concentration was not increased by AA treatment in any group. Tissue ratios of dehydroascorbic acid (DHAA)/AA, one index of oxidative stress, were not different between the diabetic and non-diabetic groups and were unaltered by AA supplementation. AA treatment of STZ-diabetic rats had no effect on elevated tissue concentrations of glucose, sorbitol and fructose or reduced myo-inositol concentration. The effect of reduced tissue AA levels in diabetes on either collagen synthesis or ability to combat increased free radical production is not known. However, correction of abnormal kidney and lens AA concentrations in experimental diabetes by AA supplementation suggests that if AA does have a role in the development or progression of the renal and ocular complications of diabetes, this treatment could be beneficial.     

The influence of albumin and calcium on human platelet arachidonic acid metabolism

The effects of in vitro changes in calcium and albumin on human platelet arachidonic acid metabolism were evaluated. Hypoalbuminemia enhanced the conversion of released 14C-arachidonic acid from prelabeled platelet phospholipids to the metabolites of the platelet cyclooxygenase and lipoxygenase pathways. This effect was, however, associated with a decreased release of arachidonic acid in the presence of hypoalbuminemia, such that the overall conversion of released 14C-arachidonic acid to platelet thromboxane B2 was similar in the presence of physiologic albumin concentration (3.5 g/dl) or at decreased albumin concentrations of 0.7 and 0.0 g/dl. External calcium was shown to be important for optimal platelet arachidonic acid release, with maximal release occurring at 1 mM calcium.     

Amino acid metabolism and the energetics of growth

The nonessential amino acids are involved in a large number of functions that are not directly associated with protein synthesis. Recent studies using a combination of transorgan balance and stable isotopic tracers have demonstrated that a substantial portion of the extra-splanchnic flux of glutamate, glutamine, glycine and cysteine derives from tissue synthesis. A key amino acid in this respect is glutamic acid. Little glutamic acid of dietary origin escapes metabolism in the small intestinal mucosa. Furthermore, because glutamic acid is the only amino acid that can be synthesized by mammals by reductive amination of a ketoacid, it is the ultimate nitrogen donor for the synthesis of other nonessential amino acids. Because the synthesis of glutamic acid and its product glutamine involve the expenditure of adenosine triphosphate (ATP), it seems possible that nonessential amino acid synthesis might have a significant bearing on the energetics of protein synthesis and, hence, of protein deposition. This paper discusses the topic of the energy cost of protein deposition, considers the metabolic physiology of amino acid oxidation and nonessential amino acid synthesis, and attempts to combine the information to speculate on the overall impact of amino acid metabolism on the energy exchanges of animals.     

Effects of ascorbic acid on trace element metabolism in the choroid-retina of streptozotocin-induced diabetic guinea pigs

In order to investigate the effect of ascorbic acid on trace element metabolism in the choroid-retina, experimental diabetes mellitus was induced in Hartley guinea pigs with intraperitoneal injection of streptozotocin. After 4 weeks, ascorbic acid-deficient feed was given for 3 weeks. Trace elements of the choroid-retina were measured with inductively-coupled plasma emission spectrometry. The activity of superoxide dismutase and lipid peroxide content also were measured. The results indicated that zinc and magnesium increased in diabetes mellitus. However, with ascorbic acid deficiency in diabetes mellitus, zinc and magnesium significantly decreased. On the other hand, the activity of superoxide dismutase showed no change between either condition and lipid peroxide content decreased under ascorbic acid deficiency in diabetes mellitus. These findings suggested that ascorbic acid played an important role in chorioretinal damage of diabetes mellitus. However, it was also suggested that lipid peroxide has little influence on the choroid-retina under these conditions.     

Effect of morphine on striatal dopamine metabolism and ascorbic and uric acid release in freely moving rats

Recent ex vivo findings have shown that morphine increases dopamine (DA) and xanthine oxidative metabolism and ascorbic acid (AA) oxidation in the rat striatum. In the present study, we evaluated the effects of subcutaneous daily morphine (20 mg/kg) administration on DA, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), AA and uric acid in the striatum of freely moving rats using microdialysis. Dialysates were assayed by high performance liquid chromatography with electrochemical detection. On the first day, morphine administration caused a significant increase in extracellular DA, DOPAC, HVA, AA and uric acid concentrations over a 3 h period after morphine. In all treated rats (n = 7), individual concentrations of DOPAC + HVA were directly correlated with individual AA and uric acid concentrations. Last morphine administration on the 4th day increased DOPAC, HVA, AA and uric acid concentrations but failed to increase those of DA. Individual DOPAC + HVA concentrations were still directly correlated with individual AA and uric acid concentrations. These results suggest that systemic morphine increases both striatal DA release and DA and xanthine oxidative metabolism. Only the former effect undergoes tolerance. The increase in DA oxidative metabolism is highly correlated with that of xanthine. The subsequent enhancement in reactive oxygen species production may account for the increase in extracellular AA.     

生产中解决镍基合金挤压荒管内壁橘皮问题的途径

在热挤压生产镍基合金荒管的过程中,挤压工艺和润滑的不匹配常常会造成荒管内壁橘皮以及凹坑等。对生产中所应用的具有不同物理特性的四种玻璃润滑剂按照不同比例进行混合,使得混合后的玻璃润滑剂具有不同于单一润滑剂的物理特性,最终通过现场实验效果验证,选出了与当前挤压工艺正确匹配的玻璃粉,解决了长期存在的内壁橘皮问题。实验均是在工厂生产中进行,其结果在实际生产中得到了应用。     

Acute growth hormone effects on amino acid and lipid metabolism

The anabolic actions of GH are well known, although specific tissue responses and the mechanism of nitrogen conservation are less well understood. This study was designed to examine the acute metabolic effects of GH on whole body and regional protein metabolism, using an experimental protocol which controlled for confounding perturbations in other hormones by a simultaneous infusion of somatostatin. Control subjects received replacement doses of insulin, glucagon, and GH for the entire 7-h study period, whereas GH subjects received an identical protocol, except for an increased dose of GH sufficient to increase serum concentrations into the high-physiological range (12-20 ng/mL) for the final 3.5 h of the study (P < 0.001). Thirteen young, healthy male subjects were studied in the postabsorptive period; five served as control subjects and eight as treatment (GH) subjects. Each received continuous iv infusions of somatostatin, L-[13-C]leucine, and L-[2H5]phenylalanine throughout the study. Femoral arterial and venous sampling allowed for simultaneous measurements across the leg and in the whole body. C-Peptide levels were suppressed throughout the infusion; insulin, glucagon, insulin-like growth factor I, cortisol, epinephrine, norepinephrine, and glucose concentrations were not different between groups. Glycerol concentrations increased 3-fold in GH subjects during the final 3.5-h period (P = 0.04). Concentrations of several amino acids declined through the study, but no differences were observed between treatment groups. Leucine oxidation was reduced in GH compared to control subjects (P = 0.04). No changes in CO2 production or whole body leucine or phenylalanine flux were observed, whereas nonoxidative disposal of leucine was marginally higher in GH compared to control subjects (P = 0.07). By contrast, rates of appearance and disappearance of both leucine and phenylalanine across the leg all were relatively lower in GH compared to control subjects; leucine balance across the leg was reduced by GH (P = 0.03), whereas phenylalanine balance was not influenced by GH. Our data thus demonstrate an acute stimulatory effect of GH on lipolysis, a decrease in leucine oxidation, and no stimulation of muscle protein synthesis in spite of enhanced protein synthesis in nonmuscle tissue.     

Oxidative DNA damage estimated by oxo8dG in the liver of guinea-pigs supplemented with graded dietary doses of ascorbic acid and alpha-tocopherol

Dietary antioxidants may influence cancer risk and aging by modifying oxidative damage. The effect of graded dietary doses of the antioxidant vitamins C and E on oxidative DNA damage was studied in the liver of guinea-pigs under normal conditions. Like human beings, guinea-pigs cannot synthesize ascorbate and alpha-tocopherol. In one experiment, three groups of 6-8 guinea-pigs were fed diets containing 15 mg of vitamin E/kg chow and three different amounts of vitamin C (33,660 or 13,200 mg/kg) for 5 weeks. In a second experiment, three groups of seven guinea-pigs were fed diets containing 660 mg of vitamin C/kg and three different amounts of vitamin E (15, 150 or 1500 mg/kg) for 5 weeks. The three graded levels of each vitamin respectively represent marginal deficiency, an optimum supplementation and a megadose. Oxidative damage to liver DNA was estimated by measuring 8-oxo-7,8-dihydro-2'-deoxyguanosine (oxo8dG) referred to deoxyguanosine (dG) by means of high-performance liquid chromatography with simultaneous electrochemical-coulometric and ultraviolet detection. The level of ascorbate in the liver was 0.034 +/- 0.051, 1.63 +/- 1.06 and 1.99 +/- 0.44 micromol/g in the low, medium and high dose ascorbate groups (59-fold variation). The liver concentration of alpha-tocopherol was 28 +/- 11, 63 +/- 18 and 187 +/- 34 nmol/g in the low, medium and high dose alpha-tocopherol groups (7-fold variation). The level of oxo8dG in the liver DNA was 1.89 +/- 0.32, 1.94 +/- 0.78 and 1.93 +/- 0.65 per 10(5) dG in the low, medium and high dose ascorbate groups (no effect: P > 0.05). In the low, medium and high dose alpha-tocopherol groups oxo8dG level in the liver DNA was 2.85 +/- 0.70, 2.74 +/- 0.66 and 2.61 +/- 0.92 per 10(5) dG (no effect: P > 0.05). It is concluded that even very large variations in the content of the antioxidant vitamins C and E in the diet and liver have no influence on the steady-state level of oxidative damage to guanine in the liver DNA of normal unstressed guinea-pigs.     

Production of an acid extract of rice straw

OBJECTIVE: Children of substance-abusing (SA) fathers have been found to have increased rates of conduct disorder (CD). Substance abuse and antisocial behavior have been linked to alterations in dopaminergic regulation and to monoamine oxidase (MAO) in adults. This study assessed the relationship between homovanillic acid (HVA), the metabolite of dopamine (DA), and MAO, the enzyme facilitating the conversion of DA to HVA, with CD in boys of SA and non-SA fathers. METHOD: Male youths (N = 65), between the ages of 6 and 15 years, admitted to a residential setting because of behavior problems, were studied through peripheral blood samples and structured interviews. RESULTS: The findings indicated that MAO activity was significantly higher in boys of SA fathers with CD than (1) in boys of non-SA fathers with CD and (2) in boys of SA fathers without CD. HVA levels did not differ significantly among the groups. CONCLUSIONS: In the context of previous studies, the findings support the concept of dopaminergic dysregulation in sons of SA fathers, manifested by alterations in MAO activity levels in those youths with CD.     

HC340LA钢冲压“桔皮”缺陷成因及措施

分析了340 MPa级冷轧低合金高强度钢“桔皮”缺陷钢板和正常钢板的微观组织结构和力学性能。结果表明,缺陷钢板的应力-应变曲线屈服点伸长率达到了3.73%,屈服延伸过大导致了所冲压的前风窗横梁连接板表面产生“桔皮”缺陷。在实验室采用对钢板预拉伸的方法模拟钢板工业化生产的平整与拉伸矫直工艺,随着预拉伸量的增加,试验样屈服平台的长度减少,当预拉伸量超过1.8%时,试验样的屈服平台消失。微观组织进一步分析显示,退火温度高导致钢板晶粒粗大和晶粒取向异常是冲压钢板 “桔皮”缺陷产生的根源。在连续退火工艺环节中合理控制平整和拉伸矫直工艺可以消除或者缩短试验钢屈服平台长度,并避免冲压件表面“桔皮”缺陷发生。     

The role of ascorbic acid in oral cancer and carcinogenesis

Severe transient focal cerebral ischemia causes brain infarction with a strong glial reaction. We have studied whether postischemic reactive glial cells express epidermal growth factor receptor (EGFR) following middle cerebral artery occlusion in the rat. We have also looked for signs of proliferating activity, as EGFR is known to be involved in cell growth and proliferation in certain non-neural cells. EGFR was studied using three different antibodies which were found to stain for a tyrosine-phosphorylated protein (p170) corresponding to the membrane-anchored EGFR. Neurons of the control brain were strongly immunoreactive to EGFR, but a decrease of EGFR-immunoreactivity was seen in the ipsilateral brain side from 24 h postischemia due to neuronal loss. However, the presence of abundant glial cells strongly immunoreactive to EGFR became apparent in this area from 4 days postischemia onward. The use of microglial (lectin or OX-42) and astroglial (GFAP) markers showed that these postischemic EGFR-stained cells were reactive microglia/macrophages and astroglia. The subcellular localization of EGFR in reactive microglia/macrophages was compatible with the network of the Golgi apparatus, as revealed with an antibody against a peripheral membrane-bound protein of the Golgi. The presence of abundant proliferating cells in the ischemic brain was detected from 4 days postischemia with an antibody against proliferating cell nuclear antigen. Proliferating reactive microglia/macrophages were abundant within the infarcted brain side, whereas proliferating astrocytes were found mainly in the immediate periphery of the infarct limiting the necrotic area from the undamaged tissue. These proliferating cells were immunoreactive to EGFR. The results show the presence of EGFR in postischemic reactive glial cells and suggest that EGFR-dependent pathways mediate signal transduction in reactive glia following transient focal cerebral ischemia.     

Dynamic parameters of maternal amino acid metabolism and fetal growth

This study presents kinetic parameters of glycine metabolism during pregnancy and the influence of fuel availability on fetal growth. The kinetic studies were done on patients with gestational diabetes mellitus (diet treated) and pre-gestational diabetes mellitus (diet and insulin treated) that was accompanied by increased fetal growth and pregnancy-induced hypertension and, during the third trimester of pregnancy, by intrauterine growth retardation. Gas chromatography-mass spectrometry was used to determine the 15N enrichment of plasma glycine, and to calculate the pool sizes, turnover rate constants, fluxes and metabolic clearance rates. Glycine pool sizes in pre-gestational diabetes were significantly larger than those in normal, hypertensive and gestational diabetes pregnancies. Glycine turnover rate constants and metabolic clearance rates were not significantly different between the normal pregnant women, the hypertensive, and the two diabetic groups of pregnant women. Glycine fluxes were significantly higher in the pre-gestational diabetic pregnant women than in those with gestational diabetes, hypertension, and normal pregnancy. Pre-gestational diabetic pregnant women delivered fetuses with higher birthweights than the other three groups. Fetal birthweight of the hypertensive women was significantly lower than among the normal and diabetic women. Stable isotope methodology using labeled amino acids provides a powerful tool for clinical studies of maternal protein metabolism and its relationship to fetal growth.     

The influence of acetylsalicylic acid on cognitive processing: an event-related potentials study

The central effects of acetylsalicylic acid (ASA) are discussed controversially. In animal models, it has been shown that ASA can interact with the central serotonergic and catecholaminergic neuronal system. However, the relevance of this interaction for humans is still unknown. We performed a study on the influence of ASA on central cognitive processing. In 25 healthy subjects (age 21-56 years), visually evoked event-related potentials (ERP) and reaction time under IV ASA medication were recorded. ERP were evoked by an oddball paradigm. As compared to placebo, ASA decreased the latency of the P3 component significantly in a time interval of 20-40 min after administration. The latency of the N2 component was significantly decreased about 25 min after administration; the latency of the exogenous P2 component was not influenced by ASA. The mean choice reaction time was significantly decreased by ASA 35 min after administration. At this time point, there was a significant correlation between decrease in reaction time and increase in ASA plasma level. The data show that IV administration of ASA has an accelerating effect on the endogenous components of visual ERP and on reaction time. This finding suggests that ASA can influence central cognitive processing, possibly by ASA induced changes of neurotransmitters. Since serotonin can be released by ASA and serotonin release leads to a decrease of ERP latencies. we assume that ASA most likely influences cognitive processing via the central serotonergic transmitter system.