The effect of nitrofurazone on the thiamin status of chickens

Nitrofurazone, given orally at doses of 10 and 20 mg/kg for seven days, decreased the activity of erythrocyte transketolase (TK) and increased the activation of TK by thiamin pyrophosphate (TPP effect %). Nitrofurazone also decreased the feed intake and growth of the chickens, and increased the concentrations of lactate and pyruvate of their blood. It was concluded that nitrofurazone has induced thiamin deficiency in the treated birds. Pair-feeding experiments showed that the decreased growth was due to anorexia, and that the effects produced by nitrofurazone treatment on the thiamin status were attributable to the drug, per se, and not to anorexia. Thiamin (100 micrograms/kg, injected subcutaneously), when given concomitantly with nitrofurazone, was effective in preventing the development of thiamin deficiency.     

A comparison of transketolase assay and transketolase and lactate dehydrogenase activity levels in whole blood and red cell hemolysates and in leukocytes

1. A study was made of transketolase activity in red and white blood cells and of conditions for assay for transketolase activity and for assessment of the "TPP effect" in human and rat blood. 2. The ratio of the transketolase activity in white cells to that in red cells varied between 23 and 93. 3. Red cells or white cells can both be used for assessment of transketolase activity and the "TPP effect", but the best source for evaluation of transketolase activity and the percent change on addition of thiamin diphosphate appears to be whole blood.     

硫胺素水平对团头鲂幼鱼生长、肝组织沉积量及血液生化指标的影响

为研究硫胺素对团头鲂幼鱼生长、组织沉积量和血液生化指标的影响,试验采用单因素浓度梯度设计,配制了6组等氮等能的半纯合饲料,各组硫胺素含量分别为0、0.51、0.98、1.59、2.13和2.68 mg/kg。选取团头鲂幼鱼720尾[初重为（0.30±0.01）g],按随机原则分为6组,每组4重复,各重复30尾,日投饵3次,饲喂8周后采集样品。结果表明,与对照组相比,0.98、1.59、2.13、和2.68 mg/kg添加组的增重率和特定生长率均显著提高（P < 0.05）。1.59和2.13 mg/kg硫胺素添加组的成活率显著高于对照组（P < 0.05）。随着饲料中硫胺素含量的升高,血浆葡萄糖含量呈现先下降后上升的趋势,血浆葡萄糖水平在1.59 mg/kg时为最小值（P < 0.05）。对照组与0.51 mg/kg硫胺素组相比血浆中丙酮酸含量差异不显著,但显著高于其他试验组（P < 0.05）。以团头鲂幼鱼的增重率和肝脏硫胺素沉积量为评价指标,进行双折线回归分析,饲料中硫胺素适宜添加水平分别为1.48和1.84 mg/kg。     

Blood vitamin values of common marmosets (Callithrix jacchus)

The blood vitamin analyses of the common marmoset (Callithrix jacchus) were determined to provide baseline reference values for the normal animal. Ascorbic acid, riboflavin (erythrocyte glutathione reductase) [ECR], measurement, thiamin (erythrocyte transketolase) measurement and vitamin A (retinol) were determined for Texas A&M colony-born animals and those obtained from the wild. The analyses were completed on the animals, three times each, for a total of 93 analyses, which included 51 colony-born and 60 wild-born marmosets. A mean value of 0.98 mg/dl for ascorbic acid was found for the colony with a range from 0.06 to 4.1 mg/dl. The normal range for the marmosets appeared to be 0.5 to 1.5 mg/dl. The mean activity coefficient (AC) for the marmosets was 1.0 indicating that the animals had adequate riboflavin in the diet. The mean transketolase activities were (ribose remaining ?30.1 IU/L) and (sedoheptulose appearance ?7.9 IU/L). The mean and range for serum vitamin A (retinol) were 20.4 mg/dl and 6.96–57.44 mg/dl, respectively. None of the animals (colony-born or wild-born) exhibited any clinical signs of vitamin deficiencies as a result of being maintained in an indoor-outdoor environment over a three-year period.     

Transketolase: observations in alcohol-related brain damage research

Thiamin, or vitamin B1, is crucial for brain function. In its active form, thiamin pyrophosphate (TPP), it is a co-enzyme for several enzymes, including transketolase. Transketolase is an important enzyme in the non-oxidative branch of the pentose phosphate pathway (PPP), a pathway responsible for generating reducing equivalents, which is essential for energy transduction and for generating ribose for nucleic acid synthesis. Transketolase also links the PPP to glycolysis, allowing a cell to adapt to a variety of energy needs, depending on its environment. Abnormal transketolase expression and/or activity have been implicated in a number of diseases where thiamin availability is low, including Wernicke-Korsakoff's Syndrome and alcoholism. Yet, the precise mechanism by which this enzyme is involved in the pathophysiology of these disorders remains controversial.     

Correlation of enzymatic,metabolic, and behavioral deficits in thiamin deficiency and its reversal

To clarify the enzymatic mechanisms of brain damage inthiamin deficiency, glucose oxidation, acetylcholine synthesis, and the activities of the three major thiamin pyrophosphate (TPP) dependent brain enzymes were compared in untreated controls, in symptomatic pyrithiamin-induced thiamin-deficient rats, and in animals in which the symptoms had been reversed by treatment with thiamin. Although brain slices from symptomatic animals produced¹⁴CO₂ and¹⁴C-acetylcholine from [U-¹⁴C]glucose at rates similar to controls under resting conditions, their K⁺-induced-increase declined by 50 and 75%, respectively. In brain homogenates from these same animals, the activities of two TPP-dependent enzymes transketolase (EC 2.2.1.1) and 2-oxoglutarate dehydrogenase complex (EC 1.2.4.2, EC 2.3.1.61, EC 1.6.4.3) decreased 60–65% and 36%, respectively. The activity of the third TPP-dependent enzyme, pyruvate dehydrogenase complex (EC 1.2.4.1, EC 2.3.1.12, EC 1.6.4.3.) did not change nor did the activity of its activator pyruvate dehydrogenase phosphate phosphatase (EC 3.1.3.43). Although treatment with thiamin for seven days reversed the neurological symptoms and restored glucose oxidation, acetylcholine synthesis and 2-oxoglutarate dehydrogenase activity to normal, transketolase activity remained 30–32% lower than controls. The activities of other TPP-independent enzymes (hexokinase, phosphofructokinase, and glutamate dehydrogenase) were normal in both deficient and reversed animals.Thus, changes in the neurological signs during pyrithiamin-induced thiamin deficiency and in recovery paralleled the reversible damage to a mitochondrial enzyme and impairment of glucose oxidation and acetylcholine synthesis. A more sustained deficit in the pentose pathway enzyme, transketolase, may relate to the anatomical abnormalities that accompany thiamin deficiency.Dedicated to Henry McIlwain.     

The properties of transketolase from photosynthetic tissue

Transketolase (E.C. 2.2.1.1.) has been partially purified from wheat (Triticum aestivum, cv. Sappo) and spinach (Spinacia oleracea) leaves. The fully-active enzyme is a tetramer of relative molecular mass (M_r) of 150 kM_r requiring thiamin pyrophosphate for maximal activity, and dissociating into a 74 kM_r dimer in its absence or in dilute solution. The chloroplastic transketolase (over 75% of the cellular total) is magnesium-stimulated but the cytosolic form is magnesium-insensitive. Both chloroplastic and cytosolic transketolase showed similar broad specificities towards several ketose phosphate substrates including fructose 6-phosphate and sedoheptulose 7-phosphate. Wheat and spinach leaf transketolases are not light-activated and closely resemble the yeast enzyme in many of their properties.Abbreviations Mr relative molecular mass - TPP thiamin pyrophosphate - Tris 2-amino-2-(hydroxymethyl)-1,3-propandiol     

GTP-specific pyrophosphorylation of thiamin in dark-grown soybean (Glycine max) seedling axes

ATP:thiamin pyrophosphotransferase (TPT: EC 2.7.6.2) was purified 5 900-fold from 48 h dark-grown soybean [ Glycine max (L.), Merr. cv. Ransom II] seedling axes. TPT activity was monitored during purification by measuring the formation of thiamin pyrophosphate (TPP) from [2-¹⁴C]-thiamin at optimal pH (7.3). Although other nucleoside triophosphates were active as pyrophosphate donors (apparent K_ms from 21 to 138 m M ), GTP was the preferred nucleotide with an apparent K_m of 0.021 m M . TPT activity was extremely sensitive to TPP formation, suggesting product feedback inhibition of TPT activity in vivo. Sulfhydryl, H⁺ and Mg²⁺ concentrations, either independently or in concert, were found to affect TPT activity.     

Properties and functions of the thiamin diphosphate dependent enzyme transketolase

This review highlights recent research on the properties and functions of the enzyme transketolase, which requires thiamin diphosphate and a divalent metal ion for its activity. The transketolase-catalysed reaction is part of the pentose phosphate pathway, where transketolase appears to control the non-oxidative branch of this pathway, although the overall flux of labelled substrates remains controversial. Yeast transketolase is one of several thiamin diphosphate dependent enzymes whose three-dimensional structures have been determined. Together with mutational analysis these structural data have led to detailed understanding of thiamin diphosphate catalysed reactions. In the homodimer transketolase the two catalytic sites, where dihydroxyethyl groups are transferred from ketose donors to aldose acceptors, are formed at the interface between the two subunits, where the thiazole and pyrimidine rings of thiamin diphosphate are bound. Transketolase is ubiquitous and more than 30 full-length sequences are known. The encoded protein sequences contain two motifs of high homology; one common to all thiamin diphosphate-dependent enzymes and the other a unique transketolase motif. All characterised transketolases have similar kinetic and physical properties, but the mammalian enzymes are more selective in substrate utilisation than the nonmammalian representatives. Since products of the transketolase-catalysed reaction serve as precursors for a number of synthetic compounds this enzyme has been exploited for industrial applications. Putative mutant forms of transketolase, once believed to predispose to disease, have not stood up to scrutiny. However, a modification of transketolase is a marker for Alzheimer’s disease, and transketolase activity in erythrocytes is a measure of thiamin nutrition. The cornea contains a particularly high transketolase concentration, consistent with the proposal that pentose phosphate pathway activity has a role in the removal of light-generated radicals.     

The effects of partial thiamin deficiency and oxidative stress (i.e., glyoxal and methylglyoxal) on the levels of alpha-oxoaldehyde plasma protein adducts in Fischer 344 rats

We hypothesized that in marginal thiamin deficiency intracellular alpha-oxoaldehydes form macromolecular adducts that could possibly be genotoxic in colon cells; and that in the presence of oxidative stress these effects are augmented because of decreased detoxification of these aldehydes. We have demonstrated that reduced dietary thiamin in F344 rats decreased transketolase activity and increased alpha-oxoaldehyde adduct levels. The methylglyoxal protein adduct level was not affected by oral glyoxal or methylglyoxal in the animals receiving thiamin at the control levels but was markedly increased in the animals on a thiamin-reduced diet. These observations are consistent with our suggestion that the induction of aberrant crypt foci with marginally thiamin-deficient diets may be a consequence of the formation of methylglyoxal adducts.     

A new crystal form of mouse thiamin pyrophosphokinase

Thiamin pyrophosphokinase (TPK) transfers a pyrophosphate group from ATP to the hydroxyl group of thiamin and produces thiamin pyrophosphate (TPP). TPP is the cofactor of metabolically important enzymes such as pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, branched-chain α-keto acid dehydrogenase, transketolase and 2-hydroxyphytanoyl-CoA lyase. Thiamin deficiency results in Wernike-Korsakof Syndrome (WKS) due to neurological disorder and wet beriberi, a potentially fatal cardiovascular disease. Mouse TPK associates as a dimer revealed by previous solved crystallographic structures. In this study, we report mouse TPK complexed with TPP-Mg²⁺ and thiamin -Mg²⁺, respectively, in a new crystal form. In these two structures, four mouse TPK molecules were found in each asymmetric unit. Although we cannot rule out this tetramer form can be an artifact from crystal packing, mouse TPK tetramer has a more closed ATP binding pocket and has the potential to provide specific interactions between mouse TPK and ATP compared with the previous dimeric structure and is likely to be an active form.     

Impact of the reduced folate carrier on the accumulation of active thiamin metabolites in murine leukemia cells

The thiamin transporter encoded by SLC19A2 and the reduced folate carrier (RFC1) share 40% homology at the protein level, but the thiamin transporter does not mediate transport of folates. By using murine leukemia cell lines that express no, normal, or high levels of RFC1, we demonstrate that RFC1 does not mediate thiamin influx. However, high level RFC1 expression substantially reduced accumulation of the active thiamin coenzyme, thiamin pyrophosphate (TPP). This decreased level of TPP, synthesized intracellularly from imported thiamin, resulted from RFC1-mediated efflux of TPP. This conclusion was supported by the following observations. (i) Efflux of intracellular TPP was increased in cells with high expression of RFC1. (ii) Methotrexate inhibits TPP influx. (iii) TPP competitively inhibits methotrexate influx. (iv) Loading cells, which overexpress RFC1 to high levels of methotrexate to inhibit competitively RFC1-mediated TPP efflux, augment TPP accumulation. (v) There was an inverse correlation between thiamin accumulation and RFC1 activity in cells grown at a physiological concentration of thiamin. The modulation of thiamin accumulation by RFC1 in murine leukemia cells suggests that this carrier may play a role in thiamin homeostasis and could serve as a modifying factor in thiamin nutritional deficiency as well as when the high affinity thiamin transporter is mutated.     

大黄鱼幼鱼对饲料硒的需求量

为确定大黄鱼(Larimichthys croceus)对饲料硒的需求量, 以Na2SeO3为饲料硒源, 配制6种饲料, 硒的添加水平分别为0(对照组)、0.05、0.2、0.4、0.6和0.9 mg/kg, 实测值分别为0.08、0.16、0.27、0.44、0.66和0.96 mg/kg。在海水浮式网箱中养殖初始体重为(9.140.09) g的大黄鱼幼鱼10周, 结果表明增重率(WG)、全鱼和骨骼中的硒含量随着饲料硒含量的升高而显著升高(P0.05)。当饲料硒含量分别超过0.27、0.66、0.66 mg/kg时, 这些指标的变化趋于平稳。饲料硒含量对存活率(SR)、饲料效率(FE)、体组成、肝体比(HSI)、脏体比(VSI)和肥满度(CF)都没有显著影响(P0.05)。在血清中谷胱甘肽过氧化物酶(GPX)活性、超氧化物歧化酶(SOD)活性和总抗氧化力(T-AOC)随着饲料硒含量的升高呈现先升高后稳定的趋势(P0.05), 并分别在饲料硒含量为0.44、0.44、0.16 mg/kg时达到最大值。肝脏中GPX活性、SOD活性、T-AOC、过氧化氢酶(CAT)活性和谷胱甘肽还原酶(GR)活性与血清中相应酶的活性有相同的趋势。在肝脏中谷胱甘肽硫转移酶(GST)活性随着饲料硒含量的升高呈现先降低后升高的趋势(P0.05), 并在饲料硒含量最高(0.96 mg/kg)时其活力取得最大值。以WG为评价指标, 得出大黄鱼幼鱼对饲料中硒的需求量为0.178 mg/kg。以全鱼和骨骼中硒含量、肝脏GPX活性为评价指标, 得出大黄鱼幼鱼对饲料中硒的最小需求量分别为0.575、0.387和0.440 mg/kg。       

Regionally selective alterations in enzymatic activities and metabolic fluxes during thiamin deficiency

To further elucidate the molecular basis of the selective damage to various brain regions by thiamin deficiency, changes in enzymatic activities were compared to carbohydrate flux through various pathways from vulnerable (mammillary bodies and inferior colliculi) and nonvulnerable (cochlear nuclei) regions after 11 or 14 days of pyrithiamin-induced thiamin deficiency. After 11 days,large decreases (–43 to –59%) in transketolase (TK) occurred in all 3 regions; 2-ketoglutarate dehydrogenase (KGDHC) declined (–45%), but only in mammillary bodies; pyruvate dehydrogenase (PDHC) was unaffected. By day 14, TK remained reduced by 58%–66%; KGDHC was now reduced in all regions (–48 to –55%); PDHC was also reduced (–32%), but only in the mammillary bodies. Thus, the enzyme changes did not parallel the pathological vulnerability of these regions to thiamin deficiency.¹⁴CO₂ production from¹⁴C-glucose labeled in various positions was utilized to assess metabolic flux. After 14 days, CO₂ production in the vulnerable regions declined severely (–46 to 70%) and approximately twice as much as those in the cochlear nucleus. Also by day 14, the ratio of enzymatic activity to metabolic flux increased as much as 56% in the vulnerable regions, but decreased 18 to 30% in the cochlear nuclei. These differences reflect a greater decrease in flux than enzyme activities in the two vulnerable regions. Thus, selective cellular responses to thiamin deficiency can be demonstrated ex vivo, and these changes can be directly related to alterations in metabolic flux. Since they cannot be related to enzymatic alterations in the three regions, factors other than decreases in the activity of these TPP-dependent enzymes must underlie selective vulnerability in this model of thiamin deficiency.Abbreviations KGDHC 2-ketoglutarate dehydrogenase complex EC 1.2.4.2., EC 2.3.1.61, EC 1.6.4.3. - PDHC pyruvate dehydrogenase complex EC 1.2.4.2., EC 2.3.1.12, EC 1.6.4.3 - TK transketolase (EC 2.2.1.1) - TPP thiamin pyrophosphate     

Thiamin pyrophosphokinase is required for thiamin cofactor activation in Arabidopsis

Thiamin pyrophosphate (TPP) is an essential enzyme cofactor required for the viability of all organisms. Whether derived from exogenous sources or through de novo synthesis, thiamin must be pyrophosphorylated for cofactor activation. The enzyme thiamin pyrophosphokinase (TPK) catalyzes the conversion of free thiamin to TPP in plants and other eukaryotic organisms and is central to thiamin cofactor activation. While TPK activity has been observed in a number of plant species, the corresponding gene/protein has until now not been identified or characterized for its role in thiamin metabolism. Here we report the functional identification of two Arabidopsis TPK genes, AtTPK1 and AtTPK2 and the enzymatic characterization of the corresponding proteins. AtTPK1 and AtTPK2 are biochemically redundant cytosolic proteins that are similarly expressed throughout different plant tissues. The essential nature of TPKs in plant metabolism is reflected in the observation that while single gene knockouts of either AtTPK1 or AtTPK2 were viable, the double mutant possessed a seedling lethal phenotype. HPLC analysis revealed the double mutant is nearly devoid of TPP and instead accumulates the precursor of the TPK reaction, free thiamin. These results suggest that TPK activity provides the sole mechanism by which exogenous and de novo derived thiamin is converted to the enzyme cofactor TPP.     

饲料中添加雨生红球藻粉对三疣梭子蟹雌体卵巢发育、色泽、抗氧化能力和生化组成的影响

研究采用雨生红球藻(Haematococcus pluvialis)藻粉作为天然虾青素源, 配制4种不同虾青素含量(含量分别为0、26.60、41.62和81.37 mg/kg)的饲料(记为饲料1#—4#), 对三疣梭子蟹(Portunus trituberculatus)雌体进行为期45d的育肥实验, 研究其对雌蟹卵巢发育、色泽、抗氧化能力、免疫性能和生化组成的影响。结果表明: (1)育肥饲料中虾青素含量对雌蟹性腺指数(GSI)和肝胰腺指数(HSI)均无显著影响。(2)肝胰腺、卵巢和头胸甲中的总类胡萝卜素含量、红度(a*)值和黄度(b*)值均随饲料虾青素含量的升高而升高, 而3种组织的亮度(L*)值呈显著下降趋势(P<0.05)。(3)对抗氧化指标而言, 虾青素添加组(饲料2#—4#)血淋巴超氧化物歧化酶(SOD)和过氧化物酶(POD)活力均显著低于无虾青素组(饲料1#); 血淋巴中的总抗氧化能力(T-AOC)、谷胱甘肽过氧化物酶(GSH-Px)及肝胰腺中的SOD和T-AOC活力均随饲料中虾青素水平升高而上升, 而血淋巴和肝胰腺中的丙二醛(MDA)含量呈下降趋势。(4)对免疫指标而言, 血淋巴和肝胰腺中的酸性磷酸酶(ACP)活力均在饲料4#组最高, 而饲料1#组血淋巴中的血蓝蛋白(Hc)含量显著高于其他组(P<0.05)。(5)对生化组成而言, 肌肉和肝胰腺中的总脂、总碳水化合物及卵巢中总脂含量均随饲料中虾青素含量的升高呈上升趋势, 饲料2#组卵巢中的总碳水化合物含量最高(P<0.05)。综上所述, 三疣梭子蟹雌体育肥饲料中添加虾青素对其卵巢发育无显著影响, 但可改善色泽和提高其抗氧化能力及可食组织中的总脂和碳水化合物含量, 三疣梭子蟹雌体育肥饲料中虾青素适宜含量为50 mg/kg饲料左右。     

Gut loading to enhance the nutrient content of insects as food for reptiles: A mathematical approach

A variety of commercially raised insects are fed to insectivorous reptiles, but information concerning appropriate diets used to feed these insects is limited. In the present study, house crickets (Acheta domesticus adults and nymphs), mealworms (Tenebrio molitor larvae), and silkworms (Bombyx mori larvae) were fed diets containing graded levels of calcium (Ca) and/or vitamin A–nutrients that are low or absent in most insects. Diets and insects were analyzed for moisture, Ca, phosphorus (P), and vitamin A. For adult crickets and cricket nymphs, body Ca and vitamin A concentrations increased in a linear fashion with increasing levels of dietary Ca or vitamin A. Ca concentrations of silkworms also increased in a linear fashion with increasing levels of dietary Ca. For mealworms, body Ca and vitamin A concentrations increased in a nonlinear fashion with increasing levels of dietary Ca or vitamin A. These regression equations, in conjunction with insect nutrient composition, allow for the calculation of the optimum nutrient concentration for gut‐loading diets. Final recommendations were based on National Research Council (NRC) requirements for rats, adjustments for the energy content of the insects, and nutrient overages as appropriate. Gut‐loading diets for crickets (adults and nymphs) should be supplemented to contain the following nutrients, respectively: Ca (51 and 32 g/kg), vitamin A (8,310 and 5,270 µg retinol/kg), vitamin D (300 and 190 µg cholecalciferol/kg), vitamin E (140 and 140 mg RRR‐α‐tocopherol/kg), thiamin (31 and 21 mg/kg), and pyridoxine (20 and 10 mg/kg). Gut‐loading diets for mealworms should be supplemented to contain the following nutrients: Ca (90 g/kg), iron (51 mg/kg), manganese (31 mg/kg), vitamin A (13,310 µg retinol/kg), vitamin D (460 µg cholecalciferol/kg), vitamin E (660 mg RRR‐α‐tocopherol/kg), thiamin (5 mg/kg), vitamin B₁₂ (650 µg/kg), and methionine (29 g/kg). Gut‐loading diets for silkworms should be supplemented to contain the following nutrients: Ca (23 g/kg), iodine (0.7 mg/kg), vitamin D (140 µg cholecalciferol/kg), vitamin E (70 mg RRR‐α‐tocopherol/kg), and vitamin B₁₂ (226 µg/kg). Zoo Biol 22:147–162, 2003. © 2003 Wiley‐Liss, Inc.     

Protective effects of taxifolin on pazopanib-induced liver toxicity: an experimental rat model

Pazopanib is a tyrosine kinase inhibitor that is generally used for the treatment of metastatic renal cell cancer and advanced soft tissue sarcoma. It can cause various degrees of hepatotoxicity. Our study aimed to investigate the effect of taxifolin on pazopanib-induced liver toxicity. A total of 18 rats were divided into three groups: the pazopanib (PP), pazopanib plus taxifolin (TPP), and control (C) group. Taxifolin was administered to the TPP (n=6) group with a dose of 50 mg/kg. Distilled water was orally admnistered to the C (n=6) and PP (n=6) groups as a solvent. Subsequently, pazopanib 200 mg/kg was administered to the TPP and PP groups via the stomach. This procedure was repeated once a day for four weeks. Then, all rats were sacrificed, and their livers were removed. Malondialdehyde (MDA), total glutathione (tGSH), total oxidant status (TOS), and total antioxidant status (TAS) levels were evaluated. MDA and TOS levels were higher in the PP group compared with the levels of the other parameters (P<0.001). tGSH and TAS levels were lower in the PP group than in the TPP and C groups (P<0.001), and the aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) levels were higher. Furthermore, liver tissue damage, including hemorrhage, hydropic degeneration, and necrosis was observed in the PP group. Administration of taxifolin before pazopanib significantly improved degenerative changes. Our study demonstrated that the administration of taxifolin is significantly effective in preventing pazopanib-induced hepatotoxicity in rats.     

An Estimation of the Manganese Requirement for Broilers from 1 to 21 Days of Age

A dose–response experiment was conducted to find the sensitive and consistent biomarker for the estimation of dietary manganese (Mn) requirement and establish the optimal Mn level for broilers fed a practical corn–soybean meal diet from 1 to 21 days of age post-hatching. A total of 480 1-day-old Arbor Acres male chicks were randomly allotted to one of eight treatments with five replicates of 12 birds each and fed diets supplemented with 0, 20, 40, 60, 80, 100, 120, or 140 mg Mn/kg from reagent grade Mn sulfate. Tissue Mn concentrations, manganese-containing superoxide dismutase (MnSOD) activity, and MnSOD mRNA concentration within heart tissue were analyzed at 7, 14, and 21 days of age. Tissue Mn concentrations and heart MnSOD activity showed significant quadratic responses, and heart MnSOD mRNA concentration showed an asymptotic response to dietary supplemental Mn level, respectively. The estimate of dietary Mn for chicks from 1 to 21 days of age was 122–128 for heart Mn concentration, 141–159 for pancreas Mn concentration, 127–138 for liver Mn concentration, and 135–156 mg/kg for heart MnSOD activity, respectively. Heart MnSOD mRNA concentration was a consistent index for the estimation of the Mn requirement of broilers. Based on this index, the estimate of dietary Mn requirement for broilers from 1 to 21 days of age post-hatching was about 130 mg/kg, which was a little more than two times of the current NRC (1994) requirement.