Amount and type of unsaturated aldehydes in chicken plasma and tissues depend more on dietary lipids than on vitamin E status.
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Biomedical subjects
Publications and source records attributed to H Fuhrmann.
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The enzymatic fundamentals of lipid metabolism of equine have not been thoroughly investigated at this point in time. It is still unclear why ponies in contrast to horses may become hyperlipaemic when coming negative energy balance. In this study, the activities of the triglyceride-cleaving key enzymes of ponies are large bred horses were investigated in order to obtain insight into the aetiology of the syndrome. The objective of the study was to measure the activities of hormone-sensitive lipase (HSL), lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) in ponies and horses in ex vivo in vitro assays. Norepinephrine (NE) stimulated pony adipocytes to release FFA in a linear fashion (4.57 +/- 2.09 nmol FFA.10(5) cells-1.min-1). This was not observed in horses. Lipolysis was significantly higher in fat cells of ponies than in horses when adenosine deaminase (ADA) and NE were added (12.71 +/- 3.12 vs. 1.96 +/- 1.22 nmol FFA.10(5) cells-1.min-1). Relative inhibition of lipolysis by the action of insulin was comparable in adipocytes of horses and ponies. However, absolute FFA release in pony fat cells was as high as the maximal NE and ADA stimulated lipolysis in horse adipocytes. Postheparin plasma lipase activities in ponies and horses did not differ between the sub-species. This finding was supported by the results obtained from measurement of LPL activity in adipose and muscle tissue showing only a tendency of increased activities in pony explants when compared to horse tissue incubations. This study further supports the hypothesis that differences in regulation of TG release from fat stores rather than clearance of TG from plasma is causative for the development of hyperlipaemia in ponies. Abbreviations used: ADA, adenosine deaminase; BW, body weight; FFA, free fatty acid; HSL, hormone-sensitive lipase; HTGL, hepatic triglyceride lipase; LPL, lipoprotein lipase; NE, norepinephrine; SDS, sodium dodecyl sulfate; TG, triglyceride; VLDL, very low density lipoprotein.
This study investigated the inhibitory efficiency of all-rac-alpha-tocopherol, 2,6-ditert-butyl-p-cresole (BHT), and 6-hydroxy-2,5,7,8-tetramethyl-chroman-2-carbonic acid (Trolox) on determination of thiobarbituric acid-reactive substances (TBARS) and short-chain alkenals in rat liver homogenates. The concentration of TBARS was measured fluorophotometrically. Aldehydes were determined after derivatization with methylhydrazine by gas chromatography (GLC). The concentrations of alkenals and TBARS in liver homogenates were diminished when antioxidants were present during the sample preparation. It is suggested that in the absence of antioxidants the samples are autoxidized further during the preparative procedures. For the aldehyde determination all-rac-alpha-tocopherol was the most effective antioxidant to reduce the bias due to autoxidation, whereas for TBARS it was Trolox.
In a prospective study from 1991-1998 plasma concentrations of alpha-Tocopherole (VitE) and Selenium (Se) were analysed in 125 sheep and 32 goats with generalised motor disturbances or elevated plasma-activities of Creatine-Kinase (CK). VitE-values < 1.0 mg/l and Se-values < 0.08 mg/l were regarded as deficiency. Diagnosis of pathological manifestations was based on blood enzyme values. CK-values in plasma > 300 U/l or Aspatate-Amino-Transferase (ASAT) > 150 U/l were regarded as myopathy, Glutamat-Dehydrogenase-values > 25 U/l indicated a hepatopathy. 92 (74%) sheep and 10 (31%) goats showed VitE and/or Se deficiency. There were no principal differences in the frequencies of myopathies (67%) and hepatopathies (46%) between pure VitE deficiencies or pure Se deficiencies or combinations of both deficiencies. In VitE deficiency and in the combinations of VitE and Se deficiency the elevations of the enzyme activities were more pronounced than in Se deficiency. The lethality was significantly higher in combined VitE + Se deficiencies (73%) than in pure VitE or Se deficiencies (35%). Combined VitE + Se deficiencies occurred more frequent in lambs (53%) and was often accompanied by anaemia (29%) and hypoproteinaemia (32%). The diagnostic reliability of ASAT and GLDH for the detection of VitE and Se deficiency was better than CK. Diagnostic and therapeutic strategies in flock diseases are discussed.
Single two-dimensional (2D) atomically thick magnetic particles of cobalt and iron with variable size and shape were fabricated by combining a mask technique with standard molecular beam epitaxy. Reduction of the lateral size of in-plane magnetized 2D cobalt films down to about 100 nanometers did not essentially modify their magnetic properties; although the separation of boundaries decreased greatly, neither domain penetrated the particle, nor was any sizable shape anisotropy observed. The mutual interaction of 2D cobalt particles was negligible, and the magnetic state of a single particle could be switched without modifying the state of the neighbors. Perpendicularly magnetized iron particles did not exhibit such responses. These results suggest that only a few atoms forming a 2D in-plane magnetized dot may provide a stable elementary bit for nanorecording.
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214 ewes suffering from pregnancy toxaemia (ketosis) were examined. Clinical signs during onset and course of disease and laboratory findings were compared between animals that survived and those which died. In the latter the onset of ketosis was earlier in pregnancy (day 143 +/- 7 vs. day 146 +/- 8) and duration of the disease was shorter (10 +/- 13 vs. 14 +/- 9 days). The animals that died showed more severe clinical signs and higher values of 3-hydroxy-butyrate (4.3 +/- 3.6 vs. 3.5 +/- 2.6 mmol/l) and cortisol (72 +/- 98 vs. 52 +/- 80 mmol/l) as well as lower values of insulin (37 + 12 vs. 3.5 + 2.6 mmol/l) and potassium (4.1 + 1.0 vs. 4.4 + 1.0 mmol/1) at onset of the disease than those which survived (all of differences with P < 0.05). Glucose levels did not differ between groups. Treated animals with glucose plus fructose infusions (n = 56) or with oral application of glucose precursors plus electrolytes (n = 126) had survival rates of 53.6% and 62.7%, respectively. Oral treatment with glucose precursors plus electrolytes and an additional subcutaneous insulin treatment (n = 15) led to an enhanced survival rate of 86.7% (P < 0.05). Low insulin levels in ketotic pregnant sheep and the therapeutic effect of insulin treatment support the hypothesis that insulin plays a causative role in the pathogenesis of ovine ketosis.
A simple and sensitive method for direct and continuous monitoring of free fatty acid (FFA) release, by measuring the pH-sensitive change in relative fluorescence intensity of seminaphthofluorescein (SNAFL-1) is described. The method was designed to use a small number of adipocytes isolated from fat pads of rats and biopsy specimens of horses for the detection of decreasing pH in fat cell suspensions caused by released FFA into the incubation medium. Species specific differences of lipolysis were demonstrated when adipocytes of rats and horses are incubated with stimulators or inhibitors of lipolysis. Norepinephrine (NE) stimulated lipolysis in fat cells of rats whereas adipocytes of horses showed a measurable release of FFA when concomitantly incubated with NE and adenosine deaminase (ADA) or NE and 8-Phenyltheophylline (8-PT), respectively). The incubation of equine fat cells with NE and ADA did not influence the antilipolytic response to insulin. The method described enables micro-scaled in vitro studies on lipolytic activity.
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The aim of the study was to gain informations about factors responsible for the higher level of plasma glucose in camels as compared to sheep and ponies. An intravenous glucose tolerance test was carried out with four camels, four ponies, and four sheep by infusing 1 mmol glucose per kg body weight intravenously within 3 min. Concentrations of glucose, insulin, and non-esterified fatty acids (NEFA) were estimated in venous plasma samples taken before and within 6 hr after infusion. Basal glucose values were higher in camels (7.1 +/- 0.3 mmol/l) than in ponies (4.2 +/- 0.4 mmol/l) and sheep (3.4 +/- 0.2 mmol/l). The rate of glucose elimination was markedly lower in camels (0.270 +/- 0.018 hr-1) than in sheep (0.804 +/- 0.036 hr-1) and ponies (0.858 +/- 0.084 hr-1). The insulin response after glucose infusion was more pronounced in ponies and sheep than in camels. Concentrations of NEFA in plasma dropped 30 min after the infusion in all species, however, NEFA level decreased slower in camels than in sheep and ponies. It is concluded that the markedly higher plasma concentration of glucose in camels compared to sheep and ponies may be caused by a poorer insulin response and/or a reduced tissue sensitivity to insulin.
Early weaned piglets were divided into eight groups of 6 animals each. The animals were fed diets differing in fat quality (4% soybean oil, POZ 5 or 176) and in the content of the vitamins A (5,000 or 20,000 I.U./kg) and E (25 or 125 I.U./kg) over a period of 7 weeks. At the beginning, on day 25 and 47 blood samples were taken and analysed for vitamin A and E. In liver, heart, M. longissimus dorsi and M. semitendinosus vitamin A, E and the TBA-reactive substances were analysed. Induced lipid peroxidation was assessed by the ethane and pentane production rate in the skeletal muscle. During the weaning period a decrease in the alpha-tocopherol level was observed. In groups with the lower doses of vitamin E this effect was more pronounced. After 47 days the alpha-tocopherol concentrations in plasma and heart and skeletal muscle fell about 25-30% by offering high doses of vitamin A compared to those groups fed low doses. Oxidized fats also led to lower tocopherol concentrations in muscle tissues. Hydrocarbon production in M. longissimus dorsi and M. semitendinosus was significantly reduced in groups with the high supplement of vitamin E. A tendentially opposite effect was seen in groups supplied with high levels of vitamin A or oxidized fat. Although retinyl esters in plasma are a minor fraction of the vitamin A activity, they present 99% of the vitamin A in the liver. The distribution pattern of the different retinyl esters was independent of the amount of supplementary vitamin A. In the present experiment 20,000 U of Vitamin A reduced plasma and tissue vitamin E levels. This effect led to an increase of lipid peroxidation indicated by the higher production of hydrocarbons. The results raise concerns about further increases of vitamin A supplementation in piglet feed.
Dietary fatty acids modify phospholipid fatty acids in brain and liver of growing chickens post-hatching. The effect of vitamin E deficiency on this process is unknown and may be relevant to the pathogenesis of chick nutritional encephalomalacia (NE). Therefore laying hens received a diet low in vitamin E (10 mg alpha-tocopherol/kg feed). Resulting chicks were assigned to nine dietary groups each fed with either oleic (18:1n-9, 58 g/kg), linoleic (18:2n-6, 57 g/kg) or linolenic (18:3n-3, 56 g/kg) acid together with 5. 25 or 125 mg alpha-tocopherol/kg feed. NE affecting the cerebellum only occurred in the group given linoleic acid and 5 mg alpha-tocopherol/kg. In 1-d-old chicks and after 1 and 2 weeks the phospholipid fatty acid composition of liver, cerebrum and cerebellum (additionally after 3 weeks) was determined. The feed fatty acids were incorporated into the liver very efficiently during the first week of life. Unsaturation of liver membranes decreased in the order dietary linolenic > linoleic > oleic acid. In liver, also, the effect of alpha-tocopherol supplementation on phospholipid fatty acids was most pronounced. The unsaturation index increased during deficiency, whereas n-9 fatty acids decreased. In the chicken brain the alterations were delayed and less distinct. The cerebellum phospholipids were rich in n-9 fatty acids and as a whole more saturated in comparison with the cerebrum. Cerebellar unsaturation increased when linolenic or linoleic acid was given. However, NE-producing dietary conditions were not accompanied by specific alterations in cerebellar phospholipid fatty acids due to the alpha-tocopherol content of the diet. Rather the alterations of membrane fatty acids in the liver seem to play a role in the pathogenesis of NE.
The consequences of different dietary fats in combination with two vitamin E levels on peroxidative tissue damage of chicken brain and liver and its meaning for development of nutritional encephalomalacia (NE) were investigated. A feeding experiment was performed with 1-day-old chickens from hens on a vitamin-E-poor diet. The animals received a vitamin-E-deficient basic diet containing 10% fat, rich in either C18:3n3-, C18:2n6- or C18:1n9-fatty acids. The fat was given either fresh or oxidized (peroxidation number: 250) and 0 or 50 ppm alpha-tocopherylacetate was added. Typical symptoms of NE occurred mainly in those groups fed with n6-fatty acids beginning on day 7. In order to evaluate oxidative tissue damage, conjugated dienes, fluorescent pigments and TBA-reactive substances were determined in liver, cerebrum and cerebellum. Brain was examined histologically. In liver and cerebrum, the feeding of oxidized fats led to a 20% increase in conjugated dienes. Fluorescent pigments could be determined only in the brain tissues. However, feeding conditions had no effect, although autofluorescence was observed histologically in the affected animals. TBA-reactive substances were heightened in cerebrum (30%) and liver (130%) as a result of feeding linolenic acid. Vitamin E deficiency doubled TBA-reactive substances only in the liver. The parameters measured did not show intensified lipid peroxidation in the cerebellum of the animals fed the NE producing diet. Rather, the liver seems to be affected by the oxidative stress.
In this study consequences of vitamin A-supplementation to the vitamin E-status was investigated in the boar. Three groups of boars, each with 9 animals were fed over a period of seven month with 30000 I.E. Vit. A/kg concentrate (group A), 90 mg b-carotene + 1000 I.E. Vit. A/kg (group B) and 1000 I.E. Vit. A/kg (group C). Every boar was given 100 mg Vit. E/kg plus 50 ml soybean oil/kg to induce oxidative stress. After four month group C showed a higher amount of tocopherol in serum (p < 0.05). The amount of tocopherol in serum of the group B were exactly between group A and C. The amount of retinol in serum of the group C began to decrease after three month due to the high reserve capacity of the liver (p < 0.01). The retinyl ester in serum reflected the state of supply. 90 mg b-carotene led to an efficiency of 15000 I.E. Vit. A. The vitamin antagonism between Vit. A and Vit. E is not based on an antagonism of the intestinal resorption. There was no influence on the daily sperm production caused by different supplementations. The sperm quality was lowered in group C; the number of defective sperm increased (p < 0.001). The supplementation of soybean oil lead to an increase of the saturated fatty acids in the fatty acid pattern of the sperm cells. The increase of saturated fatty acids was the lowest in group C that showed the highest amount of tocopherol in serum.
One of the classical vitamin E deficiency syndromes is nutritional encephalomalacia in broiler chicken. Subject of this study was the influence of dietary fatty acids and vitamin E on phospholipase A2 and alpha-tocopherol concentration in liver, cerebrum and affected cerebellum posthatching. Therefore, chicks were fed either oleic, linoleic or linolenic acid rich fats together with 5, 25, or 125 ppm vitamin E. At the end of 0, 1, 2 and 3 weeks the tocopherol content and phospholipase A2 activity of liver, cerebrum and cerebellum were determined. Dietary fatty acids did not influence tissue alpha-tocopherol and phospholipase A2. In the vitamin E-deficient cerebellum the enzyme activity of cytosolic phospholipase A2 was increased. Due to its low content of vitamin E the cerebellum is the most susceptible tissue to oxidative stress during vitamin E deficiency.
Nutritional encephalomalacia (NE) in broiler chicken is considered as a peroxidative dysfunction caused by vitamin E-deficient diets. A feeding experiment was performed to investigate the consequences of feeding different fats in combination with increasing amounts of vitamin E on liver lipid peroxidation and plasma prostanoid pattern. Newly hatched chicks from hens on a vitamin E-poor diet were fed with either mainly linolenic, linoleic or oleic acid-rich oils in a vitamin E-deficient (5 ppm) basic diet. The animals were supplemented with vitamin E on three levels (0, 20 or 120 ppm). On appearance of the first symptoms of NE after 8 days post-hatching, the animals were examined. Typical symptoms with a high incidence only occurred in the group fed linoleic acid and 5 ppm vitamin E. Plasma prostanoids and microsomal alkane production in liver as a measure of endogenous lipid peroxidation were determined. The dietary conditions affected plasma prostaglandin E2 and thromboxane A2, but not prostacyclin. However, it seems unlikely that the prostanoids are involved in the pathogenesis of NE. Liver lipid peroxidation increased in vitamin E deficiency. The level of alkanes depended on the type of fat supplied. The consequences of the different dietary fats in combination with vitamin E deficiency on peroxidative metabolism of broiler chickens are evident, indicating that a high level of oxidative stress is imposed by the linoleic acid-rich fat.
Bioefficiencies of alpha-, gamma- and delta-tocopherol in comparison with all-rac-alpha-tocopherol were established in broiler chickens. For this, 1-d-old male broiler chickens received a diet deficient in vitamin E and supplemented with increasing doses of the corresponding tocopheryl acetates. After 2 and 3 weeks of feeding, the animals were killed to obtain blood and liver samples. The ex vivo tests used were detergent-induced haemolysis and pentane production by liver microsomes. Bioefficiencies were calculated by comparison of the dose-response curves. It is concluded that haemolysis and pentane production are appropriate indicators of the bioefficiency of tocopherols in broiler chickens. The values obtained by both tests hardly differed and agree well with the figures previously obtained from rats and other species.
Fischer 344 rats were fed a low-fat high carbohydrate (HC) diet, an isocaloric fat-containing (IC) diet, a hypercaloric fat-containing (HF) diet or a commercial rodent chow. The effects of these diets were studied on the binding of aflatoxin B (AFB1) to exogenous DNA, and on the activities of hepatic glutathione transferases (GSTs), cytochromes 2B1 and 1A1. Microsome-mediated binding of [3H]AFB1 to exogenous DNA was significantly lower in the HC-rats than in the chow and IC-fed rats. No significant differences were noted between HF and either HC or IC rats. There was no significant difference in hepatic GST activity of rats fed the different diets. Our results suggest that high-carbohydrate low-fat diets reduce microsome mediated epoxidation of AFB1 to a larger extent than high-fat diets. In general, high fat diets increased cytochrome 1A1 and 2B1 activities relative to chow and high carbohydrate diet. This suggests greater detoxification of AFB1, thus reducing the amount of AFB1 available for hepatic macromolecular binding.