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G Sályi

Publications and source records attributed to G Sályi.

9 recordsLinked to original sources
PubMed1997

Nutritional metabolic diseases of poultry and disorders of the biological antioxidant defence system.

Deficiencies or disturbances of nutrition cause a variety of diseases and can arise in different ways. The amount of a particular nutrient in the diet may be insufficient to meet the requirements, the diet may contain substances that inactivate the nutrient or inhibit its absorption/utilisation, or metabolism may be upset by the interaction of dietary and environmental factors. Peroxidation of lipids or oxygen free radical generation in general is a physiological process important for cell metabolism, division and differentiation and also for the biosynthesis of hormones and prostaglandins. Free radicals generated through these processes are effectively scavenged by the antioxidant defence system. Uncontrolled lipid oxidation caused by disturbances of that system may play a crucial role in some important poultry diseases and toxicoses. The first route of lipid peroxide loading of the organism is via the feed, such as through oxidised lipids. Oxidised fatty acids are absorbed from the intestine mainly in the form of unsaturated keto compounds and initiate lipid peroxidation in the tissues. The second problem is the insufficient amount of antioxidants in the feed, e.g. vitamin E deficiency. Nutritional encephalomalacia is a problem in poultry production which depends both on the actual vitamin E supply and the dietary amount of polyunsaturated fatty acids. In young birds the primary target of vitamin E deficiency is the brain because it contains low amounts of vitamin E, and the vitamin E content of the liver acting as store decreases rapidly during the first week of life. Besides vitamin E, other components of the antioxidant system, e.g. the antioxidant enzymes (catalase and glutathione peroxidase) also have low activity in the brain as compared to other major tissues. The brain is highly susceptible to oxidative stress because of the accumulation of polyunsaturated fatty acids. The third source of free radical generation is the toxic level of different feed ingredients, e.g. toxicoses caused by vitamin A, selenium, and ionophore antibiotics. Other important aspects of antioxidants (e.g. vitamin E and selenium) in poultry are stimulation of the immune response (e.g. in the case of vaccination) and reduction of the risks of free radical formation as a result of macrophage function.

Animals↗
PubMed1994

Effect of acute selenium toxicosis on the lipid peroxide status and the glutathione system of broiler chickens.

The effect of acute oral selenium toxicosis on the rate of lipid peroxidation, on the amount of reduced glutathione as well as on glutathione-peroxidase activity of the blood (plasma and red blood cells) and liver was studied in broiler chicken. Cockerels (28-day-old) were treated with selenium (4.85 mg/kg b.w.) administered intraoesophageally in the form of sodium selenite. Samples were at the onset of clinical signs (3 h after treatment) and 2 and 4 h thereafter. The malondialdehyde content of the blood plasma rose significantly (P < 0.05) at the onset of clinical symptoms but decreased later. Malondialdehyde content of the liver was higher than the control value at the first sampling (P < 0.01) and steadily increased later. Reduced glutathione content did not change significantly in the blood plasma and liver. Glutathione peroxidase activity of the RBC was significantly elevated (P < 0.01) only at the first sampling (3 h after treatment) and decreased to the control level thereafter. Acute oral selenium toxicosis increases the rate of lipid peroxidation in a short period of time (7 h) without exerting a significant effect on the glutathione system.

Animals↗
PubMed1992

Effect of acute salinomycin-tiamulin toxicity on the lipid peroxide and antioxidant status of broiler chicken.

The combined effect, if any, of salinomycin poisoning and salinomycin-tiamulin interaction on lipid-peroxidative processes and the antioxidative defence system of the liver was studied in domestic fowl. Male broilers (28-day-old), reared on a diet containing 60 mg/kg salinomycin, were treated intraoesophageally with salinomycin (140 mg/kg body mass) or tiamulin (50 mg/kg body mass). Malondialdehyde, reduced glutathione and cytochrome P-450 concentrations as well as glutathione peroxidase and catalase activities of the liver were determined. Liver malondialdehyde concentration rose in the salinomycin-treated group while the amount of cytochrome P-450 increased in both groups treated. Glutathione concentration and glutathione peroxidase activity of the liver decreased rapidly but hepatic catalase activity increased in both groups after the treatment. Manifestation of the effect exerted by salinomycin and salinomycin-tiamulin on lipid-peroxidative processes nearly coincided with the onset of clinical signs and preceded the increase of hepatic cytochrome P-450 concentration. According to the results, the background of the previously reported incompatibility between salinomycin and tiamulin is the synergistic effect exerted on the antioxidant (glutathione) system.

Animals↗
PubMed1990

Changes in the lipid peroxide status of broiler chickens in acute monensin poisoning.

The effect exerted by overdosage of monensin, an ionophore antibiotic, on the lipid peroxide status of broiler chickens was studied. Three-week-old broiler cockerels were given 150 mg monensin/kg body mass through a tube, and the malondialdehyde (MDA) concentration, glutathione peroxidase (GSH-Px) and catalase activity of the liver and breast muscle, and MDA concentration and GSH-Px activity of the blood plasma were determined. Liver MDA and catalase values rose rapidly and significantly during the experimental period. GSH-Px activity initially decreased, then tended to rise. Blood plasma and breast muscle variables did not change during the experiment. Acute monensin poisoning induced substantial enhancement of lipid peroxidation processes in the liver, while it did not appreciably affect the lipid peroxide status of the blood plasma and breast muscle. The role of the observed phenomenon in the rather complex pathogenesis of monensin poisoning is not known sufficiently. Further studies are needed to elucidate the problem.

Animals↗
PubMed1989

Interaction of T-2 fusariotoxin and monensin in broiler chickens infected with Coccidia.

Field observations suggest that coccidiosis is a common cause of death in broiler chicken flocks fed diets containing sufficient amounts of ionophore antibiotics (monensin, narasin, etc.) and contaminated with mycotoxins, particularly with T-2 fusariotoxin. To study this phenomenon, broiler chickens fed diets containing different amounts of T-2 toxin and free from monensin, or containing a preventive dose (100 mg/kg of feed) of monensin, were infected experimentally with coccidian oocysts. In all groups fed a diet containing monensin plus T-2 toxin severe clinical symptoms of coccidiosis (blood-stained faeces etc). occurred. Deaths and retarded growth depended on the toxin dose and were considerable. The body mass gain of chicks fed a diet containing monensin and T-2 toxin but not infected with coccidia was inferior to that of groups fed diets which contained either monensin or T-2 toxin (experiment 2). On the basis of these findings a negative interaction of the two compounds is assumed. This seems to be supported by the results of experiment 3, i. e. the finding that the lethal dose of narasin, a compound closely related to monensin both in chemical structure and mechanism of action, proved to be much lower (LD50 = 102 mg/kg body mass) for chickens fed a diet supplemented with T-2 toxin than for the control chickens (LD50 = 176 mg/kg body mass). The present results suggest that the feeding of diets severely contaminated with T-2 toxin may alter the anticoccidial efficacy of monensin.

Animals↗
PubMedDate not supplied

Rapid decrease of the peripheral deiodination of thyroxine in malabsorption syndrome in artificially inoculated broilers.

Thyroid function of broilers inoculated with the intestinal homogenate from birds from a field case of malabsorption syndrome was investigated during the first 2 days postinoculation. In one experiment, different amounts of the inoculum were applied to see if there exists a dose-response relationship. As early as 3 hours after inoculation, there was a significant drop in the serum level of triiodothyronine and in the activity of the liver 5'-deiodinase (type I). Type II deiodinase activity was less impaired. A minimum of 0.3 ml of inoculum was effective, whereas 0.05 ml of the same homogenate elicited a significant (P less than 0.01) drop in liver deiodinase activity. These findings underline the importance of thyroid impairment in the pathogenesis of malabsorption syndrome.

Animals↗
PubMedDate not supplied

Decreased thyroxine, triiodothyronine, and 5'-deiodination levels in malabsorption syndrome (runting or stunting syndrome) in artificially inoculated broilers.

The effect of malabsorption syndrome (stunting or runting syndrome) on the thyroid function of broilers was investigated in control and inoculated broilers from 1 to 29 days of age. The broilers were infected at 1 day of age with intestinal homogenates from chickens naturally suffering from this syndrome. The body weight of inoculated broilers was significantly (P less than 0.05) lower 1 week after inoculation than that of controls. The level of thyroxine in the serum of inoculated birds was lower (P less than 0.05) from day 6 through the remainder of the trial. The level of triiodothyronine of inoculated birds was depressed (P less than 0.05) on day 4, but 1 week later it returned to normal. The earliest phenomenon indicative of disturbance of thyroid function was the significant depression of 5'-deiodination in liver homogenates of inoculated broilers as early as day 2. It is concluded that thyroid function is one of the earliest targets of this syndrome.

Animals↗