Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three experiments were conducted to evaluate the influence of several dietary factors on the monensin response in commercial broiler chicks fed corn-soybean meal diets varying in crude protein (CP). All experiments were conducted between 8 and 22 days posthatching. Trial 1 had a 2 X 2 X 2 factorial design wherein diets containing 16 or 24% CP and 0 or 121 mg/kg monensin were fed in the presence and absence of Eimeria acervulina infection. The monensin-induced growth depression was greater at 16% CP than at 24% CP. Coccidial infection had no effect on the monensin X protein level interaction. Monensin supplementation markedly improved performance of chicks infected with E. acervulina. Trial 2 was conducted to determine if the monensin-induced depression in performance caused by feeding a high level of monensin (140 mg/kg) could be moderated by feeding a high protein diet. Monensin supplementation reduced growth rate 18 and 10% in chicks fed 20 and 24% CP, respectively. Increasing CP to 28% alleviated the adverse effects of monensin on weight gain. Pair-feeding was used in Trial 3 to determine the extent to which the monensin-induced growth depression observed in chicks fed low protein diets was due to reduced feed intake. As expected, reducing the dietary CP from 24 to 16% resulted in a marked increase in the growth depression caused by 121 mg/kg monensin. Pair-feeding indicated that most of monensin's adverse effects in low protein diets could be attributed to its anorexic properties.
 ...
PMID:Further investigation of the dietary protein and monensin level interrelationship in broiler chicks: influence of Eimeria acervulina infection, increased dietary protein, and level of feed intake. 379 74

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.
 ...
PMID:Practical toxicologic diagnosis. 649 3

The effects of several dietary factors on the anorexigenic response to monensin in chicks fed corn-soybean meal diets varying in crude protein (CP) were investigated. In Trial 1, crossbred chicks (New Hampshire X Columbia) were fed a 16% CP diet with or without 160 mg/kg monensin and/or .53% potassium carbonate in a 2 X 2 factorial design. Monensin supplementation caused a 24.5% growth depression, and potassium carbonate had no effect on the monensin-induced depression. Trials 2 and 3 were designed to evaluate the effects of dietary energy level on the monensin response in commercial broiler chicks fed diets containing 24, 20, or 16% CP. As CP level was decreased, the depression in performance from 121 mg/kg monensin increased. Increasing the energy concentration of the 24 and 20% CP diets to that of the 16% CP diet had no consistent effect on the response of chicks to monensin. Trial 4 was conducted to determine the influence of amino acid (AA) supplementation on the monensin response in broiler chicks fed a low-protein diet. Supplementation of a 16% CP diet with an AA mixture (3% glutamic acid plus essential AA equal to the 24% CP diet) improved growth performance markedly. Deletion of methionine, arginine, and lysine from the AA mixture yielded performance well below that of chicks fed the unsupplemented 16% CP diet, indicating a severe AA imbalance. Monensin supplementation at 121 mg/kg caused a much greater growth depression in chicks fed 16% CP or 16% CP plus the complete AA mixture than in those fed 24% CP or the AA-imbalanced 16% protein diet.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Influence of dietary electrolyte balance, energy, and amino acid supplementation on the monensin response in chicks fed diets varying in protein content. 653 32

Monensin toxicosis was induced in lambs by either a single oral dose of 12 mg/kg or six daily doses of 8 mg/kg. Clinical signs of toxicosis consisted of depression, dyspnea, stiffness of gait, reluctance to move, and recumbency. Serum creatine phosphokinase activity was increased. Samples of skeletal and cardiac muscle were obtained over a six-day period and examined by light and electron microscopy. Light microscopic changes in cardiac and skeletal muscles consisted initially of vacuolation and intracellular edema of muscle cells followed by segmental necrosis. Interstitial fibrosis was present on days 5 and 6 postexposure. Muscle fiber necrosis was more severe in skeletal than cardiac muscles and most severe in sheep given 8 mg/kg of monensin daily. Macrophages were seen only in areas of severe necrosis. The earliest ultrastructural change was severe swelling of mitochondria. Secondary changes consisted of lipid accumulation and myofibrillar alterations. Myoblast proliferation was present as early as four days after initial exposure to monensin.
 ...
PMID:Light and electron microscopic changes in cardiac and skeletal muscle of sheep with experimental monensin toxicosis. 663 66

Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.
 ...
PMID:Acute monensin toxicosis in sheep: light and electron microscopic changes. 674 73

Monensin, lasalocid, salinomycin, nicarbazin, halofuginone, or arprinocid were fed to 1-week-old male broiler chicks at recommended levels and 1.5, 2, 2.5, and 3 times the recommended level, for 3 weeks. Pair-feeding experiments also were conducted to investigate the extent that growth depression with medicated diets could be attributed to the drop in feed consumption. At the recommended level of drugs, growth and feed conversion were not significantly affected. At elevated drug levels, performance was impaired; the adverse effects of drugs became more pronounced with increasing the concentrations in the diets. Weight gain was significantly depressed at 1.5X with arprinocid, halofuginone, and salinomycin, at 1 to 2X with monensin, at 2X with lasalocid, and at 2.5X with nicarbazin. Feed conversion, however, was adversely affected by 2X with halofuginone or 2.5X with salinomycin, nicarbazin, arprinocid, monensin, or lasalocid. The results of the pair-feeding experiments with 2 to 3 times drug levels indicated that most of the growth depression with medicated diets could be attributed to reduced feed consumption, but all drugs except arprinocid caused some additional growth depression.
 ...
PMID:Anticoccidial drugs: growth and performance depressing effects in young chickens. 710 61

Four experiments were conducted to investigate a possible interaction between dietary protein level and monensin on growth performance of young chicks. Crossbred chicks (New Hampshire X Columbian) or commercial broiler chicks (Hubbard X Hubbard) were fed corn-soybean meal diets containing various protein levels with or without added monensin (160 or 121 mg/kg). Monensin had little or no effect on growth performance of crossbred chicks fed diets containing 24 or 20% protein. However, growth performance of chicks fed 16% protein diets was depressed 15 and 8% by 160 and 121 mg/kg monensin, respectively. With commercial broiler chicks a marked interaction was observed between dietary protein level and monensin. As dietary protein level decreased, the depression in performance from monensin increased. At 24.0, 21.5, 19.0, and 16.5% protein, weight gains at 4 weeks of age were depressed 20, 29, 35, and 45% by 160 mg/kg monensin and 7, 14, 19, and 28% by 121 mg/kg monensin, respectively. Linear regression analysis indicated that 121 mg/kg monensin depressed growth rate an additional 2.7% for each 1% reduction in dietary protein level. A large portion of the growth depression from monensin could be explained by reduced feed intake. The results of this study indicate that level of dietary protein has a profound effect on the magnitude of growth depression caused by addition of monensin to chick diets. Thus, deficient levels of dietary protein should be avoided when using this anticoccidial drug in broiler feeds.
 ...
PMID:Effect of dietary protein level and monensin on performance of chicks. 717 99

Lasalocid was given to horses in a series of sequentially increasing single oral doses ranging between 5 and 30 mg/kg of body weight, with an appropriate washout period between treatments. One of the 5 horses died after a dosage of 15 mg/kg, 1 of 3 horses died after 21 mg/kg, 1 of 3 horses died after 22 mg/kg, and 1 of 2 horses died after 26 mg/kg. The LD50 of lasalocid for horses was estimated to be 21.5 mg/kg. Monensin was given to horses in a similar manner at dosages of 1, 2, and 3 mg/kg of body weight. One of the 2 horses died after a dosage of 2 mg/kg and 1 horse died after a dosage of 3 mg/kg. The clinical signs of toxicosis observed in horses given either drug were progressive and included depression, ataxia, paresis, and paralysis with partial anorexia. Intermittent profuse sweating was observed before death in horses given monensin.
 ...
PMID:Toxic effects of lasalocid in horses. 727 Oct 10

Four experiments were conducted to evaluate an alleged interaction between the anticoccidial drugs, monensin and lasalocid, and dietary protein source. Chicks were fed practical diets (approximately 24% crude protein) containing from 0 to 13% animal-source protein supplied by either a fish meal-meat and bone meal combination or by feather meal. Monensin (121 mg/kg) and lasalocid (125 mg/kg) were evaluated for anorexigenic activity in health birds and for growth-enhancement activity in E. acervulina-infected birds. Diet-by-coccidiostat interactions were not detected in any of these experiments. The addition of monensin or lasalocid depressed performance significantly in only one of the experiments, but the magnitude of depression was similar regardless of level of animal-source protein. Efficacy of the coccidiostats, as judged by performance of chicks infected with E. acervulina, was not altered by diet type.
 ...
PMID:Performance of healthy and Eimeria acervulina-infected chicks as influenced by anticoccidial drugs and source of dietary protein. 732 11

Monensin and lead were administered separately or concurrently at different toxic doses to broiler chicks. Administration of lead alone did not result in a significant depression of haematological parameters. Administration of higher levels of monensin caused a reduction in haematocrit and an increase in blood serum levels of alanine aminotransferase, aspartate aminotransferase and cholesterol. Concurrent administration of monensin and lead caused a severe depression of haematological profiles which indicated the existence of an interaction between the two substances. It was concluded that concurrent administration of monensin and lead potentiated the toxic effects of each other.
 ...
PMID:Oral administration of monensin and lead to broiler chicks: effects on haematological and biochemical parameters. 781 Mar 94


<< Previous 1 2 3 Next >>