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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

Ten female beef calves weighing approximately 180 kg each were allotted to 2 groups of 5 each before they were given (orally) monensin (50 mg/kg of body weight). In group A, the calves were given (IM) a commercial selenium-vitamin E (Se-E) preparation (0.25 mg of Se and 17 IU of alpha-tocopherol/kg of body weight) at 72 and 24 hours before monensin was given. The calves in group B were injected at the 2 times with isotonic saline solution. Clinical signs of monensin toxicosis, including lethargy and recumbency, appeared on day 2 in the calves given the Se-E pretreatment, compared with the onset on day 1 in the saline solution-pretreated calves. All calves in the 2 groups died, but mean survival time was longer in group A (4.4 vs 2.2 days). Lesions of monensin toxicosis were myocardial necrosis, skeletal myonecrosis, pulmonary congestion, and rumenitis. The frequency and severity of the lesions were similar for both groups of calves. The results of the present study indicate that Se-E pretreatment modifies the development of monensin toxicosis in cattle.
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PMID:Effect of pretreatment with selenium-vitamin E on monensin toxicosis in cattle. 407 30

Thirty-four adult ponies were used to determine the effects of single oral doses of copper (Cu) supplements (0, 20, and 40 mg of Cu/kg of body weight) on the toxicity of oral doses of selenium (Se) supplements (0, 2, 4, 6, and 8 mg of Se/kg of body weight) administered 24 hours after the copper was given. Signs of Se toxicosis-sweating, diarrhea, tachycardia, tachypnea, mild pyrexia, lethargy, and colic-developed in ponies given 6 and 8 mg of Se/kg of body weight without Cu pretreatment. Two of 4 ponies given 6 mg of Se/kg and both ponies given 8 mg of Se/kg without Cu pretreatment died within 36 hours after being given the Se. All ponies given either 20 or 40 mg of Cu/kg were unaffected by the subsequent Se supplement, regardless of dosage. The Cu pretreatment did not seem to inhibit absorption of Se, based on serum Se concentrations, but hastened the disappearance of the Se from the serum.
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PMID:Effects of copper pretreatment upon toxicity of selenium in ponies. 721 26

There is compelling evidence that micronutrients can profoundly affect immunity. We surveyed vitamin supplement use and circulating concentrations of 22 nutrients and glutathione in 64 HIV-1 seropositive men and women and 33 seronegative controls participating in a study of heterosexual HIV-1 transmission. We assayed antioxidants (vitamins A, C, and E; total carotenes), vitamins B6 and B12, folate, thiamin, niacin, biotin, riboflavin, pantothenic acid, free and total choline and carnitine, biopterin, inositol, copper, zinc, selenium, and magnesium. HIV-infected patients had lower mean circulating concentrations of magnesium (p < 0.0001), total carotenes (p = 0.009), total choline (p = 0.002), and glutathione (p = 0.045), and higher concentrations of niacin (p < 0.0001) than controls. Fifty-nine percent of HIV+ patients had low concentrations of magnesium, compared with 9% of controls (p < 0.0001). These abnormal concentrations were unrelated to stage of disease. Participants who took vitamin supplements had consistently fewer low concentrations of antioxidants, across HIV infection status and disease stage strata (p = 0.0006). Nevertheless, 29% of the HIV+ patients taking supplemental vitamins had subnormal levels of one or more antioxidants. The frequent occurrence of abnormal micronutrient nutriture, as found in these HIV+ subjects, may contribute to disease pathogenesis. The low magnesium concentrations may be particularly relevant to HIV-related symptoms of fatigue, lethargy, and impaired mentation.
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PMID:Micronutrient profiles in HIV-1-infected heterosexual adults. 862 65

An adult male binturong, Arctictis binturong, which had been anorexic and lethargic for seven days became acutely dyspnoeic and died under anaesthesia. A postmortem examination revealed left ventricular hypertrophy with a thrombus occluding the left ventricular chamber. Histological findings included moderate to severe multifocal, vasculocentric myocardial degeneration and necrosis with fibrosis replacing myocardiocytes. Escherichia coli and Proteus mirabilis were grown on cultures. The animal's serum vitamin E and selenium levels were considered adequate. The aetiology of the chronic myocardial changes could not be determined.
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PMID:Myocardial necrosis in a captive binturong (Arctictis binturong). 1516 Aug 46

A 9-day old Grant's zebra with a 3-day history of lethargy, weight loss, inappetance, and diarrhea was treated with ampicillin, vitamin E and selenium, and tetanus antitoxin without effect in 24 h. On transfer to the local veterinary clinic, a grade IV/VI continuous heart murmur was detected and a patent ductus arteriosus found at necropsy.
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PMID:Patent ductus arteriosus in a 9-day-old Grant's zebra. 1615 24

Pharmaceuticals are continuously dispersed into the environment, as a result of human and veterinary use, and have become a relevant environmental concern. In the present study, the acute toxicity of three therapeutic agents (diazepam, clofibrate, and clofibric acid) and a detergent, sodium dodecylsulphate (SDS), to the euryhaline fish Gambusia holbrooki was evaluated. Special attention was devoted to oxidative stress parameters. G. holbrooki males, captured in the estuary of the Minho River (NW Portugal), were exposed for 96 h to the selected compounds. The following oxidative stress biomarkers were evaluated in gills and liver tissues: reduced and oxidised glutathione, lipid peroxidation, and several antioxidant enzymes, namely (1) total and selenium-dependent glutathione peroxidase (GPx), (2) glutathione reductase (GRed), (3) copper-zinc superoxide dismutase (Cu-ZnSOD) and manganese superoxide dismutase (MnSOD), and (4) glutathione-S-transferases (GSTs). In the particular case of diazepam, swimming behaviour was also evaluated. The obtained results indicate an overall diminished oxidative stress response caused by SDS and diazepam. Oxidative-based alterations were observed after exposure to clofibrate and clofibric acid, with modifications of several enzymatic activities. Diazepam caused evident behavioural changes: animals showed dark pigmentation and also abnormal postures, namely lethargy and anomalous movement.
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PMID:Behaviour and biomarkers of oxidative stress in Gambusia holbrooki after acute exposure to widely used pharmaceuticals and a detergent. 1824 7

Phenytoin is indicated for tonic clonic seizures and status epilepticus. Phenytoin is known to deplete vital nutrients such as calcium, folic acid, vitamin D, vitamin K, biotin, carnitine, copper, selenium and zinc. Depletion of nutrients is known to cause adverse effects such as ataxia, nystagmus, lethargy, slurred speech and hematological disturbances. Spirulina is a rich source of vital nutrients including iron. It is proposed to study the effect of spirulina on the hematological disturbances induced by phenytoin. Seven groups of male albino rats weighing 130-150g were used. Each group consisted of six animals. Phenytoin at a dose of 20mg/kg/day dissolved in water, spirulina 50, 100, 200 mg/kg/day suspended in 1% tween 80 alone or in combination with phenytoin was administered for 30 days. Hemoglobin content, total leucocyte and erythrocyte count were determined on 30(th) day. Phenytoin significantly decreased the hemoglobin content, total erythrocyte and leukocyte count. Spirulina did not show any effect at the lower dose of 50 and 100mg/kg and higher dose of 200mg/ kg significantly elevated hemoglobin content. Spirulina at a dose of 200mg/kg/day in combination with phenytoin reversed the phenytoin induced decrease in hemoglobin content, total erythrocyte and leukocyte count. The results of this study indicates that supplementation of phenytoin with spirulina may reverse the hematological disturbances induced by phenytoin.
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PMID:Influence of spirulina on the phenytoin induced haematological changes. 2255 35

Selenium is a metalloid of considerable interest in the human from both a toxicological and a nutritional perspective, with a very narrow safe range of intake. Acute selenium intoxication is followed by adverse effects on the nervous system with special clinical relevance, while the neurotoxicity of long-term overexposure is less characterized and recognized. We aimed to address this issue from a public health perspective, focusing on both laboratory studies and the few epidemiologic human studies available, with emphasis on their methodological strengths and limitations. The frequently overlooked differences in toxicity and biological activity of selenium compounds are also outlined. In addition to lethargy, dizziness, motor weakness and paresthesias, an excess risk of amyotrophic lateral sclerosis is the effect on the nervous system which has been more consistently associated with chronic low-level selenium overexposure, particularly to its inorganic compounds. Additional research efforts are needed to better elucidate the neurotoxic effects exerted by selenium overexposure.
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PMID:Selenium neurotoxicity in humans: bridging laboratory and epidemiologic studies. 2426 18