Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013911 (emaciation)
 1,059 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polybrominated biphenyls (PBB) were used as a fire retardant. In common with other halogenated hydrocarbons, PBBs are lipophilic and resistant to chemical and metabolic degradation. Cattle on about 25 Michigan farms were exposed to as much as 250 g per head of PBB when it was accidentally mixed in cattle feed in 1973 to 1974. Livestock exposures several orders of magnitude lower occurred on several hundred other farms because of carryover and equipment contamination in feed mills. Approximately 85% of the Michigan population received some exposure to PBB because dairy product marketing involves mixing milk from many farms. A few cases of high human exposure, which may have been as great as 10 g, occurred when residents of the more highly exposed farms consumed their own products. Although numerous clinical signs and pathological changes were reported in exposed cattle, only anorexia, lacrimation, emaciation, hyperkeratosis, and kidney damage were confirmed in controlled studies. The acute toxicity of PBB in laboratory animals is low, but a variety of subacute effects have been reported. Induction of microsomal enzymes, enlargement and histopathological changes of the liver, fetotoxicity, and immunosuppression are among the more significant. Epidemiological studies of exposed humans have revealed no pattern of clinical signs or symptoms that were related to PBB exposure. A complete evaluation of the human consequences of exposure to PBB await the conclusion of long-term epidemiological studies.
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PMID:The PBB episode in Michigan: an overall appraisal. 300 22

Male New Zealand White rabbits were treated with microsomal enzyme inducers, inhibitors of hemoprotein synthesis or action, and glutathione precursor and depletor before they were orally given the median lethal dose (LD50) of aflatoxin B1 (AFB1; 0.4 mg/kg) at the start of a 7-day experimental period. The drugs administered, mean duration of illness (hours), and survival percentage were as follows: controls (saline solution)-85, 50%; phenobarbital (PB)-100, 100%; phenylbutazone-115, 67%; benzoflavone-39, 17%; stanozolol-67, 67%; cobaltous chloride (CoCl2)-46, 67%; piperonyl butoxide (PBO)-88, 100% cysteine (CYS)-68, 100%; ethyl maleate-71, 83%. Signs of toxicosis included decreased feed and water consumption, weight loss, dehydration, lethargy, and emaciation; some rabbits died or were euthanatized. Clinico-pathologic changes included increased serum aspartate aminotransferase (AST) activity by 24 hours and bilirubin concentration by 48 to 72 hours after AFB1 was given. Grossly, livers were pale or tan and friable, with prominent lobular architecture. Kidneys of affected rabbits were pale to dark red. Microscopically, livers were normal or had lesions as great as extensive necrosis, hemorrhage, mineralization, and bile duct proliferation. Treatment of rabbits with PB, CoCl2, PBO, and CYS protected against AFB1 hepatic pathology, and PB, PBO, and CYS also had protective effect against lethality. Ethyl maleate provided some protection against lethality and increased serum AST activity and bilirubin concentration. Toxicosis was enhanced by benzoflavone; phenylbutazone and stanozolol had litte influence.
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PMID:Effect of enzyme inducers and inhibitors and glutathione precursor and depleter on induced acute aflatoxicosis in rabbits. 680 67

Aside from the physical effects of oiling (e.g., hypothermia, dehydration, emaciation), chronic toxicity of polycyclic aromatic hydrocarbons (PAHs) contamination is an important factor influencing long-term recovery of oiled sea birds following an oil spill. Monitoring PAH exposure can help identify populations at risk from toxic effects of PAHs for further study and/or protection. This is the first studyto quantify PAH and metabolite tissue burdens in sea birds directly oiled following oil spills. PAHs and hydroxylated PAHs were quantified in liver samples from oiled Common Guillemots (Uria aalge) stranded along the East Coast of England using gas chromatography-mass spectroscopy (GC-MS). Mean parent and metabolite PAH concentrations were 0.25+/-0.09 (range 0.04-0.97) and 0.52+/-0.14 (range 0.05-1.48) microg/g (wet wt.), respectively. The main source of PAH exposure was via ingestion of crude oil during preening, resulting in PAH uptake and tissue contamination beyond levels expected from exposure via the food chain. PAH composition corresponded with number of benzene rings in each compound and was typical of contamination from petrogenic sources; pentacyclic < tri- and tetracyclic < tricyclic < dicyclic PAHs. The occurrence of PAH metabolites detected in liver samples also provided evidence of the presence and stereoselectivity of hepatic microsomal CYP1A1 in common guillemots.
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PMID:Polyaromatic hydrocarbon and PAH metabolite burdens in oiled common guillemots (Uria aalge) stranded on the east coast of England (2001 -2002). 1725 52