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)

Twenty-three ospreys (Pandion haliaetus) found dead or moribund in the eastern United States during 1975-1982 were necropsied and selected tissues were analyzed for organochlorines and metals. Major causes or factors contributing to death were trauma, impact injuries, and emaciation. DDE was detected in 96% of the osprey carcases, DDD in 65%, DDT and heptachlor epoxide in 13%, dieldrin, oxychlordane, and cis-nonachlor in 35%, cis-chlordane in 52%, trans-nonachlor in 45%, and PCB's in 83%. Carcasses of immature ospreys from the Chesapeake Bay had significantly lower concentrations of DDE, DDD + DDT, cis-chlordane, and PCB's than carcasses of adults from the same area. Concentrations of some organochlorines in ospreys from the Chesapeake Bay declined significantly from 1971-1973 to 1975-1982. Significant differences in concentrations of certain metals in the ospreys' livers were noted between time periods, and sex and age groups for birds from the Chesapeake Bay. During 1975-1982, adults had significantly lower concentrations of chromium, copper, and arsenic than immatures and nestlings, and adult males had higher mercury concentrations than adult females. Adult females had lower zinc concentrations in 1975-1982 than in 1971-1973. Immatures and nestlings had higher concentrations of chromium and lead in 1975-1982 than in 1971-1973. A slightly elevated concentration of chromium (1.7 ppm) or arsenic (3.2 ppm) was found in the livers of individual ospreys. Several ospreys had elevated concentrations of mercury in their livers; two ospreys had more than 20 ppm which may have contributed to their deaths.
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PMID:Environmental pollutant and necropsy data for ospreys from the eastern United States, 1975-1982. 358 6

From 1984 through 1992, staff at The Marine Mammal Center (TMMC, Sausalito, California, USA) examined 207 northern elephant seals (Mirounga angustirostris) with a condition of unknown etiology called northern elephant seal skin disease (NESSD). The skin lesions were characterized by patchy to extensive alopecia and hyperpigmentation, punctate or coalescing epidermal ulceration, and occasionally, massive skin necrosis. Microscopic lesions included ulcerative dermatitis with hyperkeratosis, squamous metaplasia and atrophy of sebaceous glands. All diseased seals were less than 2 years of age and suffered from emaciation, depression, and dehydration. Mortality from septicemia increased significantly with severity of skin ulceration. Compared to 14 apparently unaffected seals, diseased seals had depressed levels of circulating thyroxine, triiodothyronine, retinol, serum iron, albumin, calcium, and cholesterol. Levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transpeptidase, blood urea nitrogen, and uric acid were elevated. Morphometrically, diseased animals were approximately 15% smaller than normal seals of the same sage. Serum and blubber concentrations of 36 polychlorinated biphenyl congeners (sigma PCB) and dichloro-diphenyl-dichloroethylene (p,p'-DDE) were negatively correlated with body mass. Mean concentrations of sigma PCB and p,p'-DDE in serum in diseased seals were elevated as compared to apparently normal seals. Etiology of this syndrome remains unknown, but the possibility of PCB toxicosis cannot be ruled out.
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PMID:Clinical and pathological characterization of northern elephant seal skin disease. 924 88

Diagnostic and analytical findings are presented for 105 common loons (Gavia immer) found dead or debilitated in New York (USA) from 1972-99. Aspergillosis (23% of cases) and ingestion of lead fishing weights (21%) were the most common pathologies encountered. Stranding on land, shooting, other trauma, gill nets, air sacculitis and peritonitis, and emaciation of uncertain etiology accounted for most of the remaining causes of disease or death. Analysis for total mercury in the liver of 83 loons yielded a geometric mean (gm) of 10.3 mg/kg (wet basis) and range of 0.07 to 371 mg/kg, with emaciated birds generally showing higher levels. Organochlorine contaminant levels in brain were generally low, principally consisting of PCB's (gm = 2.02 mg/kg) and DDE (0.47 mg/kg).
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PMID:Necropsy findings and environmental contaminants in common loons from New York. 1127 94

For the first time, organochlorine (OC) contaminants were measured in blubber biopsies from free-ranging St. Lawrence River Estuary beluga whales (Delphinapterus leucas), to compare contaminant levels to those previously measured in dead stranded belugas. PCBs, DDTs, toxaphene and chlordane-related compounds were the major OC contaminants detected in 44 belugas biopsied in 1994-1998. SigmaPCB (the sum of 104 congeners) ranged from 2080 to 128,000 ng/g lipid in males (n=34; minimum estimated ages 8-22 years), and from 148 to 44,100 ng/g lipid in females (n=10; minimum estimated ages 7-22 years). The concentrations of PCBs and OC pesticides in the blubber of these whales overlapped those observed in stranded belugas from an earlier study, and demonstrated comparable age and sex-related trends. However, lower proportions of mirex, HCB, DDTs, and many of the highly chlorinated PCBs occurred in the biopsy samples compared to results for blubber from stranded carcasses. Most major OC compounds were present at lower concentrations in the biopsies, but this does not appear to be solely related to age differences between the two groups, or to emaciation in the stranded whales. Nor does it appear to be associated with the use of superficial biopsies, and the possible stratification of lipids and OCs in the blubber layer. Nevertheless, given these possible confounding factors, and the uncertainty in age estimates for the biopsied whales, the results point to the need for careful interpretation of biopsy results when comparing with data taken from the full depth of the blubber mantle in stranded whales. Taken together, results from both biopsied whales and previously studied stranded belugas indicate that PCB and OC pesticide contamination of St. Lawrence beluga whales may occur across a broader range of levels than previously thought, at least for males which formed the largest group in this study, possibly due to different degrees of dietary exposure. It also appears that measuring contaminant concentrations only in stranded whales, may overestimate OC levels in the population as a whole, especially for highly chlorinated OCs.
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PMID:PCBs and organochlorine pesticides in blubber biopsies from free-ranging St. Lawrence River Estuary beluga whales (Delphinapterus leucas), 1994-1998. 1253 17

A suppression of hepatic ethoxyresorufin-O-deethylase (EROD) activity was reported recently in large-sized Atlantic tomcod (Microgadus tomcod) from the St. Lawrence Estuary (SLE; QC, Canada), possibly related to chronic exposure to persistent contaminants and/or to emaciation. In the present study, hepatic concentrations of organochlorine contaminants and biological responses were measured in female tomcods from three estuaries located on the Canadian east coast: The SLE, the Miramichi (ME), and the Richibucto (RE) Rivers Estuaries (NB, Canada). Tomcods from the SLE had higher hepatic concentrations of organochlorine contaminants than tomcods from the ME and RE. For example, concentrations of polychlorinated biphenyls (PCBs, lipid wt) were 2.5 to 4 times higher, and concentrations of mirex and chlordanes were 6 times higher, in tomcods from the SLE than in tomcods from the other sites. Concentrations of polycyclic aromatic hydrocarbons (PAHs) metabolites in the bile did not differ among sites. The pattern of biological responses differed markedly between the SLE and the two other sites. Tomcods from the SLE had 1.5 times higher concentrations of DNA adducts and 2 times higher rates of hepatocellular proliferation, but 20 times lower hepatic EROD activity, than tomcods from the ME and RE. Lipid content was not correlated with EROD activity, indicating that low hepatic lipid content alone does not cause suppression of EROD activity in Atlantic tomcod. In contrast, for the three sites combined, EROD activity decreased as concentrations of PCBs increased. Within sites, hepatic PCB concentrations increased as lipid content decreased. This study supports the hypothesis that low EROD activity in SLE tomcods is related to chronic exposure to organochlorine contaminants.
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PMID:Low hepatic ethoxyresorufin-O-deethylase activity correlates with high organochlorine concentrations in Atlantic tomcod from the Canadian east coast. 1626 47

Anadromous arctic char (Salvelinus alpinus) undertake short feeding migrations to seawater every summer and accumulate lipids, while the rest of the year is spent in fresh water where the accumulated lipid reserves are mobilized. We tested the hypothesis that winter fasting and the associated polychlorinated biphenyls' (PCBs) redistribution from lipid depots to critical tissues impair the liver metabolic capacity in these animals. Char were administered Aroclor 1254 (0, 1, 10, and 100 mg/kg body mass) orally and maintained for 4 months without feeding to mimic seasonal winter fasting, while fed groups (0 and 100 mg Aroclor 1254/kg) were maintained for comparison. A clear dose-related increase in PCB accumulation and cytochrome P4501A (CYP1A) protein content was observed in the livers of fasted fish. This PCB concentration and CYP1A response with the high dose of Aroclor were 1.5-fold and 3-fold greater in the fasted than in the fed fish, respectively. In fed fish, PCB exposure lowered liver glycogen content, whereas none of the other metabolic indicators were significantly affected. In fasted fish, PCB exposure depressed liver glycogen content and activities of glucose-6-phosphate dehydrogenase, alanine aminotransferase, lactate dehydrogenase, and phosphoenolpyruvate carboxykinase and elevated 3-hydroxyacylcoA dehydrogenase activity and glucocorticoid receptor protein expression. There were no significant impacts of PCB on heat shock protein 70 (hsp70) and hsp90 contents in either fed or fasted fish. Collectively, our study demonstrates that winter emaciation associated with the anadromous lifestyle predisposes arctic char to PCB impact on hepatic metabolism including disruption of the adaptive metabolic responses to extended fasting.
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PMID:Fasting augments PCB impact on liver metabolism in anadromous arctic char. 1653 58

Persistent organic pollutants (POPs) encompass an array of anthropogenic organic and elemental substances and their degradation and metabolic byproducts that have been found in the tissues of exposed animals, especially POPs categorized as organohalogen contaminants (OHCs). OHCs have been of concern in the circumpolar arctic for decades. For example, as a consequence of bioaccumulation and in some cases biomagnification of legacy (e.g., chlorinated PCBs, DDTs and CHLs) and emerging (e.g., brominated flame retardants (BFRs) and in particular polybrominated diphenyl ethers (PBDEs) and perfluorinated compounds (PFCs) including perfluorooctane sulfonate (PFOS) and perfluorooctanic acid (PFOA) found in Arctic biota and humans. Of high concern are the potential biological effects of these contaminants in exposed Arctic wildlife and fish. As concluded in the last review in 2004 for the Arctic Monitoring and Assessment Program (AMAP) on the effects of POPs in Arctic wildlife, prior to 1997, biological effects data were minimal and insufficient at any level of biological organization. The present review summarizes recent studies on biological effects in relation to OHC exposure, and attempts to assess known tissue/body compartment concentration data in the context of possible threshold levels of effects to evaluate the risks. This review concentrates mainly on post-2002, new OHC effects data in Arctic wildlife and fish, and is largely based on recently available effects data for populations of several top trophic level species, including seabirds (e.g., glaucous gull (Larus hyperboreus)), polar bears (Ursus maritimus), polar (Arctic) fox (Vulpes lagopus), and Arctic charr (Salvelinus alpinus), as well as semi-captive studies on sled dogs (Canis familiaris). Regardless, there remains a dearth of data on true contaminant exposure, cause-effect relationships with respect to these contaminant exposures in Arctic wildlife and fish. Indications of exposure effects are largely based on correlations between biomarker endpoints (e.g., biochemical processes related to the immune and endocrine system, pathological changes in tissues and reproduction and development) and tissue residue levels of OHCs (e.g., PCBs, DDTs, CHLs, PBDEs and in a few cases perfluorinated carboxylic acids (PFCAs) and perfluorinated sulfonates (PFSAs)). Some exceptions include semi-field studies on comparative contaminant effects of control and exposed cohorts of captive Greenland sled dogs, and performance studies mimicking environmentally relevant PCB concentrations in Arctic charr. Recent tissue concentrations in several arctic marine mammal species and populations exceed a general threshold level of concern of 1 part-per-million (ppm), but a clear evidence of a POP/OHC-related stress in these populations remains to be confirmed. There remains minimal evidence that OHCs are having widespread effects on the health of Arctic organisms, with the possible exception of East Greenland and Svalbard polar bears and Svalbard glaucous gulls. However, the true (if any real) effects of POPs in Arctic wildlife have to be put into the context of other environmental, ecological and physiological stressors (both anthropogenic and natural) that render an overall complex picture. For instance, seasonal changes in food intake and corresponding cycles of fattening and emaciation seen in Arctic animals can modify contaminant tissue distribution and toxicokinetics (contaminant deposition, metabolism and depuration). Also, other factors, including impact of climate change (seasonal ice and temperature changes, and connection to food web changes, nutrition, etc. in exposed biota), disease, species invasion and the connection to disease resistance will impact toxicant exposure. Overall, further research and better understanding of POP/OHC impact on animal performance in Arctic biota are recommended. Regardless, it could be argued that Arctic wildlife and fish at the highest potential risk of POP/OHC exposure and mediated effects are East Greenland, Svalbard and (West and South) Hudson Bay polar bears, Alaskan and Northern Norway killer whales, several species of gulls and other seabirds from the Svalbard area, Northern Norway, East Greenland, the Kara Sea and/or the Canadian central high Arctic, East Greenland ringed seal and a few populations of Arctic charr and Greenland shark.
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PMID:Exposure and effects assessment of persistent organohalogen contaminants in arctic wildlife and fish. 1991 21