Hepatocyte changes following selenium accumulation in a freshwater teleost

Sorensen, Elsie M. B.; Harlan, Charles W.; Bell, James; Bauer, Thomas; Pradzynski, A.H.

doi:10.1097/00000433-198303000-00004

Cited by 25 publications

(4 citation statements)

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“…As the liver is one of the most important detoxifying organs in fish accumulation of arsenic in this organ would surely have some negative effects on survival and fish died in this experiment may be the above causes. The pathological alterations in the intestine of the tilapia fish are in agreement with those observed by many investigators about the effects of different toxicants on fish intestine (Shah et al 2009b;Sorensen et al 1983). Epithelial degeneration, inflammatory cells infiltration in the sumucosa as well as submucosal edema was seen in the intestine of Channa punctata fish exposed to carbofuran (Ram and Singh 1988).…”

Section: Discussionsupporting

confidence: 89%

“…Therefore, it is speculated that arsenic exposure would have effect in the regulation of metabolic functions through inactivation of these nerves. Arsenic is actively metabolized in the tissue of fishes especially in organs such as liver and intestine has the tendency to accumulate as reported in different teleots such as green sunfish (Sorensen et al 1983), and Tilapia mossambica (Suhendrayatna et al 2002). In the present study mature snakehead, Channa punctata were exposed to non-lethal levels of sodium arsenite.…”

Section: Introductionmentioning

confidence: 69%

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Effect of Arsenic (NaAsO2) on the Histological Change of Snakehead Fish, Channa punctata

Hossain

2014

J Life Earth Sci

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Sodium arsenite (NaAsO 2 ) considered effective for aquatic weed control, has been found to be harmful to several species of freshwater teleost fishes. Channa punctata was exposed to NaAsO 2 at the concentrations of 100µl/30g and 200µl//30g body weight per fish and cultured for 14 days post exposure respectively. Tissue disorientation, peliosis and vacuolization accompanied by karyolysis, apoptosis and necrosis in the liver and heart were significant on days onwards. Irregularities in the intestines including apoptotic and necrotic cells were also common, enlargement of the mucosa and submucosa was noted. Corresponding with the histopathological lesions, necrosis of liver cells and intestinal functions or induction of heart muscles at the early phase of arsenic exposure may be the possible causes of fish death.Keywords: Arsenic, Channa punctata, histology, fish pathology mvivsk: †mvwWqvg Av ‡m© bvBU ‡K Kvh© Kwi RjR AvMvQv `g ‡bi Kv ‡R e¨envi Ki ‡jI A ‡bK cÖ RvwZi wgVv cvwbi gv ‡Qi Rb¨ Gi ¶wZKi cÖ fve i ‡q ‡Q| GB M ‡elYvq 30 MÖ vg IR ‡bi UvwK gv ‡Qi Channa punctata †` ‡n intraperitoneal injection Gi gva¨ ‡g 100µl/fish I 200µl/fish Av ‡m© wbK ( †mvwWqvg Av ‡m© bvB ‡Ui `ª eY) cÖ ‡qvM K ‡i Zv 14 w`b hver ch© ‡e ¶Y Kiv nq| Gi d ‡j gv ‡Qi wjfvi I ü`wc ‡Ûi †Kvl¸ ‡jv ‡Z peliosis, apoptosis, karyolysis Ges necrosis RvZxq cwieZ© b j ¶¨ Kiv hvq| †mvwWqvg Av ‡m© bvB ‡Ui cÖ fv ‡e gv ‡Qi Lv`¨ bvwji mucosa, lumen, I submucosa-i AwaK e" w× N ‡U| GB M ‡elYvq cÖ gvwYZ nq †h, Channa punctata gv ‡Qi †h g" Zz N ‡U Zv †mvwWqvg, Av ‡m© bvB ‡Ui wµqvi dj| Av ‡m© wbK wjfvi †Kv ‡l lesion, necrosis I Lv`¨ bvwji Kvh© KvixZv wKsev ürwc ‡Ûi †cwki ms ‡KvP ‡b evav m" wó K ‡i e ‡j gv ‡Qi †Kv ‡li histological cix ¶vq Rvbv hvq|

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 69%

Effect of Arsenic (NaAsO2) on the Histological Change of Snakehead Fish, Channa punctata

Hossain

2014

J Life Earth Sci

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“…The procedure presented here was developed to address that information need. It includes the key parameters that are implicit in basic toxicological risk assessment such as concentration and exposure, but it also integrates biotic and 5) are based on a synthesis of toxicity, bioaccumulation, and sediment data from Traversy et al, 1975;Adams and Johnson, 1977;Birkner, 1978;Cumbie, 1978;Cumbie and Van Horn, 1978;Goettl and Davies, 1978;Cherry et al, 1979;Furr et al, 1979;Guthrie and Cherry, 1979;Holland, 1979;Duke Power Company, 1980;Hilton et al, 1980;Nassos et al, 1980;Speyer, 1980;Hilton and Hodson, 1983;Hodson and Hilton, 1983;Nriagu and Wong, 1983;Rudd and Turner, 1983;Sorensen and Bauer, 1983,1984a, 1984bTurner and Rudd, 1983;Bryson et al, 1984;Garrett and Inman, 1984;Hicks et al, 1984;Martin and Hartman, 1984;Sager and Cofield, 1984;Sorensen et al, 1982aSorensen et al, , 1982bSorensen et al, , 1983aSorensen et al, , 1983bSorensen et al, , 1984Wiener et al, 1984;Woock, 1984;Woock and Summers, 1984;Finley, 1985;Lemly, 1985aLemly, , 1993a…”

Section: Introductionmentioning

confidence: 99%

Assessing the toxic threat of selenium to fish and aquatic birds

Lemly

1996

Environ Monit Assess

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Abstract.A procedure is given for evaluating the toxic threat of selenium to fish and wildlife. Toxic threat is expressed as hazard, and is based on the potential for food-chain bioaccumulation and reproductive impairment in fish and aquatic birds, which are the most sensitive biological responses for estimating ecosystem-level impacts of selenium contamination. Five degrees of hazard are possible depending on the expected environmental concentrations of selenium, exposure of fish and aquatic birds to toxic concentrations, and resultant potential for reproductive impairment. The degree of hazard is given a numerical score: 5 = high hazard, 4 = moderate hazard, 3 = low hazard, 2 = minimal hazard, and 1 = no identifiable hazard. A separate hazard score is given to each of five ecosystem components; water, sediments, benthic macroinvertebrates, fish eggs, and aquatic bird eggs. A final hazard characterization is determined by adding individual scores and comparing the total to the following evaluation criteria: 5 = no hazard, 6-8 = minimal hazard, 9-11 = low hazard, 12-15 = moderate hazard, 16-25 = high hazard. An example is given to illustrate how the procedure is applied to selenium data from a typical contaminant monitoring program.

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“…The presence of excess levels of selenium in Martin Lake is currently believed to be the major factor in the increased mortality and certain abnoralities of endemic fish populations. Fish inhabiting water near the alleged selenium discharge sites in Martin Lake accumulated markedly elevated levels of selenium in tissues and organs [ 1,2]. The hepatopancreas of fish from these discharge sites, for example, was documented to contain an average of 27 ppm selenium in a winter collection [3] and an average of 10 ppm in a summer collection [2].…”

Section: Introduction I59mentioning

confidence: 99%

Planimetric analysis of redear sunfish (Lepomis microlophus) hepatopancreas following selenium exposure

Sorensen

Bauer

1984

Enviro Toxic and Chemistry

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A real ratios of pancreas cells to liver cells (P/L ratios) were determined planimetrically and compared with selenium accumulated in the hepatopancreas (liver and associated exocrine pancreas) of redear sunfish (Lepomis microlophus). Fish were collected from four locations in Martin Lake, Texas, and from a reference lake 8 km upstream in the same drainage system. Fish collected from selenium‐contaminated areas in Martin Lake had significantly higher P/L ratios than did reference fish. The increase in the P/L ratios could be explained by either pancreatic cell hyperplasia or parenchymal hepatocyte necrosis and cell loss. Since a previous publication documented both central necrosis with loss of parenchymal hepatocytes and architectural disorganization and endoplasmic reticulum changes in the exocrine pancreas cells of these same redear sunfish, both changes probably occurred simultaneously. However, in this study, P/L ratios were not correlated with selenium levels in the hepatopancreas. This contrasts with published data regarding hematological changes, condition factors, and relative hepatopancreas weight for the same redear sunfish collected for this study. Relative ratios of pancreatic cells to liver cells determined in this study, therefore, were less accurate in pinpointing biological changes due to selenium than were the other parameters previously published using these same fish.

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Hepatocyte changes following selenium accumulation in a freshwater teleost

Cited by 25 publications

References 0 publications

Effect of Arsenic (NaAsO2) on the Histological Change of Snakehead Fish, Channa punctata

Effect of Arsenic (NaAsO2) on the Histological Change of Snakehead Fish, Channa punctata

Assessing the toxic threat of selenium to fish and aquatic birds

Planimetric analysis of redear sunfish (Lepomis microlophus) hepatopancreas following selenium exposure

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