title: Physiology of acute silver toxicity in the starry flounder (Platichthys stellatus) in seawater.
abstract: Physiological effects of exposure to silver (AgClnn-1; 250 micrograms Ag l-1 or 1000 micrograms Ag l-1) in seawater fish were investigated using adult starry flounders. While all fish survived up to 10 days in 250 micrograms Ag l-1, flounders started to die after day 4 in 1000 micrograms l-1. Dose-dependent increases in plasma and hepatic silver concentrations showed that silver was available for uptake. There were minimal negative effects on hematological parameters, acid-base status, and blood gases. Plasma ammonia showed a pronounced (three- to four-fold), but transient increase in flounders exposed to either 250 micrograms Ag l-1 or 1000 micrograms Ag l-1. Whole body ammonia and acid equivalent efflux measurements indicated that ammonia retention was due to a combination of stimulated production and inhibited excretion. In the 1000-microgram Ag l-1 group there was a similar transient increase in plasma [magnesium], which was restored by day 4. In contrast, plasma chloride and sodium levels increased gradually towards the point when fish began to die. At 250 micrograms Ag l-1, the Na+/K(+)-ATPase activity of the intestine was unaffected but there was a two-fold increase in branchial Na+/K(+)-ATPase activity. The latter effect was interpreted as compensation for an elevated chloride and sodium load. The increases in plasma chloride and sodium concentrations were accompanied by a marked suppression of drinking, thereby indicating that acute silver toxicity was likely caused by a combination of elevated electrolyte concentrations and dehydration.
authors.affiliation: T. H. Morgan School of Biological Sciences, University of Kentucky, Lexington 40506-0225, USA. hogstra@pop.uky.edu
authors.forename: C
authors.initials: C
authors.lastname: Hogstrand
authors.forename: E A
authors.initials: EA
authors.lastname: Ferguson
authors.forename: F
authors.initials: F
authors.lastname: Galvez
authors.forename: J R
authors.initials: JR
authors.lastname: Shaw
authors.forename: N A
authors.initials: NA
authors.lastname: Webb
authors.forename: C M
authors.initials: CM
authors.lastname: Wood
mesh_terms: D000143:Acids / Q000032:analysis / Q000378:metabolism; D000641:Ammonia / Q000032:analysis / Q000097:blood; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D001784:Blood Gas Analysis; D001786:Blood Glucose; D001806:Blood Urea Nitrogen; D001826:Body Fluids / Q000737:chemistry / Q000378:metabolism; D002245:Carbon Dioxide / Q000097:blood; D002712:Chlorides / Q000097:blood; D003681:Dehydration / Q000139:chemically induced; D004327:Drinking Behavior / Q000187:drug effects; D005432:Flounder / Q000502:physiology*; D005880:Gills / Q000201:enzymology; D006400:Hematocrit; D006454:Hemoglobins; D006854:Hydrocortisone / Q000097:blood; D007422:Intestines / Q000201:enzymology; D008274:Magnesium / Q000097:blood; D010100:Oxygen / Q000097:blood; D012623:Seawater; D012834:Silver / Q000633:toxicity*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014882:Water-Electrolyte Balance / Q000187:drug effects*
chemical_list: D000143:Acids; D001786:Blood Glucose; D002712:Chlorides; D006454:Hemoglobins; D002245:Carbon Dioxide; D012834:Silver; D000641:Ammonia; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D010100:Oxygen; D006854:Hydrocortisone