Renal responses to acute lead waterborne exposure in the freshwater rainbow trout (Oncorhynchus mykiss)

Monika Patel, Joseph T. Rogers, Eric F. Pane, Chris M. Wood

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

The possible nephrotoxic effects of waterborne lead exposure (as Pb(NO3)2) were investigated in the freshwater rainbow trout (Oncorhynchus mykiss). Kidney lead accumulation was time-dependent, increasing upon exposure to 0.57 ± 0.01 mg dissolved Pb L-1 for up to 96 h with a significantly higher burden occurring in the posterior kidney compared to the anterior segment. Urine analyses in trout exposed to 1.20 ± 0.09 mg dissolved Pb L-1 revealed a significant increase in urinary lead excretion rate throughout 96 h of exposure. Urine flow rate and glomerular filtration rate (GFR) were not impacted with the exception of a significant decrease in GFR from 84 to 96 h in lead-exposed trout. Urine pH decreased significantly over time in lead-exposed fish. Correspondingly, urine ammonia excretion rate showed a marked increase from 48 h onwards. In experimental fish, urine glucose excretion was significantly greater by 96 h while urine lactate, urea and protein excretion were not significantly altered by lead exposure. The urine excretion rate of Ca2+ increased significantly by approximately 43% after only 24 h of lead exposure, and was maintained at a higher rate than controls for up to 96 h. Magnesium excretion increased in a time-dependent fashion, reaching a two- to three-fold rise by 96 h. In contrast, rates of Na+ and Cl- excretion were decreased in experimental fish by approximately 30% by 48 h, this trend continuing for the duration of lead-exposure. There were no changes in any of these parameters in similarly treated control fish. Clearance ratio analyses indicated progressive decreases in the net reabsorption efficiencies of the renal system for Ca2+, Mg2+, Pb, and glucose, suggesting that the active tubular transport mechanisms for these substances were inhibited by lead exposure, while Na+, K+, Cl-, lactate, and protein reabsorptions were unaffected. Net ammonia secretion increased. We conclude that changes in renal function both reflect and help to minimize some of the associated disturbances in systemic physiology. Lead-induced ionoregulatory toxicity in rainbow trout, particularly the disturbance of Ca2+ homeostasis, is not exclusively a branchial phenomenon, but is in part a result of disruption of ionoregulatory mechanisms at the kidney. This action of lead outside the gills is critical to consider when developing guidelines for water quality.

Original languageEnglish
Pages (from-to)362-371
Number of pages10
JournalAquatic Toxicology
Volume80
Issue number4
DOIs
StatePublished - Dec 30 2006

Fingerprint

Oncorhynchus mykiss
Fresh Water
rainbow
kidneys
Kidney
excretion
urine
Urine
Fishes
glomerular filtration rate
Trout
fish
Glomerular Filtration Rate
calcium
Ammonia
trout
lactates
Lactic Acid
glucose
Lead

Keywords

  • Acute toxicity
  • Calcium reabsorption
  • Ionoregulation
  • Kidney function
  • Rainbow trout
  • Waterborne lead

ASJC Scopus subject areas

  • Aquatic Science

Cite this

Renal responses to acute lead waterborne exposure in the freshwater rainbow trout (Oncorhynchus mykiss). / Patel, Monika; Rogers, Joseph T.; Pane, Eric F.; Wood, Chris M.

In: Aquatic Toxicology, Vol. 80, No. 4, 30.12.2006, p. 362-371.

Research output: Contribution to journalArticle

Patel, Monika ; Rogers, Joseph T. ; Pane, Eric F. ; Wood, Chris M. / Renal responses to acute lead waterborne exposure in the freshwater rainbow trout (Oncorhynchus mykiss). In: Aquatic Toxicology. 2006 ; Vol. 80, No. 4. pp. 362-371.
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N2 - The possible nephrotoxic effects of waterborne lead exposure (as Pb(NO3)2) were investigated in the freshwater rainbow trout (Oncorhynchus mykiss). Kidney lead accumulation was time-dependent, increasing upon exposure to 0.57 ± 0.01 mg dissolved Pb L-1 for up to 96 h with a significantly higher burden occurring in the posterior kidney compared to the anterior segment. Urine analyses in trout exposed to 1.20 ± 0.09 mg dissolved Pb L-1 revealed a significant increase in urinary lead excretion rate throughout 96 h of exposure. Urine flow rate and glomerular filtration rate (GFR) were not impacted with the exception of a significant decrease in GFR from 84 to 96 h in lead-exposed trout. Urine pH decreased significantly over time in lead-exposed fish. Correspondingly, urine ammonia excretion rate showed a marked increase from 48 h onwards. In experimental fish, urine glucose excretion was significantly greater by 96 h while urine lactate, urea and protein excretion were not significantly altered by lead exposure. The urine excretion rate of Ca2+ increased significantly by approximately 43% after only 24 h of lead exposure, and was maintained at a higher rate than controls for up to 96 h. Magnesium excretion increased in a time-dependent fashion, reaching a two- to three-fold rise by 96 h. In contrast, rates of Na+ and Cl- excretion were decreased in experimental fish by approximately 30% by 48 h, this trend continuing for the duration of lead-exposure. There were no changes in any of these parameters in similarly treated control fish. Clearance ratio analyses indicated progressive decreases in the net reabsorption efficiencies of the renal system for Ca2+, Mg2+, Pb, and glucose, suggesting that the active tubular transport mechanisms for these substances were inhibited by lead exposure, while Na+, K+, Cl-, lactate, and protein reabsorptions were unaffected. Net ammonia secretion increased. We conclude that changes in renal function both reflect and help to minimize some of the associated disturbances in systemic physiology. Lead-induced ionoregulatory toxicity in rainbow trout, particularly the disturbance of Ca2+ homeostasis, is not exclusively a branchial phenomenon, but is in part a result of disruption of ionoregulatory mechanisms at the kidney. This action of lead outside the gills is critical to consider when developing guidelines for water quality.

AB - The possible nephrotoxic effects of waterborne lead exposure (as Pb(NO3)2) were investigated in the freshwater rainbow trout (Oncorhynchus mykiss). Kidney lead accumulation was time-dependent, increasing upon exposure to 0.57 ± 0.01 mg dissolved Pb L-1 for up to 96 h with a significantly higher burden occurring in the posterior kidney compared to the anterior segment. Urine analyses in trout exposed to 1.20 ± 0.09 mg dissolved Pb L-1 revealed a significant increase in urinary lead excretion rate throughout 96 h of exposure. Urine flow rate and glomerular filtration rate (GFR) were not impacted with the exception of a significant decrease in GFR from 84 to 96 h in lead-exposed trout. Urine pH decreased significantly over time in lead-exposed fish. Correspondingly, urine ammonia excretion rate showed a marked increase from 48 h onwards. In experimental fish, urine glucose excretion was significantly greater by 96 h while urine lactate, urea and protein excretion were not significantly altered by lead exposure. The urine excretion rate of Ca2+ increased significantly by approximately 43% after only 24 h of lead exposure, and was maintained at a higher rate than controls for up to 96 h. Magnesium excretion increased in a time-dependent fashion, reaching a two- to three-fold rise by 96 h. In contrast, rates of Na+ and Cl- excretion were decreased in experimental fish by approximately 30% by 48 h, this trend continuing for the duration of lead-exposure. There were no changes in any of these parameters in similarly treated control fish. Clearance ratio analyses indicated progressive decreases in the net reabsorption efficiencies of the renal system for Ca2+, Mg2+, Pb, and glucose, suggesting that the active tubular transport mechanisms for these substances were inhibited by lead exposure, while Na+, K+, Cl-, lactate, and protein reabsorptions were unaffected. Net ammonia secretion increased. We conclude that changes in renal function both reflect and help to minimize some of the associated disturbances in systemic physiology. Lead-induced ionoregulatory toxicity in rainbow trout, particularly the disturbance of Ca2+ homeostasis, is not exclusively a branchial phenomenon, but is in part a result of disruption of ionoregulatory mechanisms at the kidney. This action of lead outside the gills is critical to consider when developing guidelines for water quality.

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