N-acetylcysteine improves renal hemodynamics in rats with cisplatin-induced nephrotoxicity

Aly M. Abdelrahman, Suhail Al Salam, Ahmed S. Almahruqi, Ishaq S. Al Husseni, Mohamed A. Mansour, Badreldin H. Ali

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

This work investigated the effect of N-acetylcysteine (NAC), on renal hemodynamics in cisplatin (CP)-induced nephrotoxicity in Wistar-Kyoto (WKY) rats. The animals were divided into four groups (n = 5 or 6). The first and second groups received normal saline (control) and intraperitoneal (i.p.) N-acetylcysteine (500 mg kg-1 per day for 9 days), respectively. The third and fourth groups were given a single intraperitoneal (i.p.) injection of CP (5 mg kg-1) and an i.p. injection of CP (5 mg kg-1) together with i.p. NAC (500 mg kg-1 per day for 9 days), respectively. At the end of the experiment, rats were anesthetized and blood pressure and renal blood flow were monitored, followed by intravenous (i.v.) injection of norepinephrine (NE) for measurement of renal vasoconstrictor responses. CP caused a significant reduction in renal blood flow but did not affect NE-induced renal vasoconstriction. In addition, CP significantly increased plasma concentrations of urea and creatinine and urinary N-acetyl-β-D-glucosaminidase (NAG) activity and kidney relative weight. CP decreased body weight and creatinine clearance. Histopathologically, CP caused remarkable renal damage compared with control. NAC alone did not produce any significant change in any of the variables measured. However, NAC significantly ameliorated CP-induced hemodynamic, biochemical and histopathological changes. The concentration of platinum in the kidneys of CP + NAC treated rats was less than in CP-treated rats by 37%. The results show that administration of i.p. NAC (500 mg kg-1 per day for 9 days) reversed the renal hemodynamic changes as well as the biochemical and histopathological indices of CP-induced nephrotoxicity in WKY rats.

Original languageEnglish
Pages (from-to)15-21
Number of pages7
JournalJournal of Applied Toxicology
Volume30
Issue number1
DOIs
Publication statusPublished - Jan 2010

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Acetylcysteine
Hemodynamics
Cisplatin
Rats
Kidney
Inbred WKY Rats
Renal Circulation
Intraperitoneal Injections
Creatinine
Norepinephrine
Blood
Hexosaminidases
Blood pressure
Vasoconstrictor Agents
Vasoconstriction
Platinum
Intravenous Injections
Urea
Animals
Body Weight

Keywords

  • Cisplatin
  • N-acetylcysteine
  • Nephrotoxicity
  • Rats
  • Renal blood 5 flow

ASJC Scopus subject areas

  • Toxicology

Cite this

N-acetylcysteine improves renal hemodynamics in rats with cisplatin-induced nephrotoxicity. / Abdelrahman, Aly M.; Al Salam, Suhail; Almahruqi, Ahmed S.; Al Husseni, Ishaq S.; Mansour, Mohamed A.; Ali, Badreldin H.

In: Journal of Applied Toxicology, Vol. 30, No. 1, 01.2010, p. 15-21.

Research output: Contribution to journalArticle

Abdelrahman, Aly M. ; Al Salam, Suhail ; Almahruqi, Ahmed S. ; Al Husseni, Ishaq S. ; Mansour, Mohamed A. ; Ali, Badreldin H. / N-acetylcysteine improves renal hemodynamics in rats with cisplatin-induced nephrotoxicity. In: Journal of Applied Toxicology. 2010 ; Vol. 30, No. 1. pp. 15-21.
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AB - This work investigated the effect of N-acetylcysteine (NAC), on renal hemodynamics in cisplatin (CP)-induced nephrotoxicity in Wistar-Kyoto (WKY) rats. The animals were divided into four groups (n = 5 or 6). The first and second groups received normal saline (control) and intraperitoneal (i.p.) N-acetylcysteine (500 mg kg-1 per day for 9 days), respectively. The third and fourth groups were given a single intraperitoneal (i.p.) injection of CP (5 mg kg-1) and an i.p. injection of CP (5 mg kg-1) together with i.p. NAC (500 mg kg-1 per day for 9 days), respectively. At the end of the experiment, rats were anesthetized and blood pressure and renal blood flow were monitored, followed by intravenous (i.v.) injection of norepinephrine (NE) for measurement of renal vasoconstrictor responses. CP caused a significant reduction in renal blood flow but did not affect NE-induced renal vasoconstriction. In addition, CP significantly increased plasma concentrations of urea and creatinine and urinary N-acetyl-β-D-glucosaminidase (NAG) activity and kidney relative weight. CP decreased body weight and creatinine clearance. Histopathologically, CP caused remarkable renal damage compared with control. NAC alone did not produce any significant change in any of the variables measured. However, NAC significantly ameliorated CP-induced hemodynamic, biochemical and histopathological changes. The concentration of platinum in the kidneys of CP + NAC treated rats was less than in CP-treated rats by 37%. The results show that administration of i.p. NAC (500 mg kg-1 per day for 9 days) reversed the renal hemodynamic changes as well as the biochemical and histopathological indices of CP-induced nephrotoxicity in WKY rats.

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