Ascorbic acid protects against the nephrotoxicity and apoptosis caused by colistin and affects its pharmacokinetics

The use of colistin in the treatment of life-threatening Gram-negative infections is associated with a high rate of nephrotoxicity that is dose limiting. This study aimed to examine the nephroprotective effect of ascorbic acid against colistin-induced nephrotoxicity. Rats were treated intravenously...

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Published inJournal of antimicrobial chemotherapy Vol. 67; no. 2; pp. 452 - 459
Main Authors YOUSEF, Jumana M, GONG CHEN, HILL, Prue A, NATIONAL, Roger L, JIAN LI
Format Journal Article
LanguageEnglish
Published Oxford Oxford University Press 01.02.2012
Oxford Publishing Limited (England)
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Abstract The use of colistin in the treatment of life-threatening Gram-negative infections is associated with a high rate of nephrotoxicity that is dose limiting. This study aimed to examine the nephroprotective effect of ascorbic acid against colistin-induced nephrotoxicity. Rats were treated intravenously twice daily with saline, colistin (cumulative dose of 36.5 mg/kg), a combination of ascorbic acid (50 or 200 mg/kg) and colistin, or ascorbic acid (200 mg/kg) over 7 days. Colistin-induced apoptosis was examined in rats over 5 days and in vitro using rat renal proximal tubular cells NRK-52E over 24 h with and without ascorbic acid. The effect of co-administered ascorbic acid on colistin pharmacokinetics was investigated. The 24 h urinary excretion of N-acetyl-β-D-glucosaminidase, a sensitive marker for tubular damage, was significantly lower (P < 0.0001) in the colistin/ascorbic acid 200 mg/kg group. Significant histological abnormalities (P < 0.01) were detected only in the kidneys of the colistin group, which also had the highest percentage (30.6 ± 7.8%) of apoptotic cells (P < 0.005). In the cell culture studies, the percentage of apoptotic cells was significantly higher in the presence of 0.1 mM colistin alone (51.8 ± 2.0%; P < 0.0001) than in the presence of ascorbic acid, which decreased the apoptotic effect in a concentration-dependent manner. Ascorbic acid (200 mg/kg) altered colistin pharmacokinetics, as the total body clearance decreased from 3.78 ± 0.36 mL/min/kg (colistin group) to 2.46 ± 0.57 mL/min/kg (P = 0.0024). This is the first study demonstrating the protective effect of ascorbic acid against colistin-induced nephrotoxicity and tubular apoptosis. Co-administration of ascorbic acid has the potential to increase the therapeutic index of colistin.
AbstractList The use of colistin in the treatment of life-threatening Gram-negative infections is associated with a high rate of nephrotoxicity that is dose limiting. This study aimed to examine the nephroprotective effect of ascorbic acid against colistin-induced nephrotoxicity. Rats were treated intravenously twice daily with saline, colistin (cumulative dose of 36.5 mg/kg), a combination of ascorbic acid (50 or 200 mg/kg) and colistin, or ascorbic acid (200 mg/kg) over 7 days. Colistin-induced apoptosis was examined in rats over 5 days and in vitro using rat renal proximal tubular cells NRK-52E over 24 h with and without ascorbic acid. The effect of co-administered ascorbic acid on colistin pharmacokinetics was investigated. The 24 h urinary excretion of N-acetyl-β-d-glucosaminidase, a sensitive marker for tubular damage, was significantly lower (P < 0.0001) in the colistin/ascorbic acid 200 mg/kg group. Significant histological abnormalities (P<0.01) were detected only in the kidneys of the colistin group, which also had the highest percentage (30.6±7.8%) of apoptotic cells (P<0.005). In the cell culture studies, the percentage of apoptotic cells was significantly higher in the presence of 0.1 mM colistin alone (51.8±2.0%; P<0.0001) than in the presence of ascorbic acid, which decreased the apoptotic effect in a concentration-dependent manner. Ascorbic acid (200 mg/kg) altered colistin pharmacokinetics, as the total body clearance decreased from 3.78±0.36 mL/min/kg (colistin group) to 2.46±0.57 mL/min/kg (P=0.0024). This is the first study demonstrating the protective effect of ascorbic acid against colistin-induced nephrotoxicity and tubular apoptosis. Co-administration of ascorbic acid has the potential to increase the therapeutic index of colistin.
The use of colistin in the treatment of life-threatening Gram-negative infections is associated with a high rate of nephrotoxicity that is dose limiting. This study aimed to examine the nephroprotective effect of ascorbic acid against colistin-induced nephrotoxicity. Rats were treated intravenously twice daily with saline, colistin (cumulative dose of 36.5 mg/kg), a combination of ascorbic acid (50 or 200 mg/kg) and colistin, or ascorbic acid (200 mg/kg) over 7 days. Colistin-induced apoptosis was examined in rats over 5 days and in vitro using rat renal proximal tubular cells NRK-52E over 24 h with and without ascorbic acid. The effect of co-administered ascorbic acid on colistin pharmacokinetics was investigated. The 24 h urinary excretion of N-acetyl-β-D-glucosaminidase, a sensitive marker for tubular damage, was significantly lower (P < 0.0001) in the colistin/ascorbic acid 200 mg/kg group. Significant histological abnormalities (P < 0.01) were detected only in the kidneys of the colistin group, which also had the highest percentage (30.6 ± 7.8%) of apoptotic cells (P < 0.005). In the cell culture studies, the percentage of apoptotic cells was significantly higher in the presence of 0.1 mM colistin alone (51.8 ± 2.0%; P < 0.0001) than in the presence of ascorbic acid, which decreased the apoptotic effect in a concentration-dependent manner. Ascorbic acid (200 mg/kg) altered colistin pharmacokinetics, as the total body clearance decreased from 3.78 ± 0.36 mL/min/kg (colistin group) to 2.46 ± 0.57 mL/min/kg (P = 0.0024). This is the first study demonstrating the protective effect of ascorbic acid against colistin-induced nephrotoxicity and tubular apoptosis. Co-administration of ascorbic acid has the potential to increase the therapeutic index of colistin.
Objectives The use of colistin in the treatment of life-threatening Gram-negative infections is associated with a high rate of nephrotoxicity that is dose limiting. This study aimed to examine the nephroprotective effect of ascorbic acid against colistin-induced nephrotoxicity. Methods Rats were treated intravenously twice daily with saline, colistin (cumulative dose of 36.5 mg/kg), a combination of ascorbic acid (50 or 200 mg/kg) and colistin, or ascorbic acid (200 mg/kg) over 7 days. Colistin-induced apoptosis was examined in rats over 5 days and in vitro using rat renal proximal tubular cells NRK-52E over 24 h with and without ascorbic acid. The effect of co-administered ascorbic acid on colistin pharmacokinetics was investigated. Results The 24 h urinary excretion of N-acetyl- beta -d-glucosaminidase, a sensitive marker for tubular damage, was significantly lower (P<0.0001) in the colistin/ascorbic acid 200 mg/kg group. Significant histological abnormalities (P<0.01) were detected only in the kidneys of the colistin group, which also had the highest percentage (30.6+/-7.8%) of apoptotic cells (P<0.005). In the cell culture studies, the percentage of apoptotic cells was significantly higher in the presence of 0.1 mM colistin alone (51.8+/-2.0%; P<0.0001) than in the presence of ascorbic acid, which decreased the apoptotic effect in a concentration-dependent manner. Ascorbic acid (200 mg/kg) altered colistin pharmacokinetics, as the total body clearance decreased from 3.78+/-0.36 mL/min/kg (colistin group) to 2.46+/-0.57 mL/min/kg (P=0.0024). Conclusions This is the first study demonstrating the protective effect of ascorbic acid against colistin-induced nephrotoxicity and tubular apoptosis. Co-administration of ascorbic acid has the potential to increase the therapeutic index of colistin.
Author YOUSEF, Jumana M
GONG CHEN
NATIONAL, Roger L
JIAN LI
HILL, Prue A
AuthorAffiliation 1 Drug Delivery, Disposition and Dynamics , Monash Institute of Pharmaceutical Sciences, Monash University , 381 Royal Parade, Parkville, VIC 3052 , Australia
2 Department of Anatomical Pathology , St Vincent's Hospital , 41 Victoria Parade, Fitzroy, VIC 3065 , Australia
AuthorAffiliation_xml – name: 1 Drug Delivery, Disposition and Dynamics , Monash Institute of Pharmaceutical Sciences, Monash University , 381 Royal Parade, Parkville, VIC 3052 , Australia
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  organization: Drug Delivery, Disposition and Dynamics, Monash Institute of Pharmaceutical Sciences, Monash University, 381 Royal Parade, Parkville, VIC 3052, Australia
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  organization: Drug Delivery, Disposition and Dynamics, Monash Institute of Pharmaceutical Sciences, Monash University, 381 Royal Parade, Parkville, VIC 3052, Australia
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ContentType Journal Article
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The Author 2011. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com 2011
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Issue 2
Keywords rat kidney tubular cells
Ascorbic acid
Urinary system disease
Colistin
Rat
Cyclic peptides
Toxicity
vitamin C
Rodentia
Vitamin
polymyxin E
In vitro
Kidney
Prevention
Vertebrata
Antibiotic
Mammalia
Polypeptide
Cell death
Animal
Antibacterial agent
Pharmacokinetics
Cell
Apoptosis
Language English
License CC BY 4.0
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Joint senior authors.
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Lopez-Novoa (21_38178149) 2011; 79
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Snippet The use of colistin in the treatment of life-threatening Gram-negative infections is associated with a high rate of nephrotoxicity that is dose limiting. This...
Objectives The use of colistin in the treatment of life-threatening Gram-negative infections is associated with a high rate of nephrotoxicity that is dose...
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SubjectTerms Animals
Anti-Bacterial Agents - administration & dosage
Anti-Bacterial Agents - adverse effects
Anti-Bacterial Agents - pharmacokinetics
Antibiotics. Antiinfectious agents. Antiparasitic agents
Apoptosis
Ascorbic Acid - administration & dosage
Ascorbic Acid - pharmacology
Bacterial infections
Biological and medical sciences
Cells, Cultured
Colistin - administration & dosage
Colistin - adverse effects
Colistin - pharmacokinetics
Injections, Intravenous
Kidney Diseases - chemically induced
Kidney Diseases - prevention & control
Kidneys
Male
Medical sciences
Original Research
Pharmacology
Pharmacology. Drug treatments
Rats
Rats, Sprague-Dawley
Rodents
Vitamin C
Vitamins - administration & dosage
Vitamins - pharmacology
Title Ascorbic acid protects against the nephrotoxicity and apoptosis caused by colistin and affects its pharmacokinetics
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