ArticleClinical and experimental nephrology2009
Nitrosative stress, protein tyrosine nitration, PARP activation and NAD depletion in the kidneys of rats after single dose of cyclophosphamide.
Article in Clinical and experimental nephrology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- Oxidative Stress-Driven Mechanisms and Biomarkers of Drug-Induced Nephrotoxicity: Translational Insights and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- Antioxidant and Cytoprotective Effects of Different Compounds on Cyclophosphamide-induced Nephrotoxicity.Current drug research reviews · 2025Review
- Protective Effect of Escin Against Kidney Injury: Histopathological and Biochemical Evaluations.Current issues in molecular biology · 2024Article
- Potential Protective Effects of Antioxidants against Cyclophosphamide-Induced Nephrotoxicity.International journal of nephrology · 2022Review
- Inhibition of gene expression of organic cation/carnitine transporter and antioxidant enzymes in oxazaphosphorines-induced acute cardiomyopathic rat models.Oxidative medicine and cellular longevity · 2012Article
- Progression of cyclophosphamide-induced acute renal metabolic damage in carnitine-depleted rat model.Clinical and experimental nephrology · 2010Article
- Effect of diethyldithiocarbamate in cyclophosphamide-induced nephrotoxicity: Immunohistochemical study of superoxide dismutase 1 in rat.Indian journal of pharmacologyArticle
- Carnitine deficiency and oxidative stress provoke cardiotoxicity in an ifosfamide-induced Fanconi Syndrome rat model.Oxidative medicine and cellular longevityArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesCyclophosphamide (CP) and its structural analogue ifosfamide are highly effective cytostatic drugs. While both cyclophosphamide and ifosfamide have severe urotoxic side effects, only ifosfamide is thought to be nephrotoxic. The nephrotoxicity of CP in generally overlooked because of normal plasma creatinine levels. Therefore, little information is available regarding the pathogenic mechanism of renal damage by CP. In the present study, we investigated the role of nitrosative stress in CP-induced renal damage.
methodsThe experimental rats received a single i.p. of 150 mg/kg body weight CP in saline and were killed 6 h or 16 h later. The control rats received saline. The kidneys were used for histological and biochemical analysis. Nitrotyrosine and poly (ADP-ribose) polymerase (PARP) were localized immunohistochemically as indicators of protein nitration and DNA damage, respectively. Nitrite, NAD and superoxide dismutase (SOD) activity were assayed in the kidney homogenates.
resultsThe nitrite level in the kidneys of CP-treated rats was elevated twofold. The kidneys of CP-treated rats stained strongly for nitrotyrosine as well as for PARP. Significant decrease in oxidized NAD levels was also observed in the kidneys of CP-treated rats. The activity of the peroxynitrite sensitive enzyme SOD was significantly reduced in the kidneys of CP-treated rats.
conclusionThe results of the present study reveal that nitrosative stress may play an important role in CP-induced renal damage. It is suggested that protein nitration, PARP activation and NAD +/- depletion may play a critical role in the pathogenesis of cyclophosphamide induced renal damage.
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