ArticleClinical and experimental nephrology2010
Progression of cyclophosphamide-induced acute renal metabolic damage in carnitine-depleted rat model.
Article in Clinical and experimental nephrology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 27 citations in OpenAlex.
- Cyclophosphamide-Induced Nephrotoxicity and Nephroprotection in Rodent Models: A Systematic Review and Random-Effects Meta-Analysis (2010-2025).Journal of xenobiotics · 2026Review
- Carnitine deficiency augments methotrexate-mediated acute renal injury in rats.Journal of the Egyptian National Cancer Institute · 2025Article
- Protective Effect ofJournal of experimental pharmacology · 2020Article
- Metabolomic analysis reveals a protective effect of Fu-Fang-Jin-Qian-Chao herbal granules on oxalate-induced kidney injury.Bioscience reports · 2019Article
- 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
- Acute renal endothelial injury during marrow recovery in a cohort of combined kidney and bone marrow allografts.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2011Article
- Protective effect of aminoguanidine against cyclophosphamide-induced oxidative stress and renal damage in rats.Redox report : communications in free radical research · 2011Article
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1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundLittle information is available regarding the mechanism of cyclophosphamide (CP)-induced renal damage. Therefore, this study examined whether carnitine deficiency constitutes a risk factor in and should be viewed as a mechanism during development of CP-induced nephrotoxicity and explored whether carnitine supplementation, using propionyl-L-carnitine (PLC), could offer protection against this toxicity.
methodsExperimental rats were assigned to one of six groups; the first three groups were injected intraperitoneally with normal saline, PLC (250 mg/kg/day) or D-carnitine (250 mg/kg/day) + Mildronate (200 mg/kg/day), respectively, for 10 successive days. The 4th, 5th and 6th groups received the same doses of normal saline, PLC or D-carnitine + Mildronate, respectively, for 5 successive days before and after a single dose of CP (200 mg/kg).
resultsCP significantly increased serum creatinine, blood urea nitrogen (BUN), intramitochondrial acetyl-coenzyme A (CoA) and thiobarbituric acid reactive substances, significantly decreased total carnitine, intramitochondrial CoA-SH, adenosine triphosphate (ATP) and ATP/adenosine diphosphate (ADP) and reduced glutathione in kidney tissues. In carnitine-depleted rats, CP resulted in dramatic increase in serum nephrotoxicity indices and acetyl-CoA and induced progressive reduction in total carnitine, CoA-SH and ATP as well as severe histopathological lesions in kidney tissues. Interestingly, PLC completely reversed the biochemical and histopathological changes induced by CP to normal values.
conclusionsOxidative stress is not involved in CP-induced renal injury in this model. Carnitine deficiency and energy starvation constitute risk factors in and should be viewed as a mechanism during CP-induced nephrotoxicity. PLC prevents development of CP-induced nephrotoxicity by increasing intracellular carnitine content, intramitochondrial CoA-SH/acetyl-CoA ratio and energy production.
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