ArticleJournal of the Egyptian National Cancer Institute2025
Carnitine deficiency augments methotrexate-mediated acute renal injury in rats.
Article in Journal of the Egyptian National Cancer Institute, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThis research aimed to explore if carnitine (CARN) deficiency is a risk factor in methotrexate (MTX)-mediated acute kidney injury (AKI) and to mechanistically reveal the potential attenuating effect of CARN against MTX-mediated nephrotoxicity.
methodsThirty-six adult male Wister albino rats were subgrouped into six groups. Groups 1, 2, and 3 received 0.9% normal saline (0.5 mL/200 g, i.p.), mildronate (MD, 200 mg/kg/day, i.p.), and L-carnitine (CARN, 200 mg/kg/day, i.p.) for 10 uninterrupted days, respectively. Groups 4, 5, and 6 received similar doses of normal saline, MD, and CARN for 5 days prior to as well as following a solo dose of methotrexate (MTX, 20 mg/kg, i.p.), respectively.
resultsTreatment with a single dose of MTX significantly boosted serum nephrotoxicity as well as hepatotoxicity indices; additionally, it increased the percentage of collagen deposition in rat kidney tissues with obvious histopathological changes. Moreover, MTX lowered kidney levels of adenosine triphosphate (ATP) and amplified acetyl-CoA carboxylase-1 (ACC-1) in kidney tissues. In MD-treated rats, MTX progressively boosted nephrotoxicity indices and collagen disposition in kidney tissues as well as progressive additional reduction in ATP as compared with MTX-treated rats and serum carnitine levels compared with MD-treated rats. Carnitine administration totally counteracted the biochemical and histopathological alterations mediated by MTX to the normal measures.
conclusionsThis research proposes that carnitine deficiency is a potential risk factor in the development of MTX-mediated AKI. MTX disrupts ACC1 signaling with the consequential inhibition of ATP production. Carnitine supplementation attenuates MTX-mediated AKI. Our results are preliminary and mandate further mechanistic study to justify the progression of AKI by MTX in CARN-deficient rats.
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