Abstract

Background:
Methotrexate (MTX) is an effective chemotherapeutic and immunosuppressive agent; however, its clinical use is limited by nephrotoxicity, primarily due to oxidative stress (OS) and inflammation.

Aim:
Coenzyme Q10 (CoQ10) is a mitochondrial electron carrier with antioxidant and anti-inflammatory properties. It has been proposed as a potential agent against MTX-induced nephrotoxicity. This study assessed its renoprotective potential.

Methods:
Twenty-four Wistar rats were randomly divided into four equal groups: Group 1 (normal control; NC) was left untreated, Group 2 (positive control; PC) was intraperitoneally injected with MTX (20 mg/kg) on day 4 of the experiment, Group 3 (CoQ10) was orally administered CoQ10 (10 mg/kg) for 8 days, and Group 4 was administered CoQ10 + MTX. The following biomarkers were measured: OS biomarkers (glutathione [GSH], superoxide dismutase [SOD], malondialdehyde [MDA], total antioxidant capacity [TAC], total oxidant status [TOS], and nitric oxide [NO]), inflammatory markers (IL-1β, TNF-α, and NF-κB), and renal function markers (serum creatinine, uric acid, blood urea nitrogen [BUN], and urinary N-acetyl-β-D-glucosaminidase [NAG]).

Results:
MTX induced nephrotoxicity, elevating BUN, creatinine, and uric acid levels, as well as urinary NAG, and increasing MDA, TOS, NO, IL-1β, TNF-α, and NF-κB, while reducing GSH, SOD, and TAC levels. In contrast, CoQ10 significantly reduced oxidative and inflammatory markers and increased the antioxidant capacity of renal tissue, even though it failed to restore values to baseline levels. CoQ10 showed significant renoprotective effects by suppressing OS and inflammatory pathways.

Conclusion:
These findings show that CoQ10 is a potential renoprotective antioxidant that could serve as an adjunct therapy to reduce MTX-associated renal injury.

Key words: Antioxidant; Coenzyme Q10; Drug-induced nephrotoxicity; Methotrexate; Oxidative damage.