Key result
Mito-TEMPO coadministration significantly lowered renal injury markers, restored normal histoarchitecture, and reduced apoptotic cell death in mice with 5-fluorouracil-induced renal injury.
Why the study?
The study evaluated the protective effect of scavenging mitochondrial oxidative stress against 5-fluorouracil-induced renal injury.
Does Mito-TEMPO prevent 5-fluorouracil-induced renal injury in male BALB/c mice?
Does Mito-TEMPO prevent 5-fluorouracil-induced renal injury in male BALB/c mice?
Mito-TEMPO, a mitochondria-targeted antioxidant, protects against 5-fluorouracil-induced renal injury in mice by reducing mitochondrial oxidative stress and apoptosis.
Mito-TEMPO may attenuate 5-FU renal injury in mice; hypothesis-generating and should not yet change clinical practice.
Background: The present study reports the protective effect conferred by scavenging mitochondrial oxidative stress (mtOS) in 5‐fluorouracil (5‐FU)‐induced renal injury. Methods: 5‐FU renal toxicity model was created by administering 5‐FU (12 mg/kg b.w. intraperitoneally [i.p.], for 4 days) to male BALB/c mice. The protective effect of mitochondria‐targeted antioxidant (MTA), Mito‐TEMPO coadministered at a dosage of 0.1 mg/kg b.w. i.p., was established in terms of levels/expressions of renal injury markers, histopathological alterations, oxidative DNA damage, proinflammatory markers, mtOS, mitochondrial dysfunction, and modulation of apoptotic proteins and apoptotic cell death. Results: A significant rise in the levels of serum urea, uric acid, and creatinine was noted after 5‐FU administration to the animals. Immunohistochemical and ELISA findings demonstrated significant decrease in podocin and conversely a significant increase in neutrophil gelatinase‐associated lipocalin (NGAL) expression after 5‐FU challenge. The histopathological analysis further revealed Bowman’s capsule dilation, glomerular condensation, and vacuolar degeneration. Mito‐TEMPO treatment significantly lowered renal injury markers, reversed the expressions of podocin and NGAL to normal, and restored normal histoarchitecture of renal tissue. Mitochondrial reactive oxygen species (mtROS), mtLPO, activity of mitochondrial enzyme complexes, and mitochondrial antioxidant defense status were significantly improved in Mito‐TEMPO protected group as compared to the 5‐FU group. Further, significantly decreased expression of 8‐OHdG, reduction in apoptotic cell death, and modulation of apoptotic proteins Bax, Bcl‐2, and caspase‐3 were noted in Mito‐TEMPO protected group, indicating its protective effect against 5‐FU‐induced renal injury. Conclusion: The approach of targeting mtOS using MTA, Mito‐TEMPO, may prove as safe adjuvant in alleviating renal toxicity during 5‐FU chemotherapy.
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Tambe et al. (2025) studied 5-fluorouracil-induced renal injury. Mito-TEMPO vs. 5-FU alone was evaluated on Renal injury markers, histopathological alterations, oxidative DNA damage, and mitochondrial dysfunction. Mito-TEMPO coadministration significantly lowered renal injury markers, restored normal histoarchitecture, and reduced apoptotic cell death in mice with 5-fluorouracil-induced renal injury.
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