Elif Ece Akgun, Esra Bilici, Busra Gulbenli Turkoglu
Background/Objectives: Cyclophosphamide (CP) can produce acute renal toxicity through overlapping oxidative, inflammatory, and apoptotic processes. Although lycopene is widely studied for antioxidant and anti-inflammatory activity, its renal effects during acute CP exposure remain incompletely defined. We investigated whether a 10-day course of oral lycopene before CP administration altered early biochemical, transcriptional, histological, and apoptosis-related renal responses. Methods: Twenty-eight male CD-1 mice were assigned equally to control, lycopene (20 mg kg-1 day-1), CP (200 mg kg-1 intraperitoneally on day 10), or CP + lycopene groups (n = 7). At 24 h after CP administration, serum BUN and creatinine were measured together with renal TBARS-derived MDA-equivalent values, SOD activity, TNF-α/IL-6/IL-1β mRNA abundance, histopathological injury, and cleaved caspase-3 immunoreactivity. Results: CP increased BUN, creatinine, and renal TBARS-derived MDA-equivalent values; decreased SOD activity; increased all three inflammatory transcripts; worsened tubular and tubulointerstitial injury; and increased cleaved caspase-3 labeling. Compared with CP alone, lycopene pretreatment reduced BUN, renal TNF-α, IL-6, and IL-1β mRNA, tubular and tubulointerstitial damage, and cleaved caspase-3 labeling. Creatinine, renal TBARS-derived MDA-equivalent values, and SOD activity were not significantly different between the CP and CP + lycopene groups. Conclusions: In this prophylactic model (20 mg kg-1 day-1 for 10 days; 24 h assessment), lycopene provided partial early protection against CP-associated renal injury. The response was evident in BUN, inflammatory transcription, tissue injury, and apoptotic labeling, but not in creatinine or the two measured redox indices. The study does not establish pathway causality and does not support extrapolation to post-injury treatment or long-term protection.