RESUMEN
Objective: Ciprofloxacin (CPFX) is frequently prescribed by fertility specialists and urologists to manage infections in male reproductive organs. However, it is toxic to the testicles and can lead to infertility. Dietary antioxidants are known to protect the testis from damage. This study aimed to investigate the effects of coenzyme Q10 (CoQ10) on the adverse side effects of CPFX using stereological methods. Methods: Sixty rats were divided into six groups: control (distilled water), CoQ10 (10 mg/kg/day), and low-dose (103 mg/kg/day) and high-dose (206 mg/kg/day) of CPFX (LD-CPFX, HD-CPFX) with or without CoQ10 consumption. The treatments lasted for 45 days. Sperm count, serum testosterone levels, and testicular parameters were evaluated. Results: Significant decreases in sperm count, motility, normal morphology, viability, and testosterone levels were observed in the LD-CPFX (p<0.003) and HD-CPFX- treated rats (p=0.0001) compared to the control groups. A 10% to 36% reduction in the volume of seminiferous tubules, tubular epithelium, and tubule length was noted in LD-CPFX (p<0.01) and HD-CPFX-treated rats (p<0.006), while the volume of the interstitium increased by 25% to 28% in LD-CPFX (p=0.03) and HD-CPFX (p=0.008) groups. The number of cells, including spermatogonia, spermatocytes, spermatids, Sertoli cells, and Leydig cells, decreased by 36% to 75% in the testes exposed to LD-CPFX (p<0.04) and HD-CPFX (p<0.01), compared to the control groups. However, these changes normalized in rats that received CoQ10. Conclusion: CPFX exposure for 45 days, regardless of the dose, has detrimental effects on testicular parameters. CoQ10 can prevent CPFX-induced testicular structural impairments.
RESUMEN
BACKGROUND: Clear cell renal cell carcinoma (ccRCC) is a form of kidney cancer characterized by dysregulated angiogenesis and multidrug resistance. Hypoxia-induced tumor progression plays a crucial role in ccRCC pathogenesis. Beta-hydroxybutyrate (BHB) and quercetin (QCT) have shown potential in targeting angiogenesis and drug resistance in various cancer types. This study investigates the combined effects of BHB and QCT in hypoxia-induced Caki-1 cells. METHODS: Caki-1 cells were subjected to normoxic and hypoxic conditions and treated with BHB, QCT, or a combination of both. Cell-viability was assessed using the MTT assay, and mRNA expression levels of key angiogenesis-related genes (HIF-1α/2α, VEGF, Ang-1, Ang-2, and MDR4) were quantified through real-time PCR during 24 and 48 h. RESULTS: BHB and QCT treatments, either alone or in combination, significantly reduced cell-viability in Caki-1 cells (p < 0.05). Moreover, the combined therapy demonstrated a potential effect in downregulating the expression of angiogenesis-related genes and MDR4 in hypoxia-induced cells, with a marked reduction in HIF-1α/2α, VEGF, Ang-1, and MDR4 expression (p < 0.05). The expression of Ang-2 increases significantly in presence of BHB combined QCT treatment. CONCLUSION: This study highlights the promising potential of a combination therapy involving BHB and QCT in mitigating angiogenesis and MDR4 expression in hypoxia-induced ccRCC cells. These findings support further investigation into the underlying mechanisms and warrant clinical studies to evaluate the therapeutic value of this combined treatment for ccRCC patients. This research provides new insights into addressing the challenges posed by angiogenesis and drug resistance in ccRCC.