Ameliorative effects of myricetin nanoparticles on carbon tetrachloride-induced spermatogenic dysfunction in mice.
Environmental toxins like carbon tetrachloride (CCl4) induce systemic oxidative stress, which can severely impair testicular function and spermatogenesis. Myricetin is a potent antioxidant, although its bioavailability is limited. Nanoformulation may enhance its absorption and effectiveness. This study evaluated the therapeutic potential of myricetin nanoparticles on CCl4-induced testicular damage. Twenty-four adult male C57BL/6 mice were divided into four groups: Sham, CCl4-induced liver injury model, empty nanoparticle, and myricetin nanoparticle treatment (25 mg/kg). Testicular histology was assessed using Johnsen's scoring, and the gene expression of TDRD5, CLCN2, and MORC1 was measured via Real-Time PCR. CCl4 treatment significantly reduced seminiferous tubule diameter (115 ± 18 vs. 188.3 ± 17.1 µm), Johnsen's score (5 ± 0 vs. 8.3 ± 1.2), and expression of spermatogenesis-related genes compared to the Sham group. Myricetin nanoparticle treatment partially ameliorated these effects, with preserved TDRD5 expression relative to sham and a less pronounced reduction in CLCN2 and MORC1 levels (p < 0.05). These findings suggest that myricetin nanoparticles confer partial amelioration on testicular tissue under systemic stress conditions, probably by preserving gene expression critical for spermatogenesis.