eugenol protection of testicular function in diabetic rats by attenuating oxidative stress and restoring catsper gene expression

Background: diabetes mellitus (dm) frequently leads to male infertility, with oxidative stress being a primary culprit in damaging testicular function. this damage may extend to key spermatogenic genes, including the sperm-specific cation channels catsper1 and catsper2, which are essential for male fertility.materials and methods: this study investigated the therapeutic potential of eugenol against testicular dysfunction in a streptozotocin (stz)-induced diabetic rat model, focusing on glycemic control, oxidative stress, histopathology, and the expression of catsper1 and catsper2 genes. in this experimental study, 32 male wistar rats were divided into control, diabetic, diabetic+eugenol (4 mg/kg/d, ip), and eugenol-only groups. diabetes was induced with a single stz injection (55 mg/kg). after 8 weeks of treatment, fasting blood glucose, serum oxidative stress markers (malondialdehyde [mda], superoxide dismutase [sod], glutathione peroxidase [gpx]), testicular histology, and catsper1/2 mrna expression were analyzed.results: eugenol treatment significantly attenuated hyperglycemia in diabetic rats (p<0.05). it also mitigated diabetes-induced testicular damage, as shown by histopathological improvement. biochemically, eugenol reversed oxidative stress by lowering elevated mda (p<0.05) and restoring depleted sod and gpx activities (p<0.05). crucially, diabetes profoundly downregulated catsper1 and catsper2 gene expression (p<0.000), and eugenol treatment significantly restored their mrna levels (p<0.001).conclusion: eugenol exerts a multifaceted protective effect against diabetic testicular damage by improving glycemic control, reducing oxidative stress, preserving testicular architecture, and restoring the expression of the critical spermatogenic genes: catsper1 and catsper2. these findings highlight eugenol's promise as a therapeutic adjunct for managing diabetic male infertility.