Akademik Veri Yönetim Sistemi
Reproductive Toxicology, cilt.140, 2026 (SCI-Expanded, Scopus)
Aim: This study investigated the harmful effects of tramadol (TRD) exposure on ovarian and uterine tissue, with a specific focus on oxidative stress and the damage pathways it triggers. It also aimed to establish whether catechin hydrate (CTH), a potent antioxidant flavonoid, could protect against or repair TRD-induced reproductive toxicity. Methods: 28 Wistar rats were randomly divided into four groups: Control, CTH, TRD, and TRD+CTH. TRD (50 mg/kg, intraperitoneal) and CTH (20 mg/kg, oral) were administered daily for a period of 14 days. Subsequent to the administration of treatment, blood, ovarian, and uterine tissues were collected for biochemical, qRT-PCR, histopathological, and immunohistochemical analyses to evaluate oxidative and ER stress, inflammation and apoptotic damage, hormonal changes, and tissue damage. Results: TRD administration significantly increased oxidative stress (MDA, p < 0.001), inflammation (NF-κB, TNF-α, IL-1β, p < 0.001), apoptosis (Caspase-3, Bax, p < 0.001), and ER stress (PERK, ATF6, p < 0.001), while suppressing antioxidant parameters, Bcl-2 and steroidogenic enzyme expression (CYP11A1, CYP17A1, CYP19A1, p < 0.001) and reducing serum AMH, E2, FSH, and LH levels (p < 0.001). Co-administration of CTH markedly reversed these effects by restoring antioxidant and hormonal balance (p < 0.05–0.001) and downregulating oxidative, inflammatory, and apoptotic markers. Histologically, CTH treatment notably improved TRD-induced ovarian and uterine degeneration, reducing inflammation, congestion, and follicular atresia while preserving tissue integrity (p < 0.05). Conclusion: The findings of this study suggest that CTH may offer protective effects against TRD-induced ovarian and uterine toxicity by mitigating oxidative stress, inflammation, apoptosis, and ER stress, thereby supporting hormonal balance and tissue integrity.