European journal of obstetrics, gynecology, and reproductive biology · 2026
Boric acid Attenuates premature ovarian insufficiency by Modulating oxidative stress in a Cyclophosphamide-Induced rat model.
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Ozcakar Tugce Guclu, Kender Erturk Nergis, Onguncan Onur, Guler Sabire, Erturk Anil
Аннотация
AIM: This study aimed to investigate whether boric acid (BA) exerts potential protective effects against cyclophosphamide (CYC)-induced premature ovarian insufficiency (POI) in rats through modulation of oxidative stress and preservation of ovarian reserve.
MATERIALS AND METHODS: Thirty female Wistar-Albino rats were randomly assigned to five groups: Control, Sham, CYC, BA, and BA + CYC. CYC was administered intraperitoneally at 50 mg/kg on Day 1 followed by 8 mg/kg/day for 14 days to induce ovarian injury. BA was administered intraperitoneally at 200 mg/kg/day, either alone or beginning 6 days before and continuing throughout CYC treatment. Serum levels of anti-Müllerian hormone (AMH), follicle-stimulating hormone (FSH), glutathione (GSH), and lipid peroxidase (LPO) were measured before and after treatment. Ovarian tissues underwent histopathological evaluation for assessment of follicular development and follicular atresia.
RESULTS: CYC administration resulted in significant follicular atresia (p = 0.002), elevated FSH levels (p = 0.015), decreased AMH levels (p = 0.008), together with reduced GSH, and increased LPO levels, indicating ovarian damage and oxidative stress. In contrast, co-administration of BA with CYC was associated with lower follicular atresia and relatively preserved AMH and FSH profiles compared with the CYC-only group. In addition, BA administration alone was associated with increased GSH levels (p = 0.001) and reduced LPO levels (p = 0.014), supporting a possible antioxidant effect. Histological findings also suggested partial attenuation of CYC-induced ovarian damage in the BA + CYC group. However, some findings, including ΔAMH comparisons, did not reach statistical significance and should therefore be interpreted cautiously.
CONCLUSION: BA demonstrated potential protective effects against CYC-induced ovarian damage in rats, possibly through modulation of oxidative stress and partial preservation of ovarian follicular integrity. However, because the present findings are derived from a small preclinical experimental model, they should be interpreted cautiously. Further mechanistic, dose-response, and long-term fertility studies are required before definitive conclusions or clinical translation can be considered.
MATERIALS AND METHODS: Thirty female Wistar-Albino rats were randomly assigned to five groups: Control, Sham, CYC, BA, and BA + CYC. CYC was administered intraperitoneally at 50 mg/kg on Day 1 followed by 8 mg/kg/day for 14 days to induce ovarian injury. BA was administered intraperitoneally at 200 mg/kg/day, either alone or beginning 6 days before and continuing throughout CYC treatment. Serum levels of anti-Müllerian hormone (AMH), follicle-stimulating hormone (FSH), glutathione (GSH), and lipid peroxidase (LPO) were measured before and after treatment. Ovarian tissues underwent histopathological evaluation for assessment of follicular development and follicular atresia.
RESULTS: CYC administration resulted in significant follicular atresia (p = 0.002), elevated FSH levels (p = 0.015), decreased AMH levels (p = 0.008), together with reduced GSH, and increased LPO levels, indicating ovarian damage and oxidative stress. In contrast, co-administration of BA with CYC was associated with lower follicular atresia and relatively preserved AMH and FSH profiles compared with the CYC-only group. In addition, BA administration alone was associated with increased GSH levels (p = 0.001) and reduced LPO levels (p = 0.014), supporting a possible antioxidant effect. Histological findings also suggested partial attenuation of CYC-induced ovarian damage in the BA + CYC group. However, some findings, including ΔAMH comparisons, did not reach statistical significance and should therefore be interpreted cautiously.
CONCLUSION: BA demonstrated potential protective effects against CYC-induced ovarian damage in rats, possibly through modulation of oxidative stress and partial preservation of ovarian follicular integrity. However, because the present findings are derived from a small preclinical experimental model, they should be interpreted cautiously. Further mechanistic, dose-response, and long-term fertility studies are required before definitive conclusions or clinical translation can be considered.