Boric acid Attenuates premature ovarian insufficiency by Modulating oxidative stress in a Cyclophosphamide-Induced rat model.

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.