Acta Scientiarum Polonorum Technologia Alimentaria

Background. Estrogen deficiency during menopause leads to time-dependent alterations in calcium metabo­lism, bone turnover, and antioxidant status. Rodent ovariectomy models replicate these processes; however, the onset of measurable changes varies with the duration of estrogen deprivation. Early post-ovariectomy stages may remain physiologically compensated, thereby masking metabolic disturbances. This study exam­ined whether a three-week estrogen deficit is sufficient to induce detectable changes in calcium content, organ mass, bone markers, and antioxidant status in rats.
Material and Methods. Twenty-four female Wistar rats were assigned to control, sham-operated, or ova­riectomized groups. Following bilateral ovariectomy or sham surgery, the animals were maintained for three weeks on a standard AIN-93M diet. Body weight and food intake were monitored throughout the study. At the end of the experiment, serum, tissues, and organs were collected for analysis. Calcium content in the diet and tissues was quantified using flame atomic absorption spectrometry. Serum concentrations of C-terminal telopeptide of type I collagen (CTX), procollagen type I N-terminal propeptide (PINP), tartrate-resistant acid phosphatase 5b (TRACP-5b), osteocalcin (OCN), parathyroid hormone (PTH), and total antioxidant status (TAS) were determined by ELISA. Data were analyzed using one-way analysis of variance (ANOVA) fol­lowed by Tukey’s post hoc test (p < 0.05).
Results. Ovariectomized rats exhibited a significant reduction in hair calcium content, whereas calcium con­centrations in serum and other tissues remained unchanged. No significant differences were detected among experimental groups in bone turnover markers, total antioxidant status, or relative organ masses. Collectively, these findings suggest that systemic calcium balance and antioxidant capacity are maintained during the early post-ovariectomy phase.
Conclusion. Three weeks of estrogen deficiency did not result in marked alterations in calcium homeostasis, bone turnover, or antioxidant status, indicating that this period duration may be insufficient to elicit the char­acteristic metabolic changes associated with postmenopausal conditions. Longer-term studies are warranted to fully capture the effects of chronic estrogen loss.