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Menopause. 2013 Nov;20(11):1184-93. doi: 10.1097/GME.0b013e31828a7f4e.

Zinc as a nutritional approach to bone loss prevention in an ovariectomized rat model.

Author information

1
From the 1Department of Biophysics, Panjab University, Chandigarh, India; and 2Faculty of Biomedical Engineering, Shobhit University, Meerut, India.

Abstract

OBJECTIVE:

In this study, we have investigated the role of zinc supplementation (a nutritional antioxidant) in an ovariectomized osteopenic rat model.

METHODS:

Forty-eight female Wistar rats were assigned to four groups: control, zinc, ovariectomy (OVX), and OVX + zinc. Analysis was performed to compare the study groups on bone metabolism markers, bone antioxidant enzymes, and zinc and copper levels in serum and bone tissues. Electron microscopy was also performed to assess morphological changes.

RESULTS:

Estradiol levels decreased and tartarate-resistant acid phosphatase 5b levels increased in the OVX group. In the OVX + zinc group, these levels were regulated; however, estradiol levels were still significantly lower than those in controls. The OVX group showed significantly higher urinary excretion of hydroxyproline, which recovered upon zinc supplementation but was higher than normal levels. The activities of catalase and superoxide dismutase decreased in ovariectomized animals and up-regulated upon zinc supplementation. Zinc supplementation in the OVX group revoked reduced glutathione levels and elevated malondialdehyde levels. Reduction in zinc and copper levels was observed in the bone tissues and serum of the OVX group. Zinc administration restored these levels to normal. Electron microscopic studies revealed a looser structure and resorbed areas in ovariectomized rat cortical bone. Zinc administration restored bone tissue morphology.

CONCLUSIONS:

These findings suggest that changes in cortical bone attributed to estrogen deficiency are arrested by zinc supplementation, which can be a sustainable approach to improving bone health.

PMID:
23571522
DOI:
10.1097/GME.0b013e31828a7f4e
[Indexed for MEDLINE]

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