Differential menopause- versus aging-induced changes in oxidative stress and circadian rhythm gene markers.

Oriol A Rangel-Zuñiga, Cristina Cruz-Teno, Carmen Haro, Gracia M Quintana-Navarro, Fernando Camara-Martos, Pablo Perez-Martinez, Antonio Garcia-Rios, Marta Garaulet, Manuel Tena-Sempere, Jose Lopez-Miranda, Francisco Perez-Jimenez, Antonio Camargo

Journal: Mechanisms of ageing and development 2018;164():41-48

PMID: 28408140

Abstract

Menopause is characterized by the depletion of estrogen that has been proposed to cause oxidative stress. Circadian rhythm is an internal biological clock that controls physiological processes. It was analyzed the gene expression in peripheral blood mononuclear cells and the lipids and glucose levels in plasma of a subgroup of 17 pre-menopausal women, 19 men age-matched as control group for the pre-menopausal women, 20 post-menopausal women and 20 men age-matched as control group for the post-menopausal women; all groups were matched by body mass index. Our study showed a decrease in the expression of the oxidative stress-related gene GPX1, and an increase in the expression of SOD1 as consequence of menopause. In addition, we found that the circadian rhythm-related gene PER2 decreased as consequence of menopause. On the other hand, we observed a decrease in the expression of the oxidative stress-related gene GPX4 and an increase in the expression of CAT as a consequence of aging, independently of menopause. Our results suggest that the menopause-induced oxidative stress parallels a disruption in the circadian clock in women, and part of the differences in oxidative stress observed between pre- and post-menopausal women was due to aging, independent of menopause. Clinical Trials.gov.Identifier: NCT00924937.

Copyright © 2017 Elsevier B.V. All rights reserved.

Address: Lipids and Atherosclerosis Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain.; Dpto de Bromatología y Tecnología de Alimentos, University of Cordoba, Cordoba, Spain.; Department of Physiology, University of Murcia, Spain.; CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain; Department of Cell Biology, Physiology, and Immunology, IMIBIC/Reina Sofia University Hospital/University of Cordoba, Cordoba, Spain.; Lipids and Atherosclerosis Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain. Electronic address: [email protected].
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