Effects of bone disease and calcium supplementation on antioxidant enzymes in postmenopausal women Marla Hahn a , Greicy M.M. Conterato a , Clarissa P. Frizzo b , Paula R. Augusti b , João C.N. da Silva c , Tais C. Unfer b , Tatiana Emanuelli b, ⁎ a Programa de Pós-Graduação em Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil b Núcleo Integrado de Desenvolvimento em Análises Laboratoriais (NIDAL), Departamento de Tecnologia e Ciência dos Alimentos, Centro de Ciências Rurais, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil c Departamento de Clínica Médica, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil Received 26 June 2007; received in revised form 17 October 2007; accepted 18 October 2007 Available online 26 October 2007 Abstract Objectives: The study was aimed at investigating the effects of osteopenia and calcium supplementation on antioxidant enzyme activities (superoxide dismutase, SOD; catalase, CAT; and glutathione peroxidase, GPx) in postmenopausal women. Design and methods: Postmenopausal women (n = 75) were divided into two groups, control (no bone disease) and osteopenia, according to their bone mineral density. Each group was still divided into calcium-supplemented and nonsupplemented sub-groups. Antioxidant enzyme activities were determined in whole blood using spectrophotometric methods. Results: CAT and SOD activities were not different among the studied groups. However, GPx activity was significantly higher in osteopenia groups as compared to control groups. Calcium supplementation had no effect on the parameters evaluated. Bone mineral density was negatively correlated with GPx activity (p b 0.05). Conclusions: Increased GPx activity could be interpreted as a defense response to counteract the overproduction of reactive oxygen species in women with osteopenia, and this effect was not prevented by calcium supplementation. © 2007 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved. Keywords: Osteopenia; Calcium supplementation; Catalase; Glutathione peroxidase; Superoxide dismutase Introduction Menopause is defined as the cessation of menstruation in women and is associated with the failure of ovulation because of depletion of oocytes. Menopause is a physiological event that occurs simultaneously with the establishment of several dis- eases like coronary heart disease, stroke, cancer, changes in neuropsychological status and immune function, and bone diseases like osteopenia and osteoporosis [1]. Osteoporosis is characterized by low bone mass, enhanced bone fragility, and fracture risk, while osteopenia is the initial bone loss that is not associated to fracture risk [2]. The diagnosis is made by bone densitometry, which allows the use of preventive therapy before the morbidity of a fracture ensues [3]. Postmen- opausal bone loss appears to be associated with the estrogen deficiency that leads to excessive osteoclastic and depressed osteoblastic activity, and possibly also impairs intestinal absorp- tion of calcium [4,5]. In addition, in elderly females other agents seem to contribute to the net negative bone balance, such as dietary changes and reduced physical activity [6]. Calcium supplements are used for aiding in osteoporosis treatment and fracture prevention. Calcium absorption efficiency is a key factor in the maintenance of calcium balance and is reduced in postmenopausal women with vertebral fractures [7]. Although the mechanisms that decrease calcium absorption efficiency are controversial and poorly defined, bone loss has been linked to numerous cytokines, hormones, and growth factors [7,8]. Available online at www.sciencedirect.com Clinical Biochemistry 41 (2008) 69 – 74 ⁎ Corresponding author. Fax: +55 55 3220 8353. E-mail address: tatiemanuelli@smail.ufsm.br (T. Emanuelli). 0009-9120/$ - see front matter © 2007 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved. doi:10.1016/j.clinbiochem.2007.10.010