Effects of bone disease and calcium supplementation on antioxidant enzymes in postmenopausal women.

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<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.

Sr and Fe relationship with hormone replacement therapy and bone mineral density.

BACKGROUND: We determined blood strontium (Sr) and iron (Fe) concentrations and their relationship with bone mineral density (BMD) and some biochemical parameters in premenopausal and postmenopausal women without or with hormone replacement therapy (HRT). METHODS: Blood Sr and Fe concentrations, BMD, follicle stimulating hormone (FSH), 17beta-estradiol (E2), creatinine, albumin, blood calcium and alkaline phosphatase activity were determined in premenopausal and postmenopausal women without or with HRT (mean ages: 47, 59, and 57 y, respectively). RESULTS: Blood Sr (microg/l) and Fe (mg/l) concentrations in premenopausal (31.65+/-2.96 and 496.05+/-14.37) and postmenopausal women without (28.85+/-2.48 and 525.27+/-8.56) or with (25.98+/-2.73 and 535.77+/-17.57) HRT were not significantly different. BMD L1-L4 and BMD femur (g/cm2) were significantly higher in premenopausal women (1.05+/-0.02 and 0.84+/-0.02) when compared both to postmenopausal women without (0.90+/-0.03 and 0.75+/-0.02) and with (0.93+/-0.03 and 0.73+/-0.01) HRT. However, BMD had no relationship with blood metal concentrations. E2 concentrations were lower in postmenopausal women without HRT, while FSH concentrations were higher in both postmenopausal groups (p<0.05). CONCLUSIONS: Physiological whole blood Sr and Fe concentrations had no significant effect in BMD and other biochemical parameters in pre and postmenopausal women. However, BMD was negatively influenced by FSH concentrations and associated with age.

Cytotoxic effects of moderate static magnetic field exposure on human periphery blood mononuclear cells are influenced by Val16Ala-MnSOD gene polymorphism.

Technological advancement has increasingly exposed humans to magnetic fields (MFs). However, more insights are necessary into the potential toxicity of MF exposure as a result of genetic variations related to oxidative metabolism. Therefore, the following study has assessed an in vitro cytotoxic effect of static magnetic field (SMF) (5 mT) on cells with Val16Ala polymorphism (AA, VA, and VV) in the manganese superoxide dismutase gene. Homozygous Val16Ala-superoxide dismutase 2 (SOD2) genotypes present oxidative imbalance that is associated with risk to several chronic degenerative diseases (VV produces less efficient and AA more efficient SOD2 enzyme). Blood samples from healthy adult subject carriers with different Val16Ala-SOD2 genotypes were obtained and exposed to MF at different times (0, 1, 3, 6 h). The cytotoxic effect as well as oxidative stress was evaluated after incubation of 24 h at 37 °C. In addition, apoptosis induction has been analyzed by flow cytometry as well as Bcl-2-associated X protein (BAX), B-cell lymphoma 2 (BCL-2), and caspases 8 and 3 gene expression. SMF cytotoxic effect has been observed in AA cells at all times of exposure, whereas AV cells presented higher mortality only after 6 h of exposure at SMF. Higher apoptosis induction has been observed in AA cells when compared to VV and AV cells. These results suggest a toxicogenetic SMF effect related to an imbalance in SOD2 activity.

Influence of hormone replacement therapy on blood antioxidant enzymes in menopausal women.

BACKGROUND: Natural loss of estrogen occurring in menopausal process may contribute to various health problems many of them possibly related to oxidative stress. Hormone replacement therapy (HRT) is the most common treatment to attenuate menopausal disturbances. This study was aimed at evaluating the influence of HRT on the activity of antioxidant enzymes (superoxide dismutase, SOD; catalase, CAT; and glutathione peroxidase, GPx) and lipid peroxidation (thiobarbituric acid reactive substances, TBARS) in menopausal women. METHODS: Blood antioxidant enzyme activities were determined in premenopausal (n=18) and in postmenopausal healthy women without (n=21) or with (n=19) HRT (mean ages: 47, 59, and 57 years, respectively). RESULTS: TBARS, CAT, and GPx activity were not significantly different among the groups of study. However, SOD activity was significantly lower in postmenopausal women without HRT (0.68+/-0.04 U/mg Hb) when compared both to premenopausal women (0.91+/-0.04 U/mg Hb) and to postmenopausal women with HRT (0.89+/-0.07 U/mg Hb). SOD activity was positively correlated to the duration of HRT in the postmenopausal groups (r=0.33, p<0.05). CONCLUSIONS: HRT antagonizes the decrease of SOD activity that occurs after menopause, suggesting that HRT may play a beneficial role in the protection against oxidative stress.