Perin Vural1, Cemil Akgül, Mukaddes Canbaz. 1. Department of Biochemistry and Clinical Biochemistry, Istanbul Medical Facility, Capa 34093, Istanbul, Turkey. pervinvural@yahoo.com [corrected]
Abstract
BACKGROUND: Oxidative stress has been implicated in the pathogenesis of ageing and menopause, and can arise through the increased production of lipid peroxides and/or a deficiency of antioxidant defence. AIM: To investigate the effects of the menopause and tibolone treatment (2.5 mg/day for six months) on plasma antioxidants and lipid peroxidation. METHODS: Plasma concentrations of ascorbic acid, alpha-tocopherol, total thiol groups, caeruloplasmin, erythrocyte glutathione (GSH) and malondialdehyde (MDA) were measured in 24 postmenopausal and 24 premenopausal healthy women. RESULTS: Data analysis indicates a significant decrease in plasma ascorbic acid, alpha-tocopherol, total thiol groups, [corrected]erythrocyte GSH and a significant increase in lipid peroxides (expressed as MDA concentrations) in postmenopausal women. There was no significant difference between control and study groups in the mean plasma caeruloplasmin concentrations. It was found that there is a significant increase in alpha-tocopherol and significant decrease in lipid peroxide concentrations in postmenopausal after tibolone treatment. CONCLUSIONS: The menopause is associated with an increase in oxidative stress and a decrease of some antioxidants, such as ascorbic acid, alpha-tocopherol, total thiols and erythrocyte GSH. Tibolone treatment leads to a decrease in concentrations of plasma lipid peroxide, probably by stimulating direct and indirect mechanisms of tocopherol regeneration and increasing plasma concentrations of vitamin E. However, due to the relatively small numbers involved this study can be regarded as a pilot. Further studies performed on a larger scale are necessary to establish the exact mechanisms of tibolone in inhibiting oxidative stress in postmenopausal women.
BACKGROUND: Oxidative stress has been implicated in the pathogenesis of ageing and menopause, and can arise through the increased production of lipid peroxides and/or a deficiency of antioxidant defence. AIM: To investigate the effects of the menopause and tibolone treatment (2.5 mg/day for six months) on plasma antioxidants and lipid peroxidation. METHODS: Plasma concentrations of ascorbic acid, alpha-tocopherol, total thiol groups, caeruloplasmin, erythrocyte glutathione (GSH) and malondialdehyde (MDA) were measured in 24 postmenopausal and 24 premenopausal healthy women. RESULTS: Data analysis indicates a significant decrease in plasma ascorbic acid, alpha-tocopherol, total thiol groups, [corrected]erythrocyte GSH and a significant increase in lipid peroxides (expressed as MDA concentrations) in postmenopausal women. There was no significant difference between control and study groups in the mean plasma caeruloplasmin concentrations. It was found that there is a significant increase in alpha-tocopherol and significant decrease in lipid peroxide concentrations in postmenopausal after tibolone treatment. CONCLUSIONS: The menopause is associated with an increase in oxidative stress and a decrease of some antioxidants, such as ascorbic acid, alpha-tocopherol, total thiols and erythrocyte GSH. Tibolone treatment leads to a decrease in concentrations of plasma lipid peroxide, probably by stimulating direct and indirect mechanisms of tocopherol regeneration and increasing plasma concentrations of vitamin E. However, due to the relatively small numbers involved this study can be regarded as a pilot. Further studies performed on a larger scale are necessary to establish the exact mechanisms of tibolone in inhibiting oxidative stress in postmenopausal women.
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