Changes in Antioxidative Mechanisms in Elderly Patients with Non-Insulin- Dependent Diabetes mellitus

• Published in: Gerontology (Basel) Vol. 47; no. 3; pp. 150 - 157
• Main Authors: Yanagawa, Kiyotaka, Takeda, Hiroshi, Egashira, Toru, Matsumiya, Teruhiko, Shibuya, Takeshi, Takasaki, Masaru
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.05.2001
• Subjects: Clinical Section; Aging; Alpha-tocopherol; Non-insulin-dependent diabetes mellitus; Elderly patients; Free radical
• ISSN: 0304-324X; 1423-0003
• DOI: 10.1159/000052789

Background: Recently, it has been suggested that the onset and aggravation of diabetes are closely related to free radicals. Also, vitamin E is a lipophilic free radical scavenger that is localized mainly in biomembranes. Objective: The purpose of this study was to clarify the defensive mechanisms against oxidative stress by investigating the differences in the redox dynamics of α-tocopherol in plasma and erythrocyte membranes between elderly patients with non-insulin-dependent diabetes mellitus (NIDDM) and healthy elderly subjects. Methods: Total, α-, β-, γ- and δ-tocopherol and α-tocopherolquinone concentrations were determined by high-performance liquid chromatography with a redox detection mode using a series of four coulometric working electrodes. Results: The α-tocopherolquinone/α-tocopherol ratio in plasma and erythrocyte membranes was not different between the two groups. Both the α-tocopherol concentrations in erythrocyte membranes and ratio of α-tocopherol in erythrocyte membranes to α- tocopherol in plasma was significantly lower in elderly NIDDM patients than in healthy subjects. Conclusion: These findings suggest that α-tocopherol is used normally in both plasma and erythrocyte membranes and α-tocopherol uptake in erythrocyte membranes is significantly decreased in elderly NIDDM patients. The functional disorder of the antioxidative activity of α-tocopherol in erythrocyte membranes due to impairment of this transfer mechanism may be associated with the pathogenesis of NIDDM.