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Free radicals and Graves' disease: the effects of therapy
Insights
Graves' disease shows altered oxidative stress markers, with reduced plasma thiols and superoxide dismutase, and increased intracellular lysate thiols. Antithyroid drug therapy modifies these levels, suggesting a role for free radicals.
Area of Science:
- Endocrinology
- Biochemistry
- Oxidative Stress Research
Background:
- Graves' disease (GD) is an autoimmune disorder affecting the thyroid gland.
- Oxidative stress plays a role in various physiological and pathological processes.
- Red-cell membrane oxidative stress markers require further investigation in GD.
Purpose of the Study:
- To investigate plasma thiol (PSH), caeruloplasmin (CP), intracellular lysate thiol (LSH), and superoxide dismutase (SOD) activity in newly diagnosed Graves' disease patients.
- To compare these markers between GD patients and control subjects.
- To assess the impact of antithyroid treatments (carbimazole, propylthiouracil, 131I) on these oxidative stress parameters.
Main Methods:
- Measurement of PSH, CP, LSH, and SOD activity in 30 newly diagnosed GD patients and control subjects.
- Statistical analysis to compare marker levels between groups and assess treatment effects.
Main Results:
- Significantly reduced PSH and SOD levels in GD patients compared to controls.
- Significantly elevated LSH levels in GD patients compared to controls.
- Carbimazole treatment increased LSH and SOD; propylthiouracil increased LSH; 131I treatment showed no significant change.
Conclusions:
- Graves' disease is associated with increased oxidative stress and altered radical scavenging activity across the red-cell membrane.
- These changes may stem from increased free-radical activity.
- Antithyroid drug therapy influences these oxidative stress markers, though the exact mechanism requires further elucidation.
Abstract:
Plasma thiol (PSH), caeruloplasmin (CP), intracellular lysate thiol (LSH) and superoxide dismutase (SOD) activity were measured in 30 patients with newly diagnosed Graves' disease (GD). Compared to control subjects (C) PSH and SOD were significantly reduced (C vs GD, 507 vs 449 mumol/l, P less than 0.01; 2.1 vs 1.6 mumol/l, P less than 0.01 respectively) and LSH was significantly raised (C vs GD 181 vs 298 mumol/l). Treatment with carbimazole produced a significant rise in LSH and SOD. Propylthiouracil (PTU) treatment raised LSH levels but 131I treatment produced no significant change. All four parameters are involved in different ways in oxygen metabolism and together provide an indication of oxidative stress across the red-cell membrane. In addition LSH is a general radical scavenger and SOD a specific O2- scavenger. In Graves' disease the increased oxidative stress and increased general radical scavenging may result from raised free-radical activity. These changes, which have not previously been reported in Graves' patients, were modified by antithyroid drug therapy, but it is not clear whether this is a direct or indirect effect.