Evaluation of Leukocyte DNA Damage and Antioxidant Defense in Graves' Disease; Effect of Medical Treatment

Background: Oxidative stress has been implicated in many pathological conditions, including hyperthyroidism. In this study, our aim was to investigate the effect of medical treatment on oxidative/antioxidative status and subsequent DNA damage in Graves’ disease, in terms of reduced glutathione (GSH) levels, superoxide dismutase (SOD), glutathione peroxidase (GPx) activity and DNA strand breaks.

Methods: Fifty female patients suffering from Graves’ disease and thirty-seven healthy female controls were recruited in the study. Blood samples were taken from the patients before and after treatment. Free T3, free T4 and thyroid stimulating hormone (TSH) levels were determined using chemiluminescent particle assay, GSH, SOD and GPx activity using photometric techniques, and comet assay was utilized to analyze strand breaks with formamidopyrimidine DNA glycosylase (FPG) sensitive sites.

Results: Free T3, free T4, GPx activity, DNA strand breaks and FPG sensitive sites were significantly higher, and TSH and GSH levels were significantly lower in patients prior to treatment compared to healthy controls. Following treatment, the levels of free T3, free T4 and TSH were restored to those of healthy controls, but the rise in GSH levels and the drop in GPx activity, strand breaks and FPG sensitive sites were not as profound, though still significantly different than pre treatment levels.

Conclusions: The markers of oxidative stress and DNA damage are not restored as quickly as thyroid function tests in Graves’ disease following treatment, suggesting the oxidative damage caused by hyperthyroidism may have long term effects.