To the Editor:
The article by Kaur et al.Citation1 presents an interesting new finding and their approach is very encouraging. The authors showed that patients with Graves’ ophthalmopathy, as defined in the study, had an oxidative stress profile as well as antioxidant capacity directly related to thyroid status. A normalization of thyroid hormone levels has led to reduced oxidative stress and the concomitant, parallel, re-establishment of blood antioxidant activity.Citation1 However, they state that “…activity of Superoxide Dismutase (SOD), Catalase (CAT), Glutathione reductase (GSHR), Glutathione peroxidise (GPx) showed decrease which could be attributed to altered metabolism and already prevalent deficiency of essential micronutrients like zinc, copper, mercury, and selenium in the Indian population.”Citation1 As physicians treating mercury-induced thyroid disorders,Citation2,Citation3 we would like to point out that mercury is a nonessential element in humans.Citation4,Citation5 Furthermore, there is evidence that inorganic and organic mercury may be a remarkable source of oxidative stress.Citation6 Also, exposure to mercury may cause thyroid dysfunction and may alter serum thyroid hormone levels,Citation7–10 both in humans and animals.
Declaration of interest: The authors declared no conflict of interest.
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