Metallothionein-I/II Knockout Mice Aggravate Mitochondrial Superoxide Production and Peroxiredoxin 3 Expression in Thyroid after Excessive Iodide Exposure

In light of previous works documented on iodide induced oxidative stress and thyrotoxicity, we have demonstrated the time-course and concentration-response effects of early acute high concentrations of iodide exposure on mitochondrial superoxide generation

Na Zhang; Lingyan Wang; Qi Duan; Laixiang Lin; Mohamed Ahmed; Tingting Wang; Xiaomei Yao


Scholarcy highlights

  • Iodine is a fundamental constituent of thyroid hormones and has stimulatory effects on hydrogen peroxide generation, which is involved in oxidative stress . 150 μg iodine is the daily requirement for thyroid hormone synthesis
  • Following 10−4 M, 10−3 M, and 10−2 M of KI or 10−3 M H2O2 exposure, we showed a significant increase in mitochondrial superoxide production with increased MitoSOX Red fluorescence intensity) and an increase in Lactate Dehydrogenase release) with a decrease in relative cell viability) in the thyroid cell suspensions of both MT-I/II Metallothionein I/II knockout and WT mice groups
  • Compared to WT mice group, a more significant increase of mitochondrial superoxide production, increase in LDH release, and decrease in a relative cell viability can be detected in MT-I/II KO mice group, 1(c), and 1(a))
  • The Peroxiredoxin 3 protein expressions were significantly increased in 10−2 M KI or 10−3 M H2O2 exposure group in both MT-I/II KO and WT mice groups
  • Prx 3 can be the target for up to 90% of hydrogen peroxide generated in the matrix
  • The present study provides evidence that high concentrations of iodide may lead to a significant increase in mitochondrial superoxide production and Prx 3 expression in both in vitro and in vivo studies

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