Percholate is an inorganic compound that is known for its thyrotoxicant nature as it affects the thyrod gland adversely by competitively inhibiting the uptake of iodide. A study conducted by tranet al. (2008) concluded that perchlorate is actively transported into the FRTL-5 cells (thyroid cells) by a thyroid stimulating hormone dependent process. The amount of percholate that is taken up is directly proportional to the amount of concentration of percholate in the medium and it gets saturated at higher concentration and the uptake is then blocked by iodide in a dose dependent manner. The transportation of percholate is mediated by sodium/iodide symporter (NIS) and some other factors may also contribute to the same (Tran et al., 2008). Percholate is associated with inhibition of iodide uptake and thereby inhibition of production of thyroid hormone and this fact was further supported by Gold et al. (2012). They concluded that if a dose of 0.5mg/kg/day of percholate was consumed, then the inhibition of iodide uptake was seen and the production of TSH was reduced. The study concluded that if the consumed levels of percholate were below the threshold dose, it did not result in adverse thyroid health (Gold et al., 2012). Many other research based evidence suggests that the exposure of expecting mother to percholate in form of contaminated drinking water or food, often results in adverse effects in the neonates. There has been evidence in the increased levels of TSH of such new borns. As long as the mothers take adequate intake of iodide, the effect of percholate is suppressed (Amitai et al., 2007).
Inanother research, in order to confirm the effect of percholate on the production of thyroid hormone, the genetic mechanism was studied. It was found that increased dosage of percholate affected the genes- NIS, tg and tPO. Further, percholate exerted its action by causing significant loss in the body weight and also lead to hypertrophy of the thyroid gland as well. This caused a decrease in the level of FT3, FT4 and a significant increase in the level of TSH (Thyroid stimulating hormone). The expression of the two genes- thyroglobulin (tg) and thyroperoxidase (TPO) were downregulated and reduced such that it directly affected the production of thyroid hormone (Wu, F. et al., 2010).
Therefore, since higher dosage of percholate is concerned with the decreased production thyroid hormone, the women, during the gestation period and the children during infancy, should avoid exposure to this inorganic compound as it may become a common cause for congenital hypothyroidism and may affect the learning capability of the neonates and the young children.
Amitai, Y, et al. (2007). Gestational exposure to high perchlorate concentrations in drinking water and neonatal thyroxine levels. Thyroid, 17(9): 843-50.
Clewell, R., Merrill, E., Narayanan, L. and Gearhart, J. (2004). Evidence for Competitive Inhibition of Iodide Uptake by Perchlorate and Translocation of Perchlorate into the Thyroid. International Journal of Toxicology, 23:17-23.
Gold, E. et al. (2012). Thyroid hormones and thyroid disease in relation to perchlorate dose and residence near a superfund site. Journal of Exposure and Environmental Epidemiology, 2012:1-10.
Steinmas, C., Miller, M. and Smith, A. (2010). Perchlorate in Drinking Water During Pregnancy and Neonatal +Thyroid Hormone Levels in California. JOEM, 52(12).
Tran, N. et al. (2008). Thyroid-stimulating hormone increases active transport of perchlorate into thyroid cells. Am J PhysiolEndocrinol Metab., 294:E802-E806.
Wu, F., Zhou, X., Zhang, R., Pan, M. and Peng, K. (2010). The Effects of Ammonium Perchlorate on Thyroid Homeostasis and Thyroid-Specific Gene Expression in Rat. Wiley periodicals, Inc.
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