Environmental pollutants as thyroid disruptors


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Environmental pollutants as thyroid disruptors

  1. 1. Environmental pollutants as Thyroid Disruptors  Importance of Thyroid Harmones Thyroid hormones are essential for:  Normal brain development in fetus.  For the control of metabolism,  For normal adult physiology. 
  2. 2. What Happens in the presence of Endocrine Disruptors? Environmental pollutants Interfere with the normal functioning of thyroid hormone and produce hazaderous effects on:  development  metabolism  adult physiology  Disturbed Thyroid Harmone signalling pathways. 
  3. 3. How Pollutants act? Structural Similarity with THs: Several Thyroid Disruptors have high degree of structural resemblance to the thyroxine (T4) and triiodothyronine (T3) due to which they get attach to receptor sites instead of THs.  Interference with regulation:  Many industrial chemicals and pollutants can interfere with thyroid function by acting on different points of regulation of thyroid hormone synthesis, release, transport through the blood, metabolism of thyroid hormone.  
  4. 4. Major Thyroid Disruptors And Their Effects Perchlorate It block uptake of Iodide in thyroid cells.As a result T3 and T4 synthesis decreased.Higher in smoker Women.  PCBs  These are lipophilic in nature and accumulate in fatty tissues.PCBs inhibit TSH receptors and decrease production of T3 and T4. It reduce T4 circulation in blood.  Acetochlor(Herbicide)  It enhance hepatic(liver) metabolism results in increase metabolism of T3 and T4 unneccesarily  
  5. 5.     Pentachlorophenol T4 transport to target tissues via serum transport proteins e.g Transthyretin(TTR) but if pentachlorophenol competitively binds to serum transport proteins then T4 would not be transported to target tissue. Bisphenol A(BPA) At high temprature BPA leach out of plastics into food.
  6. 6. In Human embryonic kidney cell and hepatoblastoma cells BPA inhibit T3 binding to TR .  Isoflavones,  especially those found in soy protein (e.g., genistein, coumesterol) cause goiter in Human infants. 
  7. 7. Abnormalities due to Thyroid Disruptors Neurodevelopmental toxicity  Goiter and thyroid diseases are associated with TH disruption.  Hypothyroidism  It results in impaired intellectual development in childrens or permanent cognitive deficiencies. 
  8. 8. Perchlorates as Thyroid Disruptors Perchlorate is a known competitive inhibitor of the sodium-iodide in humans and can inhibit iodide uptake, leading to the suppression of T3 and T4.  Effects  It has been related to lower levels of iodine in breast milk.As a result of iodine deficiency neurodevelopmental disorders occur in utero. 
  9. 9.  In an environment with perchlorate exposure may have a significant effect on thyroid hormone production particularly in the environment of dietary iodine insufficiency
  10. 10. PCBs as Thyroid Disruptors     The concept that PCBs can exert a neurotoxic effect on the developing brain by causing a state of relative hypothyroidism. Polychlorinated biphenyls belong to the class of organochlorine compounds classified as persistent organohalogenated pollutants (POPs) Disruption Mechanisms: (1)It reducing the ability of thyroid hormones to bind to transport proteins in the bloodstream
  11. 11. (2)It enhance hepatic metabolism by up-regulating the sulfotransferases that break down thyroid hormones in the liver  (3)It inhibit the production of deiodinases that allow T4 to be converted to T3  (4)it act as either an agonist or antagonist at the site of the cellular thyroid receptor. 
  12. 12. Environmental chemicals impacting the thyroid hormone receptor PCBs  BPA(4,4 isopropylidenediphenol)  PBDEs (polybrominated diphenylethers) 
  13. 13. Thyroid Cancer  The role of TSH in activating growth and differentiation of follicular cells have shown that a prolonged disruption of the pituitary-thyroid axis is linked to thyroid neoplasia. Two mechanisms involved in the disruption of the pituitary thyroid axis are chemically-induced blocking of thyroid peroxidase and inhibition of T4 deiodinases, which are known to occur with TD exposure