Acute iodine ingestion increases intrathyroidal glutathione
| Autor: | Elsie M. Allen |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
medicine.medical_specialty
Antioxidant Endocrinology Diabetes and Metabolism medicine.medical_treatment Thyroid Gland chemistry.chemical_element Iodine medicine.disease_cause Lipid peroxidation chemistry.chemical_compound Endocrinology Internal medicine medicine Ingestion Animals Rats Inbred BB Sulfhydryl Compounds Rats Wistar Staining and Labeling Chemistry Thyroid Thyroiditis Autoimmune Glutathione Phenylmercury Compounds Rats medicine.anatomical_structure Liver Dietary Iodine Lipid Peroxidation Oxidative stress |
| Zdroj: | Journal of endocrinological investigation. 16(4) |
| ISSN: | 0391-4097 |
| Popis: | In genetically predisposed individuals, autoimmune lymphocytic thyroiditis (LT) is potentiated by excess dietary iodine (I). There have been data which suggest that oxidative stress may have a role in iodine-induced LT. These in vivo studies were undertaken to examine the effect of iodine on intrathyroidal levels of the potent antioxidant glutathione (GSH) and see if the thyroids of LT-prone BB/Wor rats have aberrant GSH responses after iodine-loading. LT-prone BB/Wor, non LT-prone BB/Wor and Wistar rats were randomized to receive either 0.05% I (as Nal) or tap water. Thyroid and liver homogenates were assayed individually for GSH. Following the administration of 0.05% iodine water overnight, all of the animals demonstrated a rise in intrathyroidal GSH regardless of LT-proneness. To determine whether this was a dose-dependent response, Wis rats were randomized to receive tap, 0.0125%, 0.025%, 0.05%, or 0.075% I, overnight. Intrathyroidal GSH levels rose with increasing iodine concentrations peaking at 0.025% I. Hepatic GSH levels were unaltered by iodine treatment. Ten days of 0.05% I water did not result in any difference between the GSH levels of thyroids from treated and control rats. Frozen sections of the thyroids and livers from iodine-treated rats were compared to tap-water controls after staining with Mercury Orange for GSH and Schiffs reagent for evidence of lipid peroxidation. Iodine-treated thyroids had an apparent shift of GSH staining from the apical border to the cytoplasm. However, there was no Schiffs staining indicative of lipid peroxidation in the iodine-treated thyroids. These results show that acute iodine loads increase intrathyroidal GSH and LT-prone rats do not have an inherent deficit in this response. Therefore, we conclude that there is no role for oxidative damage in iodine-induced LT. We propose that GSH has a role in intrathyroidal iodine metabolism and thyroid hormone synthesis. |
| Databáze: | OpenAIRE |
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