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At least 613 records · Page 34Linked to original sources
PubMed2002

Antioxidant status in thyroid dysfunction.

Our study was designed to test and compare the levels of enzymatic antioxidants (ARS), endogenous peroxides (POX), non-enzymatic antioxidants (Antiox-cap) and anti-oxidized low-density lipoprotein (LDL) antibody titers (oLAb) in hyperthyroid and hypothyroid patients. We measured POX, ARS, Antiox-cap and oLAb in the plasma from 68 patients (34 patients with hyperthyroidism, thyroid-stimulating hormone (TSH) <0.04; and 34 patients with hypothyroidism, TSH >4.0) and 34 healthy euthyroid controls. POX were highest in hyperthyroid patients, but differences between hyperthyroid and hypothyroid patients and controls were not significant. ARS were significantly higher in patients compared to controls. Antiox-cap were significantly lower in patients compared to controls. oLAb were significantly higher in hypothyroid patients compared to controls and hyperthyroid patients. Our study shows that both hyperthyroidism and hypothyroidism are associated with enhanced oxidative stress involving enzymatic and non-enzymatic antioxidants. Higher POX in hyperthyroid patients might reflect the hypermetabolic state of these patients. oLAb, indicating progression of atherosclerosis, were highest in hypothyroid patients.

Adult↗
PubMed1977

Effects of thyroid dysfunction on the development of the rat cerebellum, with special reference to cell death within the internal granular layer.

The increased cell death within the internal granular layer of the cerebellar cortex, previously demonstrated by other investigators in 12-day-old rats treated with propylthiouracil, was found again in 10-, 14- and 21-day-old similarly treated young rats. In thyroid-deficient as well as in normal animals, cell death was maximal at 10 days. In hypothyroid rats, the greatest difference with the normal animals was at 14 days, when there was an increase by a factor of 20 of the number of dying cells. On day 13, the ratio of free to total N-acetyl-beta-D-glucosaminidase activities was also increased by 34%. Cell death predominantly occurred in the lower part of the internal granular layer at 10 days, in the middle part at 14 days and the upper part at 21 days. The increase in thickness of the molecular layer, which reflects the development of the Purkinje cell dendritic arborizations, was also more retarded than the acquisition of a normal ratio of granule cells to Purkinje cells. Administration of a daily dose of 0.10 mug thyroxine to thyroid-deficient animals was sufficient (and a lower dose insufficient) to return to normal the number of dying cells as well as the development of the molecular layer and the evolution of the ratio of granule cells to Purkinje cells. A daily dose of T4 as low as 0.20 or 0.25 mug already induced a marked hyperthyroid state resulting in a decrease in granule cells formation without increased cell death. Indeed, an increased cell death seemed to occur only when the normal synchronism between the development of the Purkinje cell arborizations and the laying down of granule cells was suppressed, as is the case in thyroid deficiency but not in neonatal hyperthyroidism.

Acetylglucosaminidase↗
PubMed1991

Carbaryl-induced thyroid dysfunction in the freshwater catfish Clarias batrachus.

Freshwater female catfish, Clarias batrachus, were exposed to sublethal concentrations of carbaryl (12 mg/liter for 96 hr and 5 mg/liter for 16 days) during the prespawning and spawning phases of their annual reproductive cycle. The effects on the levels of thyroxine (T4) and triiodothyronine (T3), the T3/T4 ratio, and the extrathyroidal conversion of T4 to T3 were studied in serum, pharyngeal thyroid, and anterior and posterior kidney. Carbaryl exposure for 96 hr suppressed T4 but elevated T3 and the T3/T4 ratio in serum during both phases of experimentation. However, 16 days exposure caused a decline in T4 as well as in T3 and in the T3/T4 ratio. In the pharyngeal thyroid, carbaryl increased T4 as well as peroxidase activity and decreased T3 and the T3/T4 ratio. Its treatment for 96 hr did not elicit any change in the parameters studied in the anterior kidney, whereas in the posterior kidney it suppressed the levels of T4 and T3, peroxidase activity, and the T3/T4 ratio. However, carbaryl exposure for 16 days provoked increases in T4 and peroxidase activity but decreases in T3 and the T3/T4 ratio in anterior kidney. In posterior kidney, it did not change T4 and peroxidase activity, but decreased T3 and the T3/T4 ratio. It also stimulated extrathyroidal conversion of T4 to T3.

Animals↗
PubMed2006

[Specific follow-up for pregnant patients with a thyroid dysfunction].

Association between thyroidian disease and pregnancy is a frequent event. Thyroidian hormones are mandatory for foetal development especially at the level of brain structures. Any shortage of thyroidian hormone can severely and irreversibly alter neurological development. On the other hand it is also clear that an excess of thyroidian hormone can jeopardize the embryo then the foetus. In case of maternal hyperthyroidism, strict guidelines relying mainly on foetal thyroid monitoring echographic scanning will allow in most cases the delivery of a healthy euthyroid newborn. Hypothyroidia, providing an adequate substitution, has no significant impact on pregnancy. Biological monitoring is the key of monitoring. Iodine deficiency is a matter of concern when considering neurodevelopmental outcome, however it is still an unsolved issue in France. A multidisciplinary team will sometimes be necessary for taking care of pregnant patients with active Graves' disease.

Adult↗
PubMed1997

Selenium-induced thyroid dysfunction.

Administration of the anti-oxidative trace element selenium is currently being evaluated for its benefits in patients with inflammatory diseases. However, little is known about the risks of selenium. We report on a patient in whom, along with standard therapy, administration of large intravenous doses of selenite for sepsis secondary to pneumonia resulted in development of marked hypothyroidism. In addition, severe iodine deficiency was noted, and supplementation with iodine led to normalisation of thyroid function.

Aged↗