Models of Fetal Iodine Deficiency

Escobar, Gabriel la Morreale de; Oña, Carmen Ruiz de; Obregón, Marı́a Jesús; Rey, Francisco Escobar del

doi:10.1007/978-1-4613-0765-5_17

Cited by 19 publications

(20 citation statements)

References 32 publications

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“…To prevent contamination with small amounts of T4 and T3, the LID we used previously (30-32) does not contain any component of animal origin. It is nutritionally inadequate even when supplemented with KI, as evidenced by poorer growth of the pups born from mothers that have been fed this diet for months, as compared to the growth of pups born from mothers on the standard breeding diet (34). To avoid this possible confounding factor in this study, each kilogram of the basic LID diet (6 kg corn flour, 2.5 kg wheat gluten, 1 kg brewer's yeast, 0.15 kg NaCl, and 0.15 kg CaCO 3 ) was fortified with 18 g of the macro-and 0.25 g of the micro-mineral mixtures, and 1 g of the vitamin mixture described by Bieri et al (35), KI excluded, and with 10 g of L -lysine, 1.9 g of L -trytophane, 2.2 g of L -methione, 3.4 g of L -threonine, and 2 g of L -choline, which are all deficient in the wheat gluten used as major protein source.…”

Section: Methodsmentioning

confidence: 99%

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Martinez-Galán¹,

Pedraza²,

Santacana³

et al. 1997

J. Clin. Invest.

103

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The most severe brain damage associated with thyroid dysfunction during development is observed in neurological cretins from areas with marked iodine deficiency. The damage is irreversible by birth and related to maternal hypothyroxinemia before mid gestation. However, direct evidence of this etiopathogenic mechanism is lacking. Rats were fed diets with a very low iodine content (LID), or LID supplemented with KI. Other rats were fed the breeding diet with a normal iodine content plus a goitrogen, methimazole (

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Section: Methodsmentioning

confidence: 99%

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Martinez-Galán¹,

Pedraza²,

Santacana³

et al. 1997

J. Clin. Invest.

103

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“…We used 2-ml Alzet osmotic minipumps (Alza Corp., Palo Alto, CA), implanted under the dorsal skin (16 (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30),000 cpm per pump), prepared as described further on, were added to the T4 or T3 solutions, respectively. The radioactivity of the pumps was determined before implanting them, and at the end of the experiment.…”

Section: Methodsmentioning

confidence: 99%

“…The nuclear receptor for T3 is also found in human and rat brain early in pregnancy (7,9). The adverse effects of maternal hypothyroxinemia on the central nervous system (CNS) might be related to the thyroid hormone deficiency ofthe developing embryo (5,8,(10)(11)(12). In neurologic endemic cretinism the degree ofthe developmental disorders has been correlated to with that of maternal hypothyroxinemia (1 3).…”

Section: Introductionmentioning

confidence: 99%

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Congenital hypothyroidism, as studied in rats. Crucial role of maternal thyroxine but not of 3,5,3'-triiodothyronine in the protection of the fetal brain.

Calvo¹,

Obregón²,

Oña³

et al. 1990

J. Clin. Invest.

294

143

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To study the protective effects of maternal thyroxine (T4) and 3,5,3'-triiodothyronine (T3) in congenital hypothyroidism, we gave pregnant rats methimazole (MMI), an antithyroid drug that crosses the placenta, and infused them with three different doses of T4 or T3. The concentrations of both T4 and T3 were determined in maternal and fetal plasma and tissues (obtained near term) by specific RIAs. Several thyroid hormone-dependent biological end-points were also measured. MMI treatment resulted in marked fetal T4 and T3 deficiency. Infusion of T4 into the mothers increased both these pools in a dose-dependent fashion. There was a preferential increase of T3 in the fetal brain. Thus, with a T4 dose maintaining maternal euthyroidism, fetal brain T3 reached normal values, although fetal plasma T4 was 40% of normal and plasma TSH was high. The infusion of T3 into the mothers increased the total fetal extrathyroidal T3 pool in a dose-dependent fashion. The fetal T4 pools were not increased, however, and this deprived the fetal brain (and possibly the pituitary) of local generation of T3 from T4. As a consequence, fetal brain T3 deficiency was not mitigated even when dams were infused with a toxic dose of T3. The results show that (a) there is a preferential protection of the brain of the hypothyroid fetus from T3 deficiency; (b) maternal T4, but not T3, plays a crucial role in this protection, and (c) any condition which lowers maternal T4 (including treatment with T3) is potentially harmful for the brain of a hypothyroid fetus. Recent confirmation of transplacental passage of T4 in women at term suggests that present results are relevant for human fetuses with impairment of thyroid function. Finding signs of hypothyroidism at birth does not necessarily mean that the brain was unprotected in utero, provided maternal T4 is normal. It is crucial to realize that maintainance of maternal "euthyroidism" is not sufficient, as despite hypothyroxinemia, the mothers may be clinically euthyroid if their T3 levels are normal. (J. Clin. Invest. 1990. 86:889-899.)

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“…Infants and children with iodine deficiency are at risk of poor mental and psychomotor development. [79] Vitamin E may interact with selenium additively because of their similar antioxidant roles.There is evidence to suggest that deficiency in Vitamin E may be associated with neurological functions in children and adults. [80,81] Although nutrients do not vary to the same extent in seafood as MeHg, it is important to control for fish intake in the study design and the statistical analysis.…”

Section: Cardiovascular Outcomesmentioning

confidence: 99%

Methylmercury exposure and health effects in humans

Choi¹,

Grandjean

2008

Environ. Chem.

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Environmental context. Dietary intake of fish and other seafood products is the dominant source of human exposure to methylmercury, a toxicant that can have serious adverse effects on the developing nervous system and may promote heart diseases. The existing evidence of human toxicity should inspire prudent choices in maintaining fish intakes to secure an ample supply of essential nutrients, while at the same time choosing species that are low in mercury concentrations. The combination of essential nutrients and avoidance of this toxic contaminant will benefit brain development and human health in general. In addition, current contamination levels suggest that intensified efforts are needed to reduce and eliminate mercury release to the environment.Abstract. Methylmercury (MeHg) is a worldwide contaminant found in seafood and freshwater fish, which constitute the dominant source of human exposure to this substance. The developing human brain is particularly susceptible to injury caused by MeHg, which easily passes the placental barrier. Epidemiological studies in fishing populations have found subtle though lasting adverse effects on brain functions of children who were exposed prenatally to MeHg from seafood diets. This contaminant also seems capable of promoting the development of heart disease. Fish and seafood also contain important nutrients, such as omega-3 fatty acids that may provide beneficial effects, thereby possibly counteracting or obscuring the adverse effects of MeHg. This article reviews the existing evidence on MeHg developmental neurotoxicity and the emerging evidence that MeHg may promote the development of heart diseases. MeHg risks may have been underestimated in the past, in part because of the confounding effects of nutrients from seafood and fish. Improved control of mercury release to the environment is indicated. In addition, regulatory agencies should provide better guidance to consumers in maintaining a balanced diet that includes seafood as low as possible in mercury.

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Models of Fetal Iodine Deficiency

Cited by 19 publications

References 32 publications

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

Congenital hypothyroidism, as studied in rats. Crucial role of maternal thyroxine but not of 3,5,3'-triiodothyronine in the protection of the fetal brain.

Methylmercury exposure and health effects in humans

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