Elevated T3 as marker for heavy metal toxicity

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elevated T3 as a marker for heavy metal toxicity.

high numbers of ASD kids' thyroid panels showing high T3 and really wacked

out T3/T4 ratios

high numbers of kids with T3 toxicosis

Thyrotoxicity of the chlorides of cadmium and mercury in rabbit.

Ghosh N, Bhattacharya S.

Department of Zoology, Visva-Bharati University, Santiniketan, India.

Exposure to heavy metals such as cadmium and mercury is of immediate

environmental concern. The present study was aimed at establishing a direct

relationship between heavy metal poisoning and thyroid dysfunction. Cadmium

and mercury treatment at LD50 levels resulted in severe thyrotoxicosis in

the rabbit. Within 24 h of intramuscular administration of cadmium chloride

15 mg.kg-1 body weight (bw) and mercury chloride 20 mg.kg-1 bw, thyroid

peroxidase activity increased significantly over the control with a

concomitant rise in the triiodothyronine (T3) titre. On the other hand,

there was a remarkable fall in the thyroxine (T4) level, and the T3/T4

ratio was high as compared with the control. Evidence indicates that acute

heavy metal lethality will induce immediate hyperthyroidism. It is

suggested that T3-toxicosis may be produced by a preferential synthesis of

T3 and/or preferential deiodination of T4 to T3. Measurement of T3 and T4

levels may thus be utilized as a reliable indicator of heavy metal lethality.

In utero methylmercury exposure differentially affects the activities of

selenoenzymes in the fetal mouse brain.

Watanabe C, Yoshida K, Kasanuma Y, Kun Y, Satoh H.

Department of Environmental Health Sciences, Tohoku University Graduate

School of Medicine, Seiryo-machi, Sendai, 980-8575, Japan.

chiho@...

Pregnant ICR mice were subcutaneously injected with 0,5, or 3x3 mg Hg/kg of

methylmercury (MeHg) on days 12,13, and 14(G12-14) of gestation and were

sacrificed on G17. Activity of selenoenzymes, including glutathione

peroxidase (GPx) and 5'- or 5-iodothyronine deiodinases (5'-DI, 5-DI), was

determined in fetal brain and placenta. MeHg did not affect the

concentration of Se in these tissues, while it significantly inhibited the

activity of GPx in the fetal brain and placenta, but not in the maternal

brain. Although the levels of thyroid hormones in the maternal and fetal

plasma were not affected by MeHg, 5-DI decreased and 5'-DI increased in the

fetal brain, as if they had responded to hypothyroidism. Because the level

of T4 in the fetal plasma was not affected by MeHg, these changes in

enzymatic activities may result in a harmful excess of T3 in the fetal

brain. In addition, 5-DI activity was increased in the placenta of

MeHg-treated mice. These effects of prenatal MeHg exposure on fetal and

placental DIs differed from those of dietary-induced Se deficiency, where

the activities of DIs were decreased or not affected. Further evaluation of

the effect of MeHg on selenoenzymes, especially 5-DIs, is warranted.

Copyright 1999 Academic Press.

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