Effects of manganese ions on thyroid function in rat

Buthieau, Anne Marie; Autissier, N

doi:10.1007/bf01239208

Cited by 18 publications

(12 citation statements)

References 9 publications

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“…Therefore, this theory remains to be proved. Buthieau and Autissier (1983) reported recently that the TSH level was lowered in the Mn injected rat, suggesting that Mn may depress the pituitary and thyroidal functions. If this evidence could be extended to mouse, the reduction in cell height with retained colloid due to the prolonged oral administration of Mn might be attributed to the reduced blood TSH level.…”

Section: Discussionmentioning

confidence: 96%

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Manganese ion as a goitrogen in the female mouse.

et al. 1985

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Section: Discussionmentioning

confidence: 96%

“…(Buthieau and Autissier, 1983) and monkey (Suzuki et al, 1975 The dose schedule and the method of sample preparation are described in the text.54Mn activity was expressed as the ratio of cpm/mg of each organ to that of the liver. Each value represents the mean of two determinations for each sex.…”

mentioning

confidence: 99%

Manganese ion as a goitrogen in the female mouse.

et al. 1985

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“…We also observed Mn 2+ accumulation in other organs of the head and neck region, which are not shielded by the bloodbrain barrier, such as the pituitary, thyroid and other endocrine glands. Although the specific function of Mn 2+ in these glands is not fully elucidated, it seems to be involved in important processes such as protection against oxidative injury (26,27) and post-translational modifications of components in the secretory pathway, such as those involved in thyroid hormone production (28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of manganese uptake and toxicity in mouse brain during continuous MnCl₂ administration using osmotic pumps

Sepúlveda

Dresselaers

Vangheluwe

et al. 2012

Contrast Media & Molecular

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Manganese is a vital element and cofactor of many key enzymes, but it is toxic at high levels, causing pronounced disturbances in the mammalian brain. Magnetic resonance imaging (MRI) studies using manganese ions as a paramagnetic contrast agent are often limited by the neurotoxicity of Mn(2+) . In this work, we have explored a new in vivo model to study Mn(2+) uptake, distribution and neurotoxicity in mice by subcutaneous implantation of mini-osmotic pumps delivering MnCl(2) continuously for 21 days. Fractionated injections can reduce the toxicity; however, constant administration at very low doses using osmotic pumps caused a substantial effect on the T(1) contrast in MRI while reducing toxicity. Manganese-enhanced MRI documented fast but reversible Mn(2+) deposition largely in glomerular and mitral cell layers of the olfactory bulb, in the CA3 area of the hippocampus, and in the gray matter of the cerebellum. Mn(2+) accumulated as early as the first days after implantation, with a fast dispersal 9 days after stopping a 12-days Mn(2+) exposure. Prominent Mn(2+) accumulation was also seen in salivary glands and in the endocrine thyroid and posterior pituitary gland. These structures with enhanced Mn(2+) accumulation correlated well with those showing high expression of the secretory pathway Ca(2+) /Mn(2+) -ATPase (SPCA1), i.e. a transporter that could take part in Mn(2+) detoxification. Our new experimental model for continuous low-dosage administration of Mn(2+) is an easy alternative for enhancing Mn(2+) -based contrast in MEMRI studies, and might provide insight into the etiology of neuropathologies resulting from chronic Mn(2+) exposure in vivo.

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“…Levels of plasma manganese were elevated in individuals with goiter in another study (49). In rodents, administration of manganese was reported to reduce serum levels of thyroxine or induce goiter (42,50,51). Thus, there is precedent for our discovery of manganese-induced thyroid defects in Slc30a10 knockout mice.…”

Section: Zip14 Depletion Rescues Hypothyroidism In Slc30a10 Knockoutsmentioning

confidence: 97%

Hypothyroidism induced by loss of the manganese efflux transporter SLC30A10 may be explained by reduced thyroxine production

Liu

Hutchens

Jursa

et al. 2017

Journal of Biological Chemistry

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SLC30A10 and SLC39A14 are manganese efflux and influx transporters, respectively. Loss-of-function mutations in genes encoding either transporter induce hereditary manganese toxicity. Patients have elevated manganese in the blood and brain and develop neurotoxicity. Liver manganese is increased in patients lacking SLC30A10 but not SLC39A14. These organ-specific changes in manganese were recently recapitulated in knockout mice. Surprisingly, knockouts also had elevated thyroid manganese and developed hypothyroidism. To determine the mechanisms of manganese-induced hypothyroidism and understand how SLC30A10 and SLC39A14 cooperatively mediate manganese detoxification, here we produced single and double knockout mice and compared their phenotypes with that of single knockouts. Compared with wild-type controls, single and double knockouts had higher manganese levels in the blood and brain but not in the liver. In contrast, single knockouts had elevated manganese levels in the liver as well as in the blood and brain. Furthermore, SLC30A10 and SLC39A14 localized to the canalicular and basolateral domains of polarized hepatic cells, respectively. Thus, transport activities of both SLC39A14 and SLC30A10 are required for hepatic manganese excretion. Compared with single knockouts, single and double knockouts had lower thyroid manganese levels and normal thyroid function. Moreover, intrathyroid thyroxine levels of single knockouts were lower than those of controls. Thus, the hypothyroidism phenotype of single knockouts is induced by elevated thyroid manganese, which blocks thyroxine production. These findings provide new insights into the mechanisms of manganese detoxification and manganese-induced thyroid dysfunction.

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Effects of manganese ions on thyroid function in rat

Cited by 18 publications

References 9 publications

Manganese ion as a goitrogen in the female mouse.

Manganese ion as a goitrogen in the female mouse.

Evaluation of manganese uptake and toxicity in mouse brain during continuous MnCl₂ administration using osmotic pumps

Hypothyroidism induced by loss of the manganese efflux transporter SLC30A10 may be explained by reduced thyroxine production

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Effects of manganese ions on thyroid function in rat

Cited by 18 publications

References 9 publications

Manganese ion as a goitrogen in the female mouse.

Manganese ion as a goitrogen in the female mouse.

Evaluation of manganese uptake and toxicity in mouse brain during continuous MnCl2 administration using osmotic pumps

Hypothyroidism induced by loss of the manganese efflux transporter SLC30A10 may be explained by reduced thyroxine production

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Evaluation of manganese uptake and toxicity in mouse brain during continuous MnCl₂ administration using osmotic pumps