Cobalt (Co) is an essential trace element and its cellular uptake follows a similar pattern to that of iron (Fe).Our aim was to study the effects of perinatal cobalt chloride (CoCl 2 ) exposure on iron homeostasis through changes in the expression of iron regulatorty proteins -transferrin receptor 1 (TfR1), divalent metal transporter 1 (DMT-1) and hepcidin (Hepc) in the liver of 30-day old mice.Pregnant mice and their progeny were treated with daily doses of 75 mg/kg b.w.(low dose) or 125 mg/kg b. w. (high dose) CoCl 2 until postnatal day 30.The results show that prenatal and early postnatal exposure to CoCl 2 exerts a toxic effect on the liver, reducing the organ weight index and altering the expression profile of the proteins involved in iron metabolism regulation.Weaker expression of TfR1 and DMT-1 was observed in the samples of mice exposed to the low dose CoCl 2 .
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Ilovska et al. (2025) studied this question.
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