“…Similar results for signi cantly increased Co and Fe concentrations in the serum and RBCs of Co-exposed mice were obtained in our previous studies using lower daily dose of CoCl 2 [23].…”
Cobalt (Co) is an essential trace element and its cellular uptake occurs in a similar to iron (Fe) profile. The aim was to assess the alterations in iron and Fe regulatory proteins concentrations - transferrin receptor 1 (TfR1), hepcidin and ferritin, and their effect on erythrocyte count (RBCs) in mice following chronic exposure to cobalt chloride (CoCl2). Pregnant ICR mice were subjected to 125 mg/kg body weight CoCl2x6H2O daily 2–3 days prior delivery and treatment continued 90 days after birth. CoCl2 was administrated with drinking water. Pups were sacrificed on postnatal days 18, 30, 45, 60 and 90. Exposure to CoCl2 induced significant accumulation of Co ions in blood sera and RBCs. During long-term exposure the most Co was accumulated in the serum after 30 days of exposure and decreased by day 90 of dosing indicating that serum Co concentration is a reliable marker for recent exposure. Hemoglobin content increased in a time-dependent manner. Co administration significantly elevated serum Fe but decreased it in RBCs. Exposure to Co stimulated Fe storage, enhancing hepcidin production and ferritin concentrations, and reducing TfR1 expression. Chronic exposure to CoCl2 resulted in a lower Fe content of mature mice compared to immature suggesting stimulated Fe release as a possible survival mechanism to counteract the toxic effects of Fe overload.
“…Similar results for signi cantly increased Co and Fe concentrations in the serum and RBCs of Co-exposed mice were obtained in our previous studies using lower daily dose of CoCl 2 [23].…”
Cobalt (Co) is an essential trace element and its cellular uptake occurs in a similar to iron (Fe) profile. The aim was to assess the alterations in iron and Fe regulatory proteins concentrations - transferrin receptor 1 (TfR1), hepcidin and ferritin, and their effect on erythrocyte count (RBCs) in mice following chronic exposure to cobalt chloride (CoCl2). Pregnant ICR mice were subjected to 125 mg/kg body weight CoCl2x6H2O daily 2–3 days prior delivery and treatment continued 90 days after birth. CoCl2 was administrated with drinking water. Pups were sacrificed on postnatal days 18, 30, 45, 60 and 90. Exposure to CoCl2 induced significant accumulation of Co ions in blood sera and RBCs. During long-term exposure the most Co was accumulated in the serum after 30 days of exposure and decreased by day 90 of dosing indicating that serum Co concentration is a reliable marker for recent exposure. Hemoglobin content increased in a time-dependent manner. Co administration significantly elevated serum Fe but decreased it in RBCs. Exposure to Co stimulated Fe storage, enhancing hepcidin production and ferritin concentrations, and reducing TfR1 expression. Chronic exposure to CoCl2 resulted in a lower Fe content of mature mice compared to immature suggesting stimulated Fe release as a possible survival mechanism to counteract the toxic effects of Fe overload.
“…Notably, cobalt exposure resulted in a substantial increase in serum hepcidin levels only in the 18-day-old mice. These findings imply that cobalt exposure has the potential to influence the metabolism of copper, iron, manganese, and zinc [23].…”
Section: Influence Of Cobalt Exposure On Trace Element Distribution P...mentioning
Cobalt is a crucial trace element for the human body. It serves as an essentialcomponent of vitamin B12 and plays a pivotal role in the synthesis of amino acids andselect proteins within nerve cells, as well as in the synthesis of neurotransmitters vitalfor the proper functioning of the body. Both excess and deficiency of cobalt can havedetrimental effects on the human body. Notwithstanding the paramount significanceof cobalt as a trace element, comprehensive studies are necessary to evaluate its rolein physiological processes.
Keywords: cobalt, human health, trace element, vitamin B12, physiological processes
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