Cobalt(II)-Induced Changes in Hemoglobin Content and Iron Concentration in Mice from Different Age Groups

Gluhcheva, Yordanka; Madzharova, M.; Zhorova, Rumyana; Atanasov, Vasil; Ivanova, Juliana; Mitewa, M.

doi:10.5504/50yrtimb.2011.0023

Cited by 5 publications

(3 citation statements)

References 5 publications

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“…On day-2, cells were treated with 1,25(OH) 2 D 3 in the presence or absence of cobalt (II) chloride (CoCl 2 ). CoCl 2 is a chelate interfering Fe 2+ on hemoglobin [15]. It can initiate oxygen-sensing signal transduction pathway and upregulates erythropoietin and HIFα expression [16,17].…”

Section: Methodsmentioning

confidence: 99%

1,25(OH)2D3 suppresses COX-2 up-regulation and thromboxane production in placental trophoblast cells in response to hypoxic stimulation

Sun

Zhong

et al. 2014

Placenta

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In this study, we determined if vitamin D could inhibit oxidative stress-induced thromboxane production by placental trophoblasts. Trophoblast isolated from normal placentas were stimulated with CoCl2, a hypoxic mimicking agent, with or without pretreatment of 1,25(OH)2D3. Soluble phospholipase-A2, metabolites of thromboxane-A2 and prostacyclin, and 8-isoprostane were measured. Expression of cyclooxygenase-1 (COX-1), COX-2, and heme oxygenase-1 (HO-1) were determined. We found that pretreatment of trophoblasts with 1,25(OH)2D3 significantly reduced 8-isoprostane and the ratio of thromboxane-A2 to prostacyclin production, and blocked COX-2 expression induced by CoCl2. These results provide evidence of the beneficial effects of vitamin D on placental trophoblasts.

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Section: Methodsmentioning

confidence: 99%

1,25(OH)2D3 suppresses COX-2 up-regulation and thromboxane production in placental trophoblast cells in response to hypoxic stimulation

Sun

Zhong

et al. 2014

Placenta

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“…The highest Co(II) content was measured in day 18 mice exposed to CoCl 2 treatment. Accumulation of cobalt(II) in blood plasma induced hemoglobin changes, thus affecting hematopoieis [12]. Chronic treatment with cobalt(II) compounds also induced significant accumulation of the metal ions in the spleen, liver and kidneys of the exposed mice.…”

Section: Resultsmentioning

confidence: 97%

Chronic exposure to cobalt compounds — an in vivo study

Gluhcheva¹,

Atanasov

Ivanova

et al. 2014

Open Life Sciences

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An in vivo experimental model for testing the effects of long-term chronic treatment with cobalt(II) compounds — cobalt chloride (CoCl2) and cobalt-EDTA (Co-EDTA) on mice at different stages of development was optimized. Pregnant mice and their progeny were treated with daily doses of 75 or 125 mg kg−1 body weight until postnatal day 90. The compounds were dissolved in regular tap water. Mice were sacrificed on days 18, 25, 30, 45, 60 and 90 after birth, which correspond to different stages of their development. Altered organ weight indices (calculated as a ratio of organ weight to body weight) of spleen, liver and kidneys, were found depending on the type of compound used, dose, duration of treatment, and the age of the animals. The results also showed significant accumulation of cobalt ions in blood plasma, spleen, liver and kidneys of the exposed mice. More Co(II) was measured in the organs of the immature mice (day 18, 25 and 30 pnd) indicating that they were more sensitive to treatment.

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“…The effect of increased blood concentrations of Co has been demonstrated in several species, including laboratory animals (Gluhcheva et al, 2011), dogs (Fisher, 1959) and humans (Lippi et al, 2006). The consensus from these crossspecies studies is that chronic blood concentrations in excess of 300 μg/l are required to achieve both haematological and toxicological effects (Finley et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of cobalt as a performance enhancing drug (PED) in racehorses

McKeever

Malinowski

Fenger

et al. 2020

CEP

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Cobalt is a required trace element in animals, but administration in excess is considered dangerous and potentially performance enhancing in equine athletes. This study seeks to determine if cobalt may actually act as a performance enhancing drug (PED) by altering biochemical parameters related to red blood cell production as well as markers of aerobic and anaerobic exercise performance. In addition, for adequate regulation of naturally occurring substances, such as cobalt, its distribution among the population must be defined. In order to identify this distribution, plasma Cobalt was determined from 245 Standardbred horses with no cobalt supplementation from farms in New York and New Jersey, including horses at the Rutgers University Equine Science Center. Samples were analysed by Inductively Coupled Plasma Mass Spectrometry. Seven healthy, race fit Standardbreds (4 geldings, 3 mares, age: 5±3 years, ~500 kg) were used for the PED experiment. An incremental graded exercise test (GXT) to measure maximal aerobic capacity (V̇O2max) and markers of performance, measurement of plasma volume and blood volume as well as the measurement of lactate, erythropoietin (EPO), and various blood haematological factors were determined 7 days prior to cobalt administration. Each horse was administered a sterile solution of cobalt salts (50 mg of elemental Co as CoCl2 in 10 ml of saline, IV) at 9 AM on three consecutive days via the jugular vein. Blood samples were obtained from the contralateral jugular vein before and at 1, 2, 4 and 24 h after administration. Plasma and blood volume were measured one day after the last dose of cobalt, and a post administration GXT was performed the next day. Horses were observed for signs of adverse effects of the cobalt administration (agitation, sweating, increased respiration, etc.). Plasma cobalt concentration increased from a pre-administration mean of 1.6±0.6 to 369±28 μg/l following 3 doses of the cobalt solution (P<0.05). This Co concentration was unaccompanied by changes in aerobic or anaerobic performance, plasma EPO concentration, plasma volume, resting blood volume, total blood volume, or estimated red blood cell volume (P>0.05). There were no observed adverse effects.

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Cobalt(II)-Induced Changes in Hemoglobin Content and Iron Concentration in Mice from Different Age Groups

Abstract: Cobalt (Co)

Cited by 5 publications

References 5 publications

1,25(OH)2D3 suppresses COX-2 up-regulation and thromboxane production in placental trophoblast cells in response to hypoxic stimulation

1,25(OH)2D3 suppresses COX-2 up-regulation and thromboxane production in placental trophoblast cells in response to hypoxic stimulation

Chronic exposure to cobalt compounds — an in vivo study

Evaluation of cobalt as a performance enhancing drug (PED) in racehorses

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