Induction of Micronuclei in Mice Bone Marrow Cells by Cobalt and Copper Chlorides

Rasgele, Pınar Göç; Kekeçoğlu, Meral; Gökalp, Fulya Dilek

doi:10.2478/aep-2013-0007

Cited by 4 publications

(3 citation statements)

References 48 publications

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“…However, at the same time, toxicokinetic experiments demonstrated systemic exposure. By contrast, a recent paper by Rasgele et al (2013) reported significant induction of MN in bone marrow of mice treated intraperitoneally with cobalt chloride. Mice were sacrificed 24 and 48 h after injection and there were statistically significant increases in MN frequency at the top two doses of cobalt chloride at 24 h, and at all three doses (but not dose-related) at 48 h. There was no evidence of bone marrow toxicity (based on PCE:NCE ratio) at any dose level, although the ratio in control animals was higher than usually experienced.…”

Section: In Vivo Studiesmentioning

confidence: 61%

New investigations into the genotoxicity of cobalt compounds and their impact on overall assessment of genotoxic risk

Kirkland¹,

Brock

Haddouk³

et al. 2015

Regulatory Toxicology and Pharmacology

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The genotoxicity of cobalt metal and cobalt compounds has been widely studied. Several publications show induction of chromosomal aberrations, micronuclei or DNA damage in mammalian cells in vitro in the absence of S9. Mixed results were seen in gene mutation studies in bacteria and mammalian cells in vitro, and in chromosomal aberration or micronucleus assays in vivo. To resolve these inconsistencies, new studies were performed with soluble and poorly soluble cobalt compounds according to OECD-recommended protocols. Induction of chromosomal damage was confirmed in vitro, but data suggest this may be due to oxidative stress. No biologically significant mutagenic responses were obtained in bacteria, Tk(+/-) or Hprt mutation tests. Negative results were also obtained for chromosomal aberrations (in bone marrow and spermatogonia) and micronuclei at maximum tolerated doses in vivo. Poorly soluble cobalt compounds do not appear to be genotoxic. Soluble compounds do induce some DNA and chromosomal damage in vitro, probably due to reactive oxygen. The absence of chromosome damage in robust GLP studies in vivo suggests that effective protective processes are sufficient to prevent oxidative DNA damage in whole mammals. Overall, there is no evidence of genetic toxicity with relevance for humans of cobalt substances and cobalt metal.

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Section: In Vivo Studiesmentioning

confidence: 61%

New investigations into the genotoxicity of cobalt compounds and their impact on overall assessment of genotoxic risk

Kirkland¹,

Brock

Haddouk³

et al. 2015

Regulatory Toxicology and Pharmacology

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show abstract

“…Co, an indispensable ferromagnetic transition metal, plays a vital role in supporting mammalian well-being [17], that plays an important role in the vitamin B12 synthesis [14]. Co is frequently used as a dietary supplement, preservative, in beverages, cosmetics, and medical equipment as well as a medicinal agent to treat various disorders [18]. The main sources of Co include meat, vegetables, and drinking water.…”

Section: Introductionmentioning

confidence: 99%

Acute Toxicity of Aluminum, Cobalt, and Lithium Chlorides in Albino wistar Mice: Determination of Lethal Doses

Taha,

Mohammed,

Mohammed

2024

IJDNE

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Chlorides are considered one of the dangerous pollutants that pose a threat to human and animal health. The study aims to determine the acute lethal doses (LD50) of aluminum, cobalt, and lithium chlorides in Albino wistar mice. Albino wistar mice were divided into four groups with the mice were randomly divided into 4 groups, 8 mice for experimental group and 6 mice for control group. Short tests were conducted to determine the acute lethal dose of the metals under study. Over 168 hours, mice were exposed to four different concentrations of (AlCl2) metal in concentrations of 40, 50, 60 and 70 mg/kg per liter of water, where 1 liter of water was placed in each bottle, while the second group was exposed to cobalt chloride (CoCl2) in concentrations 75, 100, 125 and 150 mg/kg per liter of water, where 1 liter of water was placed in each bottle. As well as, the third group, it was exposed to (LiCl2) at concentrations 75, 100, 125 and 150 mg/kg per liter of water, while the fourth group included the control group. 1 liter of water was placed in each bottle and it was given orally. LC50 was calculated by use Finney's probit analysis method where LC50 it is abbreviation "lethal concentration 50%" or "intermediate lethal concentration". It is the concentration of a material (in the water) which it killed a half the members of populations after a specific during of exposed to toxic metal. This value is so importance in toxicology because it gives an indicated of materials poisoning. The LC50 is inverse proportionate to toxicity. The current study concluded the dose that killed 50% of the Albino wistar mice was 50mg/kg of AlCl2, 100mg/kg of CoCl2, while it was 125mg/kg of lithium chloride. Long-term use of greater doses of chlorides can have varying degrees of negative impact on various organs in mice. This study provides context for a more thorough investigation of the toxicity of chlorides compounds on humans, which may be significant for public health.

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“…Due to its advantages, including a high melting point and resistance to oxidation, it is widely used to produce different types of alloys and steel (Lison, 2007). Co 2+ compounds are now considerably involved in the petroleum and plastic industries, rechargeable battery manufacturing, and also nanoproduction of carbon tubes (Lison et al, 2001;Goc Rasgele, 2013). Anthropogenic activities, such as agricultural fertilizers, mining activities, and smelting, in addition to natural sources of this element, might provide unexpected amounts of Co 2+ in our environment and pose a threat to animal and human health (Domingo, 1989;Hamilton, 1994).…”

Section: Introductionmentioning

confidence: 99%

Cobalt induces alterations in serum parameters associated with bone metabolism in male adult rat

Moshtaghie¹,

Malekpouri²,

Moshtaghie³

et al. 2014

Turk J Biol

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The intention of this study was to investigate the toxic effect of cobalt on the bone metabolism of rats, including calcium, inorganic phosphorus, and bone-specific alkaline phosphatase of serum during short-and long-term experiments. Rats were injected intraperitoneally (IP) with either 16 mg kg -1 BW of cobalt for 5 and 10 days or 6 mg kg -1 BW for 20 and 40 days. It was found that IP administrations of cobalt could increase all serum parameters associated with bone metabolic processes. The observed effect was greatest for 16 mg kg -1 BW when used for 10 continuous days. By using gel filtration chromatography, we found that most of the activity of total serum alkaline phosphatase was related to low molecular weight isoenzymes, which can be used as a biomarker for bone metabolic disturbances. These results suggest that cobalt can induce bone resorption in adult rats and, therefore, behave as an osteoporotic agent.

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Induction of Micronuclei in Mice Bone Marrow Cells by Cobalt and Copper Chlorides

Cited by 4 publications

References 48 publications

New investigations into the genotoxicity of cobalt compounds and their impact on overall assessment of genotoxic risk

New investigations into the genotoxicity of cobalt compounds and their impact on overall assessment of genotoxic risk

Acute Toxicity of Aluminum, Cobalt, and Lithium Chlorides in Albino wistar Mice: Determination of Lethal Doses

Cobalt induces alterations in serum parameters associated with bone metabolism in male adult rat

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