Acute copper intoxication after a Cu–Ca EDTA injection in rats

Giuliodori, Mauricio J.; Ramírez, Carlos E.; Ayala, M Ahumada

doi:10.1016/s0300-483x(97)00148-0

Cited by 7 publications

(8 citation statements)

References 12 publications

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“…Cu is an essential trace element required for normal function of proteins, which is bound to specific amino acid residues in an active site [249][250][251]. However, its accumulation causes hepatitis, cholestasis, cirrhosis and ultimately death [252][253][254]. On the other hand, zinc is an essential trace element with catalytic, structural and regulatory properties, involved in antioxidant, anti-inflammatory, and antiapoptotic processes [255][256][257].…”

Section: Anticholestatic Properties Of Eamentioning

confidence: 99%

Ellagic acid: Pharmacological activities and molecular mechanisms involved in liver protection

García-Niño

Zazueta

2015

Pharmacological Research

214

120

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Section: Anticholestatic Properties Of Eamentioning

confidence: 99%

Ellagic acid: Pharmacological activities and molecular mechanisms involved in liver protection

García-Niño

Zazueta

2015

Pharmacological Research

214

120

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“…On the dead animals liver function cannot be tested and cupraemia changes to values within normal range within few hours (Bohman et al 1984, Underwood & Suttle 1999 as happened in the calves evaluated (Table 2). In these fatal cases of ACP, liver Cu concentration has no value, because there is no longer Cu accumulation period in the liver as occurs in CCP (Humann-Ziehank et al 2001, Mendel et al 2007, when the high transference rate of Cu is the lethal factor (Giuliodori et al 1997). The liver Cu values found conϐirm this statement (Table 3).…”

Section: Discussionmentioning

confidence: 93%

“…In cases of acute Cu poisoning (ACP) this value is not useful since the cause of death is not the total amount of Cu in liver, but the high transference rate from the injection site to the organ (Radostits et al 2002, Fazzio et al 2004, Stöber et al 2005. Thus, liver concentration values do not increase so much as they do in CCP (Uzal 1992et al 1992, Giuliodori et al 1997, Fazzio et al 2004). The kidney is another organ to be analyzed in cases of suspected Cu poisoning (Uzal et al 1992, Giuliodori et al 1997, Roubies et al 2008, Mozaffari et al 2009 ).…”

Section: Introductionmentioning

confidence: 95%

“…Thus, liver concentration values do not increase so much as they do in CCP (Uzal 1992et al 1992, Giuliodori et al 1997, Fazzio et al 2004). The kidney is another organ to be analyzed in cases of suspected Cu poisoning (Uzal et al 1992, Giuliodori et al 1997, Roubies et al 2008, Mozaffari et al 2009 ). The transference rate is lower in the kidney when compared with the liver; additionally it is more efϐicient in the control of Cu deposition (Giuliodori et al1997, Roubies et al 2008.…”

Section: Introductionmentioning

confidence: 95%

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Renal cortex copper concentration in acute copper poisoning in calves

et al. 2012

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The aim of this study was to estimate the diagnostic value of renal cortex copper (Cu) concentration in clinical cases of acute copper poisoning (ACP). A total of 97 calves that died due to subcutaneous copper administration were compiled in eleven farms. At least, one necropsy was conducted on each farm and samples for complementary analysis were taken. The degree of autolysis in each necropsy was evaluated. The cases appeared on extensive grazing calf breeding and intensive feedlot farms, in calves of 60 to 200 kg body weight. Mortality varied from 0.86 to 6.96 %, on the farms studied. The first succumbed calf was found on the farms between 6 and 72 hours after the susbcutaneous Cu administration. As discrepancies regarding the reference value arose, the local value (19.9 parts per million) was used, confirming the diagnosis of acute copper poisoning in 93% of the analyzed kidney samples. These results confirm the value of analysis of the cortical kidney Cu concentration for the diagnosis of acute copper poisoning.

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“…Hematological data indicate a hemolytic toxicity determined by the reduction of hemoglobin concentration, hematocrit, and RBC which was pronounced at 48 h; these findings were confirmed by the development of hemoglobinuria. Additionally, previous investigations reported a severe hemolytic toxicity, tissue hemorrhage and necrosis from copper excess in sheep, rabbits, dogs, and rats [38][39][40][41][42]. The rise in MCHC concentration at 24 h was considered without clinical relevance.…”

Section: Discussionmentioning

confidence: 99%

Pharmacokinetics and hematotoxicity of a novel copper‐based anticancer agent: Casiopeina III‐Ea, after a single intravenous dose in rats

Vértiz¹,

García-Ortuño²,

Bernal

et al. 2012

Fundamemntal Clinical Pharma

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Casiopeina III-Ea is a mixed chelate copper (II) complex that has shown cytotoxic and antitumor activity in vitro and in vivo. The aim of this study was to investigate the pharmacokinetics of total copper derived from casiopeina III-Ea administered by intravenous bolus injection to Wistar rats. Other objective was to evaluate the hematotoxicity produced by this compound in those animals. Wistar rats received a single intravenous dose of 4 mg/kg of casiopeina III-Ea. Blood samples were taken and pharmacokinetics evaluated. Furthermore, erythrocyte copper levels were determined to identify a potential target and Zn levels were analyzed to determine a possible change. For the evaluation of hematotoxicity, both blood and urine samples were collected for hematological and biochemical analyses; moreover, Fe determination was performed. Blood copper and zinc levels, red blood cell copper levels as well as copper, zinc, and iron amounts excreted into urine were analyzed by ICP-MS. The blood concentration-time profile of copper derived from casiopeina III-Ea was fitted to a two-compartment model with a zero-order input. Cumulative amounts of Cu, Zn, and Fe excreted into rat urine after administration of casiopeina III-Ea were different with respect to control. Hematological and biochemical data indicated a hemolytic toxicity. Pharmacokinetic analysis of total copper derived from casiopeina III-Ea provided a general knowledge about distribution and elimination process of this compound. Additionally, the systemic exposure of the copper derived from casiopeina III-Ea accounts for the hematotoxicity of this complex at test dose.

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Acute copper intoxication after a Cu–Ca EDTA injection in rats

Cited by 7 publications

References 12 publications

Ellagic acid: Pharmacological activities and molecular mechanisms involved in liver protection

Ellagic acid: Pharmacological activities and molecular mechanisms involved in liver protection

Renal cortex copper concentration in acute copper poisoning in calves

Pharmacokinetics and hematotoxicity of a novel copper‐based anticancer agent: Casiopeina III‐Ea, after a single intravenous dose in rats

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