Changes in ceruloplasmin activity and lactate concentration in patients at high risk of acute organ system failure

doi:10.1016/0009-8981(91)90108-O

Clinica Chimica Acta

Volume 199, Issue 2, 14 June 1991, Pages 167-172

https://doi.org/10.1016/0009-8981(91)90108-O Get rights and content

Abstract

In 241 critically ill patients at a high risk of acute organ system failure (OSF) the activity of ceruloplasmin (CPL) and the concentration of lactate in blood was measured. In patients with acute OSF the lactate concentration is high, and the CPL activity is lower in comparison with patients without OSF. These changes are particularly distinct in nonsurviving patients with OSF. The results are discussed in connection with the development of a tissue oxygen debt and the decrease of antioxidative capacity of blood.

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Cited by (5)

Acidic pH promotes oxidation-induced dissociation of C-reactive protein
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Citation Excerpt :
However, it has been reported that general hydrogen peroxide could not generate mCRP (Singh et al., 2017). Notably, serum ceruloplasmin is a main risk factor in many diseases, such as cardiovascular risk and cancer (Tang et al., 2012; Aguilar Cordero et al., 2011; Yarets et al., 2009; Gocmen et al., 2008; Tungtrongchitr et al., 2002; Manttari et al., 1994; Reunanen et al., 1992; Knekt et al., 1992; Dauberschmidt et al., 1991; Rosenfeld et al., 1986), and deposits at inflammatory loci (Stadler et al., 2004), similar to CRP (Genest, 2010; Ridker et al., 2004; Ridker, 2016; Habersberger et al., 2010; Wald and Bestwick, 2010; Cohen and Singh, 2005; Ridker et al., 2002; Allin et al., 2010; Wu et al., 2015; Khreiss et al., 2004). In addition, the deposited ceruloplasmin could release copper in the presence of hydrogen peroxide (Kim et al., 2000).
Circulating levels of the systemic inflammation marker C-reactive protein (CRP) have been associated with increased risk and poor outcomes of many diseases, such as cardiovascular events and cancer. Accumulating evidence has indicated that the conformational rearrangement of human pentameric CRP (pCRP) to monomeric CRP (mCRP) is a prerequisite for participation in the pathogenesis. Therefore, determining the mechanism of the dissociation of pCRP into pro-inflammatory mCRP under physiological/pathological circumstances has been intriguing.
The effects of oxidative and acidic stress occurring in inflammation on pCRP were examined by electrophoresis, electron microscopy, protein fluorescence, neoepitope expression and endothelial cell responses.
Reactive oxygen species (ROS) generated by the copper-hydrogen peroxide system could rapidly induce the dissociation of CRP at mild acidic pH within four hours, but not at physiological pH of 7.4. Meanwhile, mannitol, a ROS scavenger, could not protect against dissociation, which implied that local ROS from accessible histidine residues may be crucially beneficial to the formation of mCRP in a redox-balanced microenvironment. Furthermore, mCRP generated by ROS could be reduced by DTT, which indicated the exposure of functional motif aa35-47, and showed potent proinflammatory actions on endothelial cells, comparable to mCRP generated by urea.
dissociation of pCRP to mCRP could be rapidly induced by ROS from copper- hydrogen peroxide system in dependence on mildly acidic stress regardless of a redox-balanced microenvironment.
Physiological responses to endotoxin in copper deficient rats
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Copper deficient rats show high mortality after a normally sublethal dose of endotoxin. To begin examining the mechanisms, this study examined copper deficiency effects on certain responses to endotoxin. Weanling rats were fed 0.2 or 8 ppm copper for 5 weeks; endotoxin was given at 10 mg/kg, ip. Copper deficiency was confirmed by low activities of ceruloplasmin, and liver and serum superoxide dismutase. Compared to adequate rats, deficients showed the following responses to endotoxin: elevated serum transaminase activities (an indication of liver injury), prolonged hyperglycemia, slightly enhanced liver glycogen depletion, high resistance to hepatic lysosomel enzyme leakage, normal degree of rapid onset hypotension, no microvascular injury based on albumin clearance, slightly higher acute phase response based on serum zinc, and normal increase of tumor necrosis factor at typical time of peak accumulation. Thus, endotoxin-induced mortality in copper deficient rats may derive, at least in part, from a selective liver injury, but not from excessive serum glucose or liver glycogen depletion, impaired acute phase response, aggravated short term hypotension, exaggerated tumor necrosis factor release, fragile lysosomes or excessive microvascular injury.
Engineering Therapeutics to Detoxify Hemoglobin, Heme, and Iron
2023, Annual Review of Biomedical Engineering
Serum micronutrient levels in critically ill patients receiving continuous renal replacement therapy: A prospective, observational study
2022, Journal of Parenteral and Enteral Nutrition
Ceruloplasmin and hypoferremia: Studies in burn and non-burn trauma patients
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View full text

Changes in ceruloplasmin activity and lactate concentration in patients at high risk of acute organ system failure

Abstract

J Biol Chem

Chest

Multiple-organ-failure

Arch Surg

Prognosis in acute organ-system failure

Ann Surg

Basic mechanisms of lung injury

Pulm Dis Rev

Posttraumatic complications and inflammatory mediators

Arch Surg

Ist der Organfehler im hypovolämisch-traumatischen Schock die Folge eines Reperfusionssyndroms oder auch anderer Mediatoren? Anaesthesist

Tissue oxygen debt as a determinant of lethal and non-lethal postoperative organ failure

Crit Care Med

Oxygen radicals, neutrophils, and acute tissue injury

Fate of oxygen free radicals in extracellular fluids

Biochem Soc Transact

Absorption, transport, and hepatic metabolism of copper and zinc: Special reference to metallothionein and ceruloplasmin

Physiol Rev