Paraquat and diquat interference in the analysis of creatinine by the Jaffé reaction

Price, Lee; Newman, Keith J.; Clague, Alan; Wilson, Peter R.; Wenck, Drew J.

doi:10.1080/00313029500169772

Cited by 16 publications

(5 citation statements)

References 6 publications

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“…We first excluded interference in the creatinine assays by non-creatinine chromogens since the creatinine assay is susceptible to interference by non-renal factors such as the concentration of paraquat in body fluids, and assay methods [ 28 ], co-administered drugs such as co-formulants of dexamethasone [ 18 ], and cephalosporin which may also interfere with creatinine concentrations [ 17 , 18 , 29 , 30 ]. The Jaffe serum creatinine assay cross-reacts with plasma paraquat concentrations greater than 10 mg/L, but marked increases were only seen at levels greater than 100 mg/L [ 16 , 29 ].…”

Section: Discussionmentioning

confidence: 99%

Mechanisms Underlying Early Rapid Increases in Creatinine in Paraquat Poisoning

et al. 2015

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BackgroundAcute kidney injury (AKI) is common after severe paraquat poisoning and usually heralds a fatal outcome. The rapid large increases in serum creatinine (Cr) exceed that which can be explained by creatinine kinetics based on loss of glomerular filtration rate (GFR).Methods and FindingsThis prospective multi-centre study compared the kinetics of two surrogate markers of GFR, serum creatinine and serum cystatin C (CysC), following paraquat poisoning to understand and assess renal functional loss after paraquat poisoning. Sixty-six acute paraquat poisoning patients admitted to medical units of five hospitals were included. Relative changes in creatinine and CysC were monitored in serial blood and urine samples, and influences of non-renal factors were also studied.ResultsForty-eight of 66 patients developed AKI (AKIN criteria), with 37 (56%) developing moderate to severe AKI (AKIN stage 2 or 3). The 37 patients showed rapid increases in creatinine of >100% within 24 hours, >200% within 48 hours and >300% by 72 hours and 17 of the 37 died. CysC concentration increased by 50% at 24 hours in the same 37 patients and then remained constant. The creatinine/CysC ratio increased 8 fold over 72 hours. There was a modest fall in urinary creatinine and serum/urine creatinine ratios and a moderate increase in urinary paraquat during first three days.ConclusionLoss of renal function contributes modestly to the large increases in creatinine following paraquat poisoning. The rapid rise in serum creatinine most probably represents increased production of creatine and creatinine to meet the energy demand following severe oxidative stress. Minor contributions include increased cyclisation of creatine to creatinine because of acidosis and competitive or non-competitive inhibition of creatinine secretion. Creatinine is not a good marker of renal functional loss after paraquat poisoning and renal injury should be evaluated using more specific biomarkers of renal injury.

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Section: Discussionmentioning

confidence: 99%

Mechanisms Underlying Early Rapid Increases in Creatinine in Paraquat Poisoning

et al. 2015

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“…It is important to highlight that DQ interfere with creatinine assays using the Jaffe method causing a false elevation, although this largely occurs at concentrations exceeding 100 mg L À1 , which is rarely observed and likely to be associated with severe clinical toxicity. 33…”

Section: Other Laboratorial Analysismentioning

confidence: 99%

Human and experimental toxicology of diquat poisoning: Toxicokinetics, mechanisms of toxicity, clinical features, and treatment

2018

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Diquat (1,1′-ethylene-2,2′-bipyridinium ion; DQ) is a nonselective quick-acting herbicide, which is used as contact and preharvest desiccant to control terrestrial and aquatic vegetation. Several cases of human poisoning were reported worldwide mainly due to intentional ingestion of the liquid formulations. Its toxic potential results from its ability to produce reactive oxygen and nitrogen species through redox cycling processes that can lead to oxidative stress and potentially cell death. Kidney is the main target organ due to DQ toxicokinetics and redox cycling. There is no antidote against DQ intoxications, and the efficacy of treatments currently applied is still unsatisfactory. The aim of this work was to review the most relevant human and experimental findings related to DQ, characterizing its chemistry, activity as herbicide, mechanisms of toxicity, consequences of poisoning, and potential therapeutic approaches taking into account previous experience in developing antidotes for paraquat, a more toxic bipyridinium herbicide.

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“…As an herbicide, PQ is often mixed in preparation with another bipyridyl herbicide diquat (DQ) (Price et al 1995). Similar to PQ, DQ's mechanism of action is the generation of high levels of O 2 .– through redox cycling.…”

Section: Role Of Ros Producing Toxicants and Pesticides In Pdmentioning

confidence: 99%

Mitochondrial mechanisms of redox cycling agents implicated in Parkinson’s disease

Lopert

Patel

2015

J Neural Transm

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Environmental agents have been implicated in Parkinson's disease (PD) based on epidemiological studies and the ability of toxicants to replicate features of PD. However, the precise mechanisms by which toxicants induce dopaminergic toxicity observed in the idiopathic form of PD remain to be fully understood. The roles of ROS and mitochondria are strongly suggested in the mechanisms by which these toxicants exert dopaminergic toxicity. There are marked differences and similarities shared by the toxicants in increasing steady-state levels of mitochondrial ROS. Furthermore, toxicants increase steady-state mitochondrial ROS levels by stimulating the production, inhibiting the antioxidant pathways of both. This review will focus on the role of mitochondria and ROS in PD associated with environmental exposures to redox-based toxicants.

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Paraquat and diquat interference in the analysis of creatinine by the Jaffé reaction

Cited by 16 publications

References 6 publications

Mechanisms Underlying Early Rapid Increases in Creatinine in Paraquat Poisoning

Mechanisms Underlying Early Rapid Increases in Creatinine in Paraquat Poisoning

Human and experimental toxicology of diquat poisoning: Toxicokinetics, mechanisms of toxicity, clinical features, and treatment

Mitochondrial mechanisms of redox cycling agents implicated in Parkinson’s disease

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