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The impact of chronic untreated hyperglycaemia on the long-term stability of paraoxonase 1 (PON1) and antioxidant status in human sera
  1. Muiruri Macharia1,
  2. Andre P Kengne2,
  3. Diane M Blackhurst3,
  4. Rajiv T Erasmus1,
  5. Tandi E Matsha4
  1. 1Division of Chemical Pathology, Faculty of Health Sciences, National Health Laboratory Service (NHLS) and University of Stellenbosch, Cape Town, South Africa
  2. 2NCRP for Cardiovascular and Metabolic Diseases, South African Medical Research Council & University of Cape Town, Cape Town, South Africa
  3. 3Lipid Laboratory, Department of Clinical Laboratory Sciences, University of Cape Town, Cape Town, South Africa
  4. 4Department of Biomedical Sciences, Faculty of Health and Wellness Science, Cape Peninsula University of Technology, Cape Town, South Africa
  1. Correspondence to Professor Tandi E Matsha, Department of Biomedical Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, PO Box 1906, Bellville, Cape Town 7530, South Africa; matshat{at}


Aims Paraoxonase 1 (PON1) is increasingly measured on samples that have been stored for extended durations. The impact of storage and baseline conditions on the stability of the enzyme is however not well documented. We investigated the influence of hyperglycaemia on the stability of PON1 activity and antioxidant status in human sera stored for 12 months.

Methods Blood was collected from 60 individuals aged 35–80 years with chronic hyperglycaemia (HbA1c≥6.5%) or normoglycaemia (HbA1c<6.5%) in Cape Town. At baseline and after 12 months at −80°C, levels of PON1 activity (paraoxoase and arylesterase), antioxidant activity (ferric reducing antioxidant power (FRAP) and Trolox equivalent antioxidant capacity (TEAC)) and lipid peroxidation (malondialdehyde and oxidised low density lipoprotein (ox-LDL)) were measured and compared.

Results In normoglycaemic samples, 12-month storage led to minor alterations of <10% for the six target variables. In hyperglycaemic samples, alterations ranged from 13% for AREase activity to about 23% for ox-LDLs indicating a twofold to fourfold difference between the two groups in the variables assessed. Changes in levels of FRAP, TEAC and ox-LDL were both statistically and clinically significant. Furthermore, there was evidence of significant statistical interaction by baseline glycaemic status on the alteration of FRAP, TEAC, thiobarbituric acid reactive substances and ox-LDL, but not for PON1 activity.

Conclusions The results indicate that baseline glycaemic status may contribute to a decline in the stability of antioxidant activity and extent of lipid peroxidation but not PON activity.

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