Serum paraoxonase-1 activity and genetic polymorphisms: common errors in measurement and interpretation of results

Abstract

Paraoxonase-1 (PON1) is an esterase and lipolactonase which degrades lipid peroxides and participates in an organism’s antioxidant system (1). Alterations in circulating PON1 levels have been reported in a variety of diseases involving oxidative stress, such as cardiovascular disease, Alzheimer’s disease, chronic renal failure, HIV infection, metabolic syndrome, and chronic liver impairment (2, 3). Increased knowledge of the pathophysiological significance of PON1 and the involvement in human pathology are of critical importance. Thus, research of this enzyme has recently grown exponentially. Unfortunately, however, the increased popularity of PON1 among biomedical researchers has often led to a decrease in the methodological rigour of the studies being performed. This letter is intended to highlight some errors that are becoming common in manuscripts submitted to, and published by, biomedical journals. Our goal is to help researchers improve the accuracy and validity of their results and conclusions. 1. Serum PON1 activity is strongly determined by the enzyme genotype. Several polymorphisms in the promoter and the coding regions of the PON1 gene have been described, of which PON1192, PON155, PON1–108, PON1–909 and PON1–1741 are the most significantly associated with changes in enzyme activity (4, 5). In case-control studies to evaluate enzyme activity, it is imperative that cases and controls are matched for genotype. If not matched, it would not be possible to ascertain whether the observed changes are due to disease or to coincidental differences in allelic frequencies between cases and controls. This is especially true when sample sizes are small. It is also common for authors to state that the PON1 gene contains two common polymor-