Invited critical review
Malondialdehyde as biomarker of oxidative damage to lipids caused by smoking

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Abstract

Thiobarbituric acid reactive substances (TBARS) and malondialdehyde (MDA) have been used as biomarkers of lipid oxidation for more than thirty years. The validity of these biomarkers has been rightfully criticized for a lack of specificity and problems with post sampling formation. Numerous assays have been published for their analysis giving rise to reference intervals for healthy non‐smoking humans varying more than to orders of magnitude. In spite of these problems, these biomarkers remain among the most commonly reported indices of oxidative damage and the present review focuses on the problems associated with MDA/TBARS analysis, their potential as biomarkers of oxidative stress and the effect of smoking on MDA status.

Section snippets

Oxidants, oxidation and cellular targets

As originally defined by Sies [1], oxidative stress is an imbalance between oxidants and antioxidants on a cellular or individual level. Oxidative damage is one result of such an imbalance and includes oxidative modification of cellular macromolecules, induction of cell death by apoptosis or necrosis, as well as structural tissue damage. The present review is going to focus on one particular source of oxidative stress (smoking) and one particular biomarker of oxidative damage (malondialdehyde,

Biomarker criteria

Halliwell and Poulsen recently published a set of 8 criteria describing the ideal biomarker of oxidative stress including both an established relationship to disease and various practical considerations on stability and cost of analysis [4].

Although several criteria are without doubt required to adequately describe a biomarker, the entire basis of the biomarker phenomenon is the measurement of a compound that directly reflects certain biological events related to the pathogenesis of a disease

Measurement of malondialdehyde

One highly important criterion to be fulfilled by a potential biomarker is that it should produce identical results when a given sample is analyzed in different laboratories [4]. For MDA, this criterion remains a major challenge due to an almost unlimited number of assay variations in use worldwide the diversity of which by itself prevents a general acceptance of MDA as valid biomarker of oxidative damage to lipids. MDA has been quantified since the sixties and the original principles of

Oxidative stress and smoking

As mentioned earlier, tobacco smoke contains large numbers of gas and tar phase radicals and other oxidants capable of inducing oxidative stress. Measurements of antioxidants as biomarkers of oxidative stress have consistently confirmed that smokers suffer from increased oxidative stress compared with non‐smokers [23], [24], [25], [26], [27]. Although smokers also have a poorer diet than non‐smokers, more detailed studies with matched dietary intakes have shown that at least vitamin C and

Conclusion

The present review focuses on two aspects of MDA as a biomarker of lipid oxidation: the validity of MDA as a biomarker of oxidative stress in general and the specific effect of smoking on MDA/TBARS status. In the evaluation of MDA and TBARS as possible biomarkers of lipid oxidation, the wide ranges of data reported for healthy non‐smoking volunteers are important. Clearly, these ranges demonstrate that MDA so far can only be regarded as a relative rather than an absolute biomarker of lipid

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