Lipid peroxidation status, somatic mutations and micronuclei in peripheral lymphocytes: a case observation on a possible interrelationship
Introduction
Lipid peroxidation (LPO) products are regarded as one of the major sources for endogenous genotoxic compounds. The toxicological significance of this process has been linked to spontaneous mutagenesis and carcinogenesis [2]. The main precursors of LPO-products are derived from dietary polyunsaturated fatty acids and from arachidonic acid present in membrane lipids. As a consequence, LPO might be influenced by individual dietary habits. Within a larger trial on dietary fat-related adverse effects [1], a subset of ten female volunteers was analyzed for different biomarkers at two repeated time points: Plasma malondialdehyde (MDA) levels and urinary 8-isoprostaglandin-F2αwere measured as markers for LPO, while hprt (hypoxanthine guanine phosphoribosyl transferase) mutants and micronuclei frequencies in peripheral blood lymphocytes were analyzed as indicators of genotoxic effects. This pilot study revealed a good reproducibility between blood samples of the same individual taken at two different time points. Here, we report a case observation, which suggests an association between the LPO status on one hand and genotoxicity in lymphocytes on the other.
Section snippets
Subjects and study design
The data presented are derived from a larger controlled nutritional intervention trial carried out at the University of Helsinki, Finland as described in detail by Freese et al. [1]. Ten healthy, non-smoking female volunteers with normal body weight (body mass index 19.2–28.4 kg/m2) and a mean age of 34 (26–45) years consumed a controlled diet containing 27 energy% as fat, with 8% from saturated, 9% from monounsaturated and 10% from polyunsaturated fatty acids (mainly linoleic acid from
Results and discussion
Four different biomarkers, i.e. plasma MDA levels, urinary 8-iso-PGF2α and frequencies of hprt mutants and micronuclei in peripheral blood lymphocytes, were studied in ten female volunteers at two different time points being 4 weeks apart. Individual results are shown in Fig. 1. In nine out of ten subjects the number of isolated lymphocytes were sufficient for hprt mutation analysis by T-cell cloning (value for participant ‘H’ missing). The cloning efficiencies under non-selective conditions
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