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Letters |
ek Sto
ick
2 Zima5
tina6
1
Medica Centrum, 301 22 Plzen, Czech Republic
2
Department of Pediatrics, and,
3
Institute of Clinical Biochemistry, and Laboratory Diagnostics, Charles University Hospital, 304 60 Plzen, Czech Republic
4
University Clinic for Nuclear Medicine, A-1090 Vienna, Austria
5
Institute of Clinical Biochemistry, 1st Faculty of Medicine, Charles University, 120 00 Prague, Czech Republic
6
Purkyne Military Medical Academy, Department of Toxicology, 500 01 Hradec Kralove, Czech Republic
aAuthor for correspondence. Fax 420-19-7104234; e-mail racek{at}fnplzen.cz.
To the Editor:
We conducted two studies of serum antibodies against oxidized LDL (IgoxLDL) in mothers and their infants during the past 2 years. We used an ELISA (oLAb; Eli-Tec Laborreagenzien GmbH) based on the use of Cu2+-oxidized LDL particles bound to the surface of microtiter plate wells and an anti-human IgG-peroxidase conjugate. In the first study of mothers and their infants at birth and again at the age of 3 months (1), we found that the values were not homogeneous in the sera of 3-month-old infants: some infants had markedly increased IgoxLDL, whereas others had values below those in newborns. The mean value was 815 ± 469 units/L compared with 337 ± 214 units/L in newborns. At that time, we were unable to explain these findings.
One year later, we repeated the study and obtained similar results. All
mothers were familiar with the aim of the study and gave informed
consent. Of the fourteen 3-month-old infants in the study, 8 had low
serum IgoxLDL, but 6 subjects had extremely high values. In this study,
we had the opportunity to analyze the records of these infants in
detail. Surprisingly, the infants with extremely high IgoxLDL had not
been breast-fed during the first 3 months of life, whereas the others
had been (Table 1
). The difference between the values in breast-fed and
formula-fed infants was statistically significant (P
<0.001, Wilcoxon unpaired test).
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The Spearman rank correlation between IgoxLDL concentrations in the sera of mothers and their newborns was statistically significant (r = 0.79; P <0.001); on the other hand, no significant correlation was found between values for 3-month-old infants and their mothers. The early correlation reflects transplacental transport of class G IgoxLDL, whereas the infants were later able to produce their own antibodies. The production rate was individual and could be influenced by nutrition type. We also compared the number of DNA breaks in peripheral lymphocytes from 3-month-old infants by single-cell gel electrophoresis (comet assay). This method in combination with endonuclease III (endoIII) treatment of cells is able to detect oxidized pyrimidines (2). When compared with breast-fed infants, formula-fed infants had a higher number of DNA strand breaks (0.39 ± 0.06 vs 0.14 ± 0.02 DNA strand breaks/109 Da) and endoIII-sensitive sites representing predominantly oxidized pyrimidines (0.24 ± 0.10 vs 0.07 ± 0.04 endoIII sites/109 Da; P = 0.027 and 0.007, respectively, Mann–Whitney). Because the nutrition of infants contributes for their future health (3), our preliminary data may be important.
There are several possible ways to interpret our findings. One possibility is that milk formulas contain higher concentrations of IgAoxLDL than breast milk; this explanation can be omitted because our method was sensitive only to IgGoxLDL. Another explanation for these results is that milk formula diminishes oxidative stress more than breast milk and consequently leads to increased free IgGoxLDL in the circulation of infants because these antibodies are unable to bind to oxidized LDL (4). A completely different explanation is that formula feeding might cause some kind of gastrointestinal inflammatory reaction followed by early production of IgGoxLDL in these children. This may be likely if the milk formula is of nonhuman, e.g., bovine, origin, but we are also aware of the hypothesis that self-non-self recognition develops after the third month of life. On the other hand, our results show a significant increase of oxidative DNA damage in formula-fed infants compared with breast-fed infants. This increase may be a consequence of a higher oxidative load in formula-fed children, resulting from metabolic processes, or a consequence of higher antioxidative protection in breast-fed infants. The higher number of oxidized LDL particles, which are cytotoxic and able to induce apoptosis (5), may explain the enhanced oxidative DNA damage.
On the basis of our preliminary findings, we are not able to answer these questions properly, but we are convinced that additional studies should be initiated to get clearer recommendations regarding optimal nutrition for children during the first months of life.
References
ick F, Tatzber F, Lapin A. Autoantibodies against oxidized LDL in the first phase of life. Clin Chem Lab Med 1999;37:913-917.[Medline]
[Order article via Infotrieve]
inská M, Gedik CM,
ttina R. Oxidative damage to DNA; do we have a reliable
biomarker? Environ Health Perspect 1996;104(Suppl 3):465–9..
The following articles in journals at HighWire Press have cited this article:
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  A. E. Fraley, G. G. Schwartz, A. G. Olsson, S. Kinlay, M. Szarek, N. Rifai, P. Libby, P. Ganz, J. L. Witztum, S. Tsimikas, et al. Relationship of oxidized phospholipids and biomarkers of oxidized low-density lipoprotein with cardiovascular risk factors, inflammatory biomarkers, and effect of statin therapy in patients with acute coronary syndromes: Results from the MIRACL (Myocardial Ischemia Reduction With Aggressive Cholesterol Lowering) trial. J. Am. Coll. Cardiol., June 9, 2009; 53(23): 2186 - 2196. [Abstract] [Full Text] [PDF]
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