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Eur J Clin Invest. 2003 Feb;33(2):134-40.

No acute impact of lipid apheresis treatment on free radical scavenging enzyme gene expression in white blood cells.

Author information

1
Department of Nephrology and Rheumatology, Georg-August University, Göttingen, Germany. vschett@gwdg.de

Abstract

BACKGROUND:

Lipid apheresis (LA) treatment has been suggested to cause oxidative stress. Defense against oxygen-radical-mediated damage is provided by nonenzymatic and enzymatic antioxidants. In the present investigation we have investigated whether gene expression of free radical scavenging enzymes (FRSE) is affected in leukocytes of patients undergoing LDL-apheresis.

MATERIALS AND METHODS:

For this purpose cellular glutathione peroxidase (GPx-1), phospholipid glutathione peroxidase (GPx-4), glutathione reductase (GSSG-R), glutathione synthetase (GSH-S), Cu/Zn-superoxide dismutase (SOD-1) and catalase (CAT) mRNA expression were followed at the start (SA) and immediately after (EA) LA treatment (n = 25). Gene expression was determined by quantitative RT-PCR with the LightCycler(R) instrument (Roche Diagnostics, Mannheim, Germany) and transcription elongation factor-2 as reference gene.

RESULTS:

The expression of GPx-1, GPx-4, GSSG-R, GSH-S, SOD-1, CAT mRNA was not affected by a single LA treatment. Free radical scavenging enzymes mRNAs were significantly (P < 0.05) increased in the LA patients (GPx-1: 2.00 +/- 1.37; GPx-4: 0.52 +/- 0.46; GSSG-R: 0.07 +/- 0.03; GSH-S: 0.04 +/- 0.03; SOD-1: 1.12 +/- 0.74; CAT: 0.15 +/- 0.07) when compared with 26 healthy blood donors (GPx-1: 1.1 +/- 0.6; GPx-4: 0.35 +/- 0.19; GSSG-R: 0.02 +/- 0.01; GSH-S: 0.03 +/- 0.01; SOD-1: 0.16 +/- 0.08; CAT: 0.09 +/- 0.05; mean +/- SD).

CONCLUSIONS:

These results show that the LA procedure does not acutely affect the antioxidant defense system on the gene level but suggests that the chronic stress resulting from hyperlipidaemia and/or LA may cause FRSE gene induction.

[Indexed for MEDLINE]

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