Tick-borne encephalitis – lipid peroxidation and its consequences

Abstract

Background: The purpose of this study was to assess the processes of lipid peroxidation with prostaglandin derivatives and reactive aldehydes being its major indicators in cerebrospinal fluid (CSF), plasma and urine of patients with tick-borne encephalitis (TBE). Materials and methods: This study included 60 patients with TBE and 56 healthy subjects. Lipid peroxidation was estimated by the measurement of 4-hydroxynonenal (4-HNE), 4-hydroxyhexenal (4-HHE), malondialdehyde (MDA), acrolein, crotonaldehyde, and 4-oxononenal (4-ONE), determined by GC-MS, F₂-isoprostanes and neuroprostanes (NPs) level determined by LC-MS. The level of 4-HNE-protein adducts was determined by ELISA. Phospholipase A₂ (PLA₂), platelet-activating factor acetylhydrolase (PAF-AH) and glutathione peroxidase (GSH-Px) activities and vitamin E level were determined spectrophotometrically and by HPLC, respectively. In parallel, the plasma levels of phospholipid acids such as arachidonic acid (AA), linoleic acid (LA) and docosahexaenoic acid (DHA) were monitored. Results: A significant decrease in AA, LA, DHA level and GSH-Px activity (by about 20, 69, 11 and 18%, respectively) was observed. The consequence of enhanced phospholipid peroxidation was almost 7 times higher plasma level of F₂-isoprostanes and 3-fold increase in NPs level in CSF of TBE patients. Additionally a 3.5-fold increase in the CSF level of MDA, 5-fold increase in the plasma level of 4-HNE and urine level of 4-HHE in TBE patients was observed. Decreased plasma activity of PLA₂ with an increase in the PAF-AH activity was observed. Conclusion: Lipid peroxidation occurring during TBE development indicates its relevance in pathophysiology of this disease. Moreover lipid peroxidation products might be useful for the diagnosis of TBE.

Key Words::

• 4-hydroxynonenal
• CSF
• isoprostanes
• MDA
• phospholipase A₂
• plasma
• urine

Acknowledgements

This work was supported by the National Science Centre, Poland (grant number NSC 99-2314-B-002-010-MY3). The support from the side of the European Cooperation in Science and Technology project CM1001 is kindly acknowledged.

Declaration of interest:

The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.

Note

1. Genuine monoclonal mouse anti 4-HNE-His antibody in cell culture supernatant (clone 4-HNE 1g4; produced and kindly provided by Dr Georg Waeg, Karl-Franzen’s University in Graz, Institute of Molecular Biosciences, Austria).