Lipid peroxidation in the cerebrospinal fluid of patients with neurocysticercosis
Received 14 March 2008; received in revised form 6 June 2008; accepted 6 June 2008.
Summary
The variety of symptoms observed in patients with neurocysticercosis (NCC) is associated with the generation of reactive species by inflammatory cells. Reactive species can damage the cell membrane, inducing lipid peroxidation (LP) and giving rise to genotoxic free radicals. In this study we investigated the presence of LP products in cerebrospinal fluid (CSF) and the frequency of DNA damage in peripheral lymphocytes from 25 patients with NCC. Patients with NCC showed higher LP levels compared to controls (n=7), especially patients presenting with severe symptoms. There was a significant correlation between LP and the inflammatory response (Spearman's correlation coefficient 0.75, P<0.01). The presence of free radicals in the central nervous system (CNS) may favour the development of severe clinical symptoms, even in patients under anti-inflammatory treatment but with a poor response. DNA damage correlated with the presence of LP and with symptom severity (correlation coefficient 0.30, P<0.05, and 0.54, P<0.01, respectively). These results demonstrate the generation of oxidative damage in the CNS of patients with NCC, which may be responsible for the severity of the symptoms. LP determination in the CSF of patients with NCC could be used to determine the inflammatory reaction developed.
aInstituto Nacional de Neurología y Neurocirugía (INNN), Secretaría de Salud (SSA), Mexico City, Mexico
bUnidad de Investigación Biomédica en Cáncer, Instituto de Investigaciones Biomédicas/Instituto Nacional de Cancerología (IIB-INCan), Mexico City, Mexico
cInstituto de Investigaciones Biomédicas (IIB), Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico
Corresponding author. Instituto de Investigaciones Biomédicas, Departamento de Medicina Genómica y Toxicología Ambiental, UNAM, P.O. Box 70-228, Ciudad Universitaria, 04510 México, D.F., México. Tel.: +52 55 5628 0425; fax: +52 55 5628 0432.