Assessment of serum S100B and neuron specific enolase levels to evaluate the neurotoxic effects of organic solvent exposure


Zungun C., Yilmaz F. M. , Tutkun E., Yilmaz H., Uysal S.

CLINICAL TOXICOLOGY, cilt.51, ss.748-751, 2013 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 51 Konu: 8
  • Basım Tarihi: 2013
  • Doi Numarası: 10.3109/15563650.2013.820831
  • Dergi Adı: CLINICAL TOXICOLOGY
  • Sayfa Sayısı: ss.748-751

Özet

Objectives. Long-term organic solvent exposure may cause toxic effects in central nervous system. Trichloroethylene (TCE) is known to be one of the neurotoxic chlorinated organic solvents. Trichloroacetic acid (TCA) is an oxidative pathway metabolite of TCE. S100B, a calcium-binding protein in glial cells, and neuron specific enolase (NSE) in neuron cytoplasma are protein markers of astrocyte and neuron damage, respectively. Materials and methods. Clinical and laboratory assesments were performed in 25 participants with organic solvent exposure history. Control group included 25 healthy age and sex-matched individuals. Measurements of serum S100B and NSE were performed using Roche Cobas E 601 compatible kits and elechtrochemiluminescence immunoassay. The levels of TCA in urine were measured by the headspace GC technique, after methyl esterification by methanol. Results. Median value of urine TCA in solvent-exposed group was 12.30 mg/L with 10.20 mg/L and 35.00 mg/L minimum and maximum values, respectively. The difference between serum S100B levels of solvent-exposed group (0.064 mu g/L) and control group (0.049 mu g/L) was statistically significant (p < 0.05). Serum NSE levels of control group (15.61 ng/ml) were higher than solvent-exposed group (13.90 ng/ml) but difference was not statistically significant (p > 0.05). Conclusions. Serum S100B levels were found to be higher in solvent-exposed group when compared with control group. NSE levels were comparable between two groups. Increased Serum S100B levels in organic solvent exposure may indicate a preventive response to neuronal damage caused by reactive oxygen species (ROS) produced through oxidative metabolic pathways of organic solvents.