Chronic chlorinated benzene exposure induces glial cytoskeleton disturbance in the mouse brain and enteric glia

Abstract

Chlorinated benzenesare widely used solvent for various targets including industrial production of adhesives, drugs, rubber, paints and dry cleaning, and as well as fiber-swelling agent in the textile processing. Similar with other thinners chlorobenzeneis potent to induce detrimental effects in different cell types and could cause the functional disorders of the central nervous system. In spite of the progress in xenobiotic toxicity study, the molecular mechanisms of chlorobenzenecytotoxicity remain undiscovered. The search of molecular markers that are potent to characterize toxic risk chronic thinner exposure is an actual task whole world. Cytoskeleton protein expression is modulated with number of the environmental pollutants. Intermediate filament proteins are histology-specific components of cytoskeleton in the mosteukaryotic cells. The glial fibrillar acid protein (GFAP) is a basic component of the astrocyte cytoskeletonand could be used as reliable biomarker of cytotoxicity. Сhlorobenzene effect on mouse CNS and enteric glial cells was studied chronic (30 days) low dose exposure to thinner in vivo model. Obtained results demonstrated that cellular response against thinner toxicity is accompanied by both redox and cytoskeleton disturbance. In the present study, we investigated the GFAP level in the brain and thin intestine to estimate its prognostic value in the model of chlorobenzene chronic intoxication.Prolonged treatment with low doses of chlorobenzene induced in both brain and intestine tissue statistically significant (P < 0.01) upregulation of GFAP and redox imbalance. Observed results have shown that low doses of chlorobenzene develop uniquegliotoxic features in respect to CNS astrocytes and enteric glial cells.

Keywords

• cytoskeleton
• gfap
• biomarkers
• chlorobenzene