TY - JOUR
T1 - Dose-dependent biochemical changes in rat central nervous system after 12-week exposure to 1-bromopropane
AU - Wang, Hailan
AU - Ichihara, Gaku
AU - Ito, Hidenori
AU - Kato, Kanefusa
AU - Kitoh, Junzoh
AU - Yamada, Tetsuya
AU - Yu, Xiaozhong
AU - Tsuboi, Seiji
AU - Moriyama, Yoshinori
AU - Takeuchi, Yasuhiro
PY - 2003/3/1
Y1 - 2003/3/1
N2 - 1-Bromopropane is used as a cleaning agent or adhesive solvent in the workplace. The present study investigated the long-term effects of exposure to 1-bromopropane on biochemical components in the central nervous system (CNS) of rats. Four groups, each of nine male Wistar rats, were exposed to 200, 400, or 800 ppm 1-bromopropane or fresh air only, 8 h per day, 7 days a week for 12 weeks. We measured the levels of neuron-specific γ-enolase, glia-specific β-S100 protein, creatine kinase (CK) subunits B and M, heat shock protein Hsp27 (by enzyme immunoassay), enzymatic activity of CK and levels of glutathione (GSH), oxidized glutathione (GSSG) and sulfhydrul (SH) base in the cerebrum, cerebellum, brainstem and spinal cord. γ-Enolase decreased dose-dependently in the cerebrum, which showed a decrease in wet weight, at 400 ppm or over, but no change was noted in β-S100 protein in any brain region or spinal cord. Hsp27 decreased in the cerebellum, brainstem and spinal cord. Protein-bound SH base, non-protein SH base and total glutathione decreased in every brain region. CK activity decreased dose-dependently at 200 ppm or over, and the ratio of CK activity to CK-B concentration tended to decrease in all regions. The decrease in γ-enolase in the cerebrum suggests the involvement of biochemical changes in neurons with decrease in the wet weight of the cerebrum. Glutathione depletion and changes in proteins containing SH base as a critical site might be the underlying neurotoxic mechanism of 1-bromopropane. The biochemical changes in the cerebrum indicate that long-term exposure to 1-bromopropane has effects on the CNS.
AB - 1-Bromopropane is used as a cleaning agent or adhesive solvent in the workplace. The present study investigated the long-term effects of exposure to 1-bromopropane on biochemical components in the central nervous system (CNS) of rats. Four groups, each of nine male Wistar rats, were exposed to 200, 400, or 800 ppm 1-bromopropane or fresh air only, 8 h per day, 7 days a week for 12 weeks. We measured the levels of neuron-specific γ-enolase, glia-specific β-S100 protein, creatine kinase (CK) subunits B and M, heat shock protein Hsp27 (by enzyme immunoassay), enzymatic activity of CK and levels of glutathione (GSH), oxidized glutathione (GSSG) and sulfhydrul (SH) base in the cerebrum, cerebellum, brainstem and spinal cord. γ-Enolase decreased dose-dependently in the cerebrum, which showed a decrease in wet weight, at 400 ppm or over, but no change was noted in β-S100 protein in any brain region or spinal cord. Hsp27 decreased in the cerebellum, brainstem and spinal cord. Protein-bound SH base, non-protein SH base and total glutathione decreased in every brain region. CK activity decreased dose-dependently at 200 ppm or over, and the ratio of CK activity to CK-B concentration tended to decrease in all regions. The decrease in γ-enolase in the cerebrum suggests the involvement of biochemical changes in neurons with decrease in the wet weight of the cerebrum. Glutathione depletion and changes in proteins containing SH base as a critical site might be the underlying neurotoxic mechanism of 1-bromopropane. The biochemical changes in the cerebrum indicate that long-term exposure to 1-bromopropane has effects on the CNS.
KW - 1-Bromopropane
KW - Creatine kinase
KW - Glutathione
KW - Sulfhydryl
KW - γ-Enolase
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U2 - 10.1016/S0161-813X(02)00195-X
DO - 10.1016/S0161-813X(02)00195-X
M3 - Article
C2 - 12606292
AN - SCOPUS:0037334985
SN - 0161-813X
VL - 24
SP - 199
EP - 206
JO - NeuroToxicology
JF - NeuroToxicology
IS - 2
ER -