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Expression of Bcl-2, Bax and Caspase-3 in Nerve Tissues of Rats Chronically Exposed to 2,5-hexanedione

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Abstract

Occupational exposure and experimental intoxication with n-hexane or its metabolite 2,5-hexanedione (HD) produce a central-peripheral neuropathy. However, the mechanism remains unknown. We hypothesized that HD affected the expression of Bcl-2, Bax and Caspase-3 in the central nervous system (CNS) and the peripheral nervous system (PNS). Male adult Wistar rats were administered by intraperitoneal injection at a dosage of 200 or 400 mg/kg HD, five days per week for 8 weeks. Samples of the cerebral cortex, cerebellum, spinal cord and sciatic nerves were collected and examined for Bcl-2, Bax and Caspase-3 expression using Western blotting. Subchronic exposure to HD resulted in significantly increased expression of both anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax and Caspase-3 in cerebral cortex and cerebellum, which exhibited a dose-dependent pattern. Though little change was detected in spinal cord, our results showed that the expression of Bcl-2, Bax and Caspase-3 was markedly enhanced in the sciatic nerves. These findings suggested that the changes of apoptosis-related protein level in rat nerve tissues were associated with the intoxication of HD, which might be involved in early molecular regulatory mechanism of apoptosis in the HD-induced neuropathy.

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Acknowledgements

This work was supported by grants from the Ministry of Science and Technology of China (No. 2002CB512907), and National Natural Science Foundation of China (No. 30271138).

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Correspondence to Keqin Xie.

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Cui, N., Li, S., Zhao, X. et al. Expression of Bcl-2, Bax and Caspase-3 in Nerve Tissues of Rats Chronically Exposed to 2,5-hexanedione. Neurochem Res 32, 1566–1572 (2007). https://doi.org/10.1007/s11064-007-9359-0

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