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Toxicological Sciences 67, 114-120 (2002)
Copyright © 2002 by the Society of Toxicology

NEUROTOXICOLOGY

Biochemical Changes in the Central Nervous System of Rats Exposed to 1-Bromopropane for Seven Days

Hailan Wang*,1, Gaku Ichihara*, Hidenori Ito{dagger}, Kanefusa Kato{dagger}, Junzoh Kitoh{ddagger}, Tetsuya Yamada*, Xiaozhong Yu*, Seiji Tsuboi§, Yoshinori Moriyama§, Rie Sakatani*, Eiji Shibata, Michihiro Kamijima*, Seiichiro Itohara* and Yasuhiro Takeuchi*

* Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine, Nagoya, Japan; {dagger} Department of Biochemistry, Institute for Developmental Research, Aichi Human Service Center, Kasugai, Japan; {ddagger} Nagoya University Graduate School of Medicine, Nagoya, Japan; § Faculty of Pharmaceutical Sciences, Okayama University, Okayama, Japan; and Department of Medical Technology, Nagoya University School of Health Sciences, Nagoya, Japan

1-Bromopropane is used widely as an alternative to ozone-depleting solvents. The neurotoxic effects of this agent have been described in humans and experimental animals. Here we investigated the underlying mechanisms of the neurotoxic effects of 1-bromopropane by examining the initial biochemical changes in the central nervous system. Four groups of 9 Wistar male rats each were exposed to 200, 400, or 800 ppm 1-bromopropane or only fresh air, 8 h per day for 7 days. At the end of the experiment, the cerebrum, cerebellum, brain stem and lumbar enlargement of the spinal cord were dissected out from each rat (n = 8) for biochemical analyses. Morphological examinations of the nervous system were performed in the remaining rat of each group. 1-Bromopropane dose-dependently decreased neurospecific {gamma}-enolase, total glutathione, and nonprotein sulfhydryl groups in the cerebrum and cerebellum. Creatine kinase activity decreased dose-dependently in the brain and spinal cord. Histopathological examination showed swelling of preterminal axons in gracile nucleus and degeneration of myelin in peripheral nerves. Our results of low levels of {gamma}-enolase suggested that 1-bromopropane might primarily cause functional or cellular loss of neurons in the cerebrum and cerebellum. Glutathione depletion or modification to functional proteins containing a sulfhydryl base as a critical site might be the underlying mechanism of 1-bromopropane neurotoxicity.

Key Words: 1-bromopropane; creatine kinase; glutathione; {gamma}-enolase; peripheral nerve; neurotoxicity.


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