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EC number: 200-843-6
CAS number: 75-15-0
In the present study, male Wistar rats were
randomly divided into three experimental groups and one control group.
The rats in experimental groups were treated with CS2 by gavage at
dosages of 200, 400 and 600 mg/ kg bw/d respectively, six times per week
for 6 weeks. During the first week of exposure, rats kept the normal
growth of body weight. Afterwards, the mean weight gain of animal began
to slow down gradually. On week 3, the rats exposed to 600 mg/kg bw/d
CS2 showed slightly gait abnormality. At the end of the experiment, most
of the animals showed moderately abnormal gait and about 30% of animals
showed severely abnormal gait. Rats exposed to 400 mg/kg bw/d CS2 showed
slight to moderate gait abnormality until 5 week after exposure, and
lasted to the end of exposure. By contrast, no clinical signs were
observed in the control and 200 mg/kg bw/d CS2 groups throughout the
experiment. The formation of autophagosomes and lysosomes in motor
neurons of rat spinal cord was observed by transmission electron
microscopy, the level of autophagy-related proteins, lysosome-associated
membrane protein 1 (LAMP-1), and cathepsin B in spinal cord tissues was
determined by Western blot analysis, and the activity of cathepsin B was
measured by fluorescence assay. The results demonstrated that the number
of lysosomes in motor neurons was markedly increased in CS2-treated
rats. In the meantime, the administration of CS2 significantly increased
the level of microtubule-associated protein light chain 3-II (LC3-II),
Atg1, UVRAG and LAMP-1 in rat spinal cord. Furthermore, the content and
activity of cathepsin B in rat spinal cord also showed a significant
elevation. Taken together, this study suggested that CS2 intoxication
was associated with the activation of lysosomal degradative machinery,
which might play a protective role against CS2-induced neuronal damage.
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