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Carbon Disulfide-Induced Changes in Cytoskeleton Protein Content of Rat Cerebral Cortex

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Abstract

To investigate the mechanism of carbon disulfide-induced neuropathy, male wistar rats were administrated by gavage at dosage of 300 or 500 mg/kg carbon disulfide, five times per week for 12 weeks. By the end of the exposure, the animals produced a slight or moderate level of neurological deficits, respectively. Cerebrums of carbon disulfide-intoxicated rats and their age-matched controls were Triton-extracted and centrifuged at a high speed (100,000 × g) to yield a pellet fraction of NF polymer and a corresponding supernatant fraction, which presumably contained mobile monomer. Then, the contents of six cytoskeletal protein (NF-L, NF-M, NF-H, α-tubulin, β-tubulin, and β-actin) in both fractions were determined by immunoblotting. Results showed that the contents of the three neurofilament subunits in the pellet and the supernatant fraction decreased significantly regardless of dose levels (P < 0.01). As for microtubule proteins, in the pellet fraction of cerebrum, the levels of α-tubulin and β-tubulin demonstrated some inconsistent changes. However, in the supernatant fractions, the content of α-tubulin and β-tubulin increased significantly in both two dose groups (P < 0.01). In comparison to neurofilament and tubulin proteins, the content of β-actin changed less markedly, only the supernatant fraction of the high dose group displayed significant increase (P < 0.01), but the others remained unaffected. These findings suggested that the changes of cytoskeleton protein contents in rat cerebrum were associated with the intoxication of carbon disulfide, which might be involved in the development of carbon disulfide neurotoxicity.

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  1. Institute of Toxicology, Shandong University, 44 West Wenhua Road, Jinan, Shandong, 250012, P. R. China

    Fuyong Song, Sufang Yu, Xiulan Zhao, Cuili Zhang & Keqin Xie

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Song, F., Yu, S., Zhao, X. et al. Carbon Disulfide-Induced Changes in Cytoskeleton Protein Content of Rat Cerebral Cortex. Neurochem Res 31, 71–79 (2006). https://doi.org/10.1007/s11064-005-9140-1

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