Despite the great number of clinical and experimental studies on carbon disulphide neuropathy, the mechanism whereby CS 2 produces neurotoxic lesions is far from being entirely understood. Several hypotheses have been suggested to explain the neurotoxic action of CS 2, such as direct enzymatic inhibition, toxic effect of its metabolities and chelation of oligoelements. This paper reports the results of an inhalation experiment on rats exposed to 700 ppm CS 2 5hrs/day, 5 days/week for 12 weeks. In the morphologic study on peripheral nervous structures, the first and most pronounced alterations observed were axonal swelling, marked increase in neurofilaments and disappearance of neurotubules, with no alteration of myelin sheaths. In the biochemical study on brain synaptosomal fractions, a slight decrease in 5'-nucleotidase (E.C. 22.214.171.124.) and particularly a significant decrease in ATPase (Na +-K + dependent) (E.C. 126.96.36.199.)activity were observed. These results seem to suggest that carbon disulphide induces primary axonal lesions, like those observed with other neurotoxic substances such as methyl-n-buthylketone and acrylamide. Together with axoplasmic flow derangement, the axonal membrane energetic impairment might be one of the most promising hypothesis to explain the development of the 'dying back' neuropathies.
|Number of pages||9|
|Journal||Medicina del Lavoro|
|Publication status||Published - 1979|
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health