Hexacarbon neuropathy: tracking a toxin.
This paper will present the progression of hexacarbon studies which followed the investigation of circumstances surrounding the occurrence of peripheral neuropathy in an occupational setting. The identification of methyl n-butyl ketone as the neurotoxin led to systematic studies of the biotransformation and mechanism of neurotoxicity. A consistent line of evidence showed that the neurotoxic potential of hexacarbons is directly related to the formation of the gamma-diketone metabolite, 2,5-hexanedione. The precise nature of the chemical interaction at the neurofilament is the subject of continuing investigation.
D000818:Animals; D001711:Biotransformation; D006586:Hexanes / Q000633:toxicity; D006588:Hexanones / Q000633:toxicity*; D006801:Humans; D007381:Intermediate Filament Proteins / Q000378:metabolism; D007536:Isomerism; D007659:Ketones / Q000633:toxicity*; D008742:Methyl n-Butyl Ketone / Q000378:metabolism / Q000633:toxicity*; D016900:Neurofilament Proteins; D009784:Occupational Diseases / Q000139:chemically induced*; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced*; D011758:Pyrroles / Q000378:metabolism; D051381:Rats; D013783:Textile Industry
D006586:Hexanes; D006588:Hexanones; D007381:Intermediate Filament Proteins; D007659:Ketones; D016900:Neurofilament Proteins; D011758:Pyrroles; C026385:n-hexane; D008742:Methyl n-Butyl Ketone; C011269:2,5-hexanedione