2 hexanone/atrophy

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Ultrastructural studies of the dying-back process. VI. Examination of nerve fibers undergoing giant axonal degeneration in organotypic culture.

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Organotypic tissue cultures, composed of structurally and functionally coupled explants of mouse spinal cord, dorsal root ganglia, and striated muscle, have been used to create a model of the distal (dying-back) axonopathy found in animals and humans with aliphatic hexacarbon neuropathy. Mature

Neuroprotein Targets of γ-Diketone Metabolites of Aliphatic and Aromatic Solvents That Induce Central-Peripheral Axonopathy.

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Peripheral neuropathy associated with chronic occupational and deliberate overexposure to neurotoxic organic solvents results from axonal degeneration in the central and peripheral nervous system. Human and experimental studies show that axonopathy is triggered by the action of neuroprotein-reactive

Microwave-assisted derivatization of 2,5-hexanedione in urine: evaluation using GC-MS and GC-ECD.

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2,5-Hexanedione, the main metabolite of n-hexane, can be responsible for axonal degeneration symptoms via formation of pyrrol-adducts with several amino acids. In order to make it amenable to gas chromatographic analysis, a protocol including microwave assisted derivatization is presented and

Dose-response relationships in ketone-induced potentiation of chloroform hepato- and nephrotoxicity.

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Chloroform (CHCl3)-induced hepato- and nephrotoxicity was evaluated in male, Fischer 344 rats pretreated with various dosages (1.0 to 15.0 mmol/kg, po) of acetone (Ac), 2-butanone (Bu), 2-pentanone (Pn), 2-hexanone (Hx), or 2-heptanone (Hp). The CHCl3 challenge dosage (0.5 ml/kg, ip) produced slight

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