Pathogenetic Studies of Hexane and Carbon Disulfide Neurotoxicity

References

• Spencer P. S., Schaumburg H. H., Sabri M. I., Veronesi B. V. The enlarging view of hexacarbon neurotoxicity. CRC Crit. Rev. Toxicol. 1980; 7: 279
   Web of Science ®Google Scholar
• Beauchamp R. O., Bus J. S., Popp J. A., Boreiko C. J., Golberg L. A critical review of the literature on carbon disulfide toxicity. CRC Crit. Rev. Toxicol. 1983; 11: 169
   Web of Science ®Google Scholar
• Herskowitz A., Ishii N., Schaumburg H. n-Hexane neuropathy: a syndrome occurring as a result of industrial exposure. N. Engl. J. Med. 1971; 285: 82
   PubMed Web of Science ®Google Scholar
• Yamada S. An occurrence of polyneuritis byn-hexane in the polyethylene laminating plants. Jpn. J. Ind. Health 1964; 6: 192
   Google Scholar
• Rizzuto W., Terzian H., Galiazzo-Rizzuto S. Toxic polyneuropathies in Italy due to leather cement poisoning in shoe industries. J. Neurol. Sci. 1977; 31: 343
   PubMed Web of Science ®Google Scholar
• Saida K., Mendell J. R., Weiss H. S. Peripheral nerve changes induced by methyln-butyl ketone and potentiation by methyl ethyl ketone. J. Neuropathol. Exp. Neurol. 1976; 35: 207
   PubMed Web of Science ®Google Scholar
• Altenkirch H., Mager J., Stoltenburg G., Helmbrecht J. Toxic polyneuropathies after sniffing a glue thinner. J. Neurol. 1977; 214: 137
   PubMed Web of Science ®Google Scholar
• Goto I., Matsumura M., Inoue N., Murai Y., Shida K., Santa T., Kuroiwa Y. Toxic polyneuropathy due to glue sniffing. J. Neurol. Neurosurg. Psychiatry 1974; 37: 848
   PubMed Web of Science ®Google Scholar
• Korobkin R., Asbury A. K., Sumner A. J., Nielsen S. L. Glue-sniffing neuropathy. Arch. Neurol. 1975; 32: 158
   PubMed Web of Science ®Google Scholar
• Towfighi J., Gonatas N. K., Pleasure D., Cooper H. S., McCree L. Glue sniffer's neuropathy. Neurology 1976; 26: 238
   PubMed Web of Science ®Google Scholar
• Allen N., Mendell J. R., Billmaier J., Fontaine R. E., O'Neill J. Toxic polyneuropathy due to methyln-butyl ketone, an industrial outbreak. Arch. Neurol. 1975; 32: 209
   PubMed Web of Science ®Google Scholar
• Allen N. Identification of methyln-butyl ketone as the causative agent. Experimental and Clinical Neurotoxicology, P. S. Spencer, H. H. Schaumburg. Williams and Wilkins, Baltimore 1980; 834
   Google Scholar
• Billmaier D., Yee H. T., Allen N., Craft B., Williams N., Epstein S., Fontaine R. Peripheral neuropathy in a coated fabrics plant. J. Occup. Med. 1974; 16: 665
   PubMedGoogle Scholar
• Altenkirch H., Stoltenburg G., Wagner H. M. Experimental studies on hydrocarbon neuropathies. J. Neurol. 1978; 219: 159
   PubMed Web of Science ®Google Scholar
• Spencer P. S., Bischoff M. C., Schaumburg H. H. On the specific molecular configuration of neurotoxic aliphathic hexacarbon compounds causing central-peripheral distal axonopathy. Toxicol. Appl. Pharmacol. 1978; 44: 17
   PubMed Web of Science ®Google Scholar
• DiVincenzo G. D., Kaplan C. J., Dedinas J. Characterization of the metabolites of methyln-butyl ketone, methyliso-butyl ketone, and methyl ethyl ketone in guinea pig serum and their clearance. Toxicol. Appl. Pharmacol. 1976; 36: 511
   PubMed Web of Science ®Google Scholar
• Seppalainen A. M., Haltia M. Carbon disulfide. Experimental and Clinical Neurotoxicology, P. S. Spencer, H. H. Schaumburg. Williams and Wilkins, Baltimore 1980; 356
   Google Scholar
• Aaserud O., Hommeren O. J., Tvedt B., Nakstad P., Mowe G., Efskind J., Russell D., Jorgensen E. B., Nyberg-Hansen R., Rootwelt K., Gjerstad L. Carbon disulfide exposure and neurotoxic sequelae among viscose rayon workers. Am. J. Ind. Med. 1990; 18: 25
   PubMedGoogle Scholar
• Aaserud O., Russell D., Nyberg-Hansen R., Jergensen E. B., Nakstad P., Hommeren O. J., Tvedt B., Gjerstad L. Regional cerebral blood flow after long-term exposure to carbon disulfide. Acta Neurol. Scand. 1992; 85: 266
   PubMedGoogle Scholar
• Egaland G. M., Burkhart G. A., Schnorr T. M., Hornung R. W., Fajen J. M., Lee S. T. Effects of exposure to carbon disulfide in low density lipoprotein cholesterol concentration and diastolic blood pressure. Br. J. Indust. Med. 1992; 49: 287
   PubMedGoogle Scholar
• Vanhoorne M., DeBacquer D., DeBacker G. Epidemiologic study of the cardiovascular effects of carbon disulfide. Int. J. Epidem. 1992; 21: 745
   PubMedGoogle Scholar
• Lewey F. H., Alpers B. J., Bellet S., Creskoff A. J., Drabkin D. L., Ehrich W. E., Frank J. H., Jonas L., McDonald R., et al. Experimetal chronic carbon disulfide poisoning in dogs. A clinical, biochemical and pathological study. J. Ind. Hyg. Toxicol. 1941; 23: 415
   Google Scholar
• Richter R. Degeneration of the basal ganglia in monkeys from chronic carbon disulfide poisoning. J. Neuropath. Exp. Neurol. 1945; 4: 324
   PubMed Web of Science ®Google Scholar
• Yamamura Y. n-Hexane polyneuropathy. Folia. Psychiat. Neurol. Jpn. 1969; 23: 45
   PubMedGoogle Scholar
• Gottfried M. R., Graham D. G., Morgan M., Casey H. W., Bus J. S. The morphology of carbon disulfide neurotoxicity. Neurotoxicology 1985; 6: 89
   PubMedGoogle Scholar
• Schaumburg H. H., Spencer P. S. Degeneration in central and peripheral nervous systems produced by puren-hexane: an experimental study. Brain 1976; 99: 183
   PubMed Web of Science ®Google Scholar
• Spencer P. S., Schaumburg H. H. Experimental neuropathy produced by 2,5-hexanedione—a major metabolite of the neurotoxic industrial solvent methyln-butyl ketone. J. Neurol. Neurosurg. Psychiatry 1975; 38: 771
   PubMed Web of Science ®Google Scholar
• Spencer P. S., Schaumburg H. H. Ultrastructural studies of the dying-back process. IV. Differential vulnerability of PNS and CNS fibers in experimental central-peripheral distal axonopathies. J. Neuropathol. Exp. Neurol. 1977; 36: 300
   PubMed Web of Science ®Google Scholar
• Spencer P. S., Schaumburg H. H. Ultrastructural studies of the dying-back process. III. The evolution of experimental peripheral giant axonal degeneration. J. Neuropathol. Exp. Neurol. 1977; 36: 276
   PubMed Web of Science ®Google Scholar
• Cavanagh J. B., Bennetts R. J. On the pattern of changes in the rat nervous system produced by 2,5-hexanediol. A topographical study by light microscopy. Brain 1981; 104: 297
   PubMedGoogle Scholar
• Couri D., Abdel-Rahman M. S., Hetland L. B. Biotransformation ofn-hexane and methyln-butyl ketone in guinea pigs and mice. Am. Ind. Hyg. Assoc. J. 1978; 39: 295
   PubMed Web of Science ®Google Scholar
• Krasavage W. J., O'Donoghue J. L., DiVincenzo G. D., Terhaar C. J. The relative neurotoxicity of methyl-n-butyl ketone,n-hexane and their metabolites. Toxicol. Appl. Pharmacol. 1980; 52: 433
   PubMed Web of Science ®Google Scholar
• Robertson P. J., White E. L., Bus J. S. Effects of methyl ethyl ketone pretreatment on hepatic mixed-function oxidase activity and on in vivo metabolism ofn-hexane. Xenobiotica 1989; 19: 721
   PubMed Web of Science ®Google Scholar
• Lam C. W., DiStefano V. Behavior and characterization of blood carbon disulfide in rats after inhalation. Toxicol. Appl. Pharmacol. 1982; 64: 327
   PubMedGoogle Scholar
• Leonis J. La reaction des fonctions amines avec le sulfure de carbone. C. R. Trav. Lab. Carlsberg, Ser. Chim. 1948; 26: 315
   Google Scholar
• Valentine W. M., Amarnath V., Graham D. G., Anthony D. C. Covalent cross-linking of proteins by carbon disulfide. Chem. Res. Toxicol. 1992; 5: 254
   PubMed Web of Science ®Google Scholar
• Lam C. W., DiStefano V. Blood-bound carbon disulfide: an indicator of carbon disulfide exposure, and its accumulation in repeatedly exposed rats. Toxicol. Appl. Pharmacol. 1983; 70: 402
   PubMedGoogle Scholar
• Lam C. W., DiStefano V. Characterization of carbon disulfide binding in blood and to other biological substances. Toxicol. Appl. Pharmacol. 1986; 86: 235
   PubMedGoogle Scholar
• Campbell L., Jones A. H., Wilson H. K. Evaluation of occupational exposure to carbon disulfide by blood, exhaled air, and urine analysis. Am. J. Ind. Med. 1985; 8: 143
   PubMed Web of Science ®Google Scholar
• Meuling W. J., Bragt P. C., Braun C. L. Biological monitoring of carbon disulfide. Am. J. Ind. Med. 1990; 17: 247
   PubMed Web of Science ®Google Scholar
• Rosier J., Veulemans H., Masschelein R., Vanhoorne M., Van P. C. Experimental human exposure to carbon disulfide. II. Urinary excretion of 2-thiothiazolidine-4-carboxylic acid (TTCA) during and after exposure. Int. Arch. Occup. Environ. Health 1987; 59: 243
   PubMed Web of Science ®Google Scholar
• Kitamura S., Ferrari F., Vides G., Filho D. C. M. Biological monitoring of workers occupationally exposed to carbon disulfide in a rayon plant in Brazil: validity of 2-thiothiazolidine-4-carboxylic acid (TTCA) in urine samples taken in different times, during and after the real exposure period. Int. Arch. Occup. Health 1993; 65(Suppl)S1–77
   PubMedGoogle Scholar
• De Matteis F., Seawright A. A. Oxidative metabolism of carbon disulfide by the rat: effect of treatments which modify the liver toxicity of carbon disulfide. Chem. Biol. Interactions 1973; 7: 375
   PubMed Web of Science ®Google Scholar
• Masuda Y., Yasoshima M. Loss of 3-methyl-cholanthrene-inducible form of cytochrome P-450 in liver microsomes following administration of carbon disulfide in C57BL/6 Cr mice. Biochem. Pharmacol. 1988; 37: 2363
   PubMedGoogle Scholar
• Catignani G. L., Neal R. A. Evidence for formation of a protein bound hydrodisulfide resulting from the microsomal mixed function oxidase catalyzed desulfuration of carbon disulfide. Biochem. Biophys. Res. Comm. 1975; 65: 629
   PubMed Web of Science ®Google Scholar
• Savolainen H., Vainio H. High binding of CS2 sulfur in spinal cord axonal fraction. Acta Neuropath. (Berlin) 1976; 36: 251
   PubMedGoogle Scholar
• Graham D. G., Gottfried M. R. Cross-species extrapolation in hydrocarbon neuropathy. Neurobehav. Toxicol. Teratol. 1984; 6: 433
   PubMedGoogle Scholar
• Spencer P. S., Sabri M. I., Moore C. L. Does a defect in energy metabolism in the nerve fiber underlie axonal degeneration in polyneuropathies?. Ann. Neurol. 1979; 5: 683
   Google Scholar
• Graham D. G., Abou-Donia M. B. Studies of the molecular pathogenesis of hexane neuropathy. I. Evaluation of the inhibition of glyceraldehyde-3-phosphate dehydrogenase by 2,5-hexanedione. J. Toxicol. Environ. Health 1980; 6: 621
   PubMed Web of Science ®Google Scholar
• Gillies P. J., Norton R. M., Bus J. S. Effect of 2,5-hexanedione on lipid biosynthesis on sciatic nerve and brain of the rat. Toxicol. Appl. Pharmacol. 1980; 54: 210
   PubMedGoogle Scholar
• Brieger H. Carbon disulfide in the living organism — retention, biotransformation, and pathophysiologic effects. Toxicology of Carbon Disulfide, H. Brieger. Excerpta Medica Foundation, Amsterdam 1967; 27
   Google Scholar
• Mc Kenna M. J., DiStefano V. Carbon disulfide. II. A proposed mechanism for the action of carbon disulfide on dopamine β-hydroxylase. J. Pharmacol. Exp. Ther. 1977; 202: 253
   PubMedGoogle Scholar
• Teisinger J. New advances in the toxicology of carbon disulfide. Am. Ind. Hyg. Assoc. J. 1974; 35: 55
   PubMed Web of Science ®Google Scholar
• Schoentai R., Cavanagh J. B. Mechanisms involved in the “dying-back” process — an hypothesis implicating coenzymes. Neuropathol. Appl. Neurobiol. 1977; 3: 145
   Google Scholar
• Savolainen H., Lehtonen E., Vainio H. Carbon disulfide binding to rat spinal neurofilaments. Acta Neuropath. (Berlin) 1977; 37: 219
   PubMedGoogle Scholar
• Graham D. G., Anthony D. C., Boekelheide K., Maschmann N. A., Richards R. G., Wolfram J. W., Shaw B. R. Studies of the molecular pathogenesis of hexane neuropathy. II. Evidence that pyrrole derivatization of lysyl residues leads to protein crosslinking. Toxicol. Appl. Pharmacol. 1982; 64: 415
   PubMed Web of Science ®Google Scholar
• De Caprio A. P., Olajos E. J., Weber P. Co-valent binding of a neurotoxicn-hexane metabolite: conversion of primary amines to substituted pyrrole adducts by 2,5-hexanedione. Toxicol. Appl. Pharmacol. 1982; 65: 440
   PubMedGoogle Scholar
• Amarnath V., Anthony D. G., Amarnath K., Valentine W. M., Wetterau L. A., Graham D. G. Intermediates in the Paal-Knorr synthesis of pyrroles. J. Org. Chem. 1991; 56: 6924
   Web of Science ®Google Scholar
• Szakal-Quin G., Graham D. G., Millington D. S., Maltby D. A., McPhail A. T. Stereoisomer effects on the Paal-Knorr synthesis of pyrroles. J. Org. Chem. 1986; 51: 621
   Google Scholar
• De Caprio A. P. Molecular mechanisms of diketone neurotoxicity. Chem. Biol. Interactions 1985; 54: 257
   PubMedGoogle Scholar
• Sayre L. M., Autilio-Gambetti L., Gambetti P. Pathogenesis of experimental giant neuro-filamentous axonopathies: a unified hypothesis based on chemical modification of neurofilaments. Brain. Res. Rev. 1985; 10: 69
   Google Scholar
• Carden M. J., Lee V. M., Schlaepfer W. W. 2,5-Hexanedione neuropathy is associated with the covalent crosslinking of neurofilament proteins. Neurochem. Pathol. 1986; 5: 25
   PubMedGoogle Scholar
• Graham D. G., Szakal-Quin G., Priest J. W., Anthony D. C. In vitro evidence that covalent crosslinking of neurofilaments occurs in γ-diketone neuropathy. Proc. Natl. Acad. Sci. U.S.A. 1985; 81: 4979
   Google Scholar
• Griffin J. W., Anthony D. C., Fahnestock K. E., Hoffman P. N., Graham D. G. 3,4-dimethyl-2,5-hexanedione impairs the axonal transport of neurofilament proteins. J. Neurosci. 1984; 4: 1516
   PubMedGoogle Scholar
• Lapadula D. M., Irwin R. D., Suwita E., Abou-Donia M. B. Cross-linking of neurofilament proteins of rat spinal cordin vivo after administration of 2,5-hexanedione. J. Neurochem. 1986; 46: 1843
   PubMed Web of Science ®Google Scholar
• St. Clair M. B. G., Anthony D. C., Wikstrand C. J., Graham D. G. Neurofilament protein crosslinking in γ-diketone neuropathy:in vitro andin vivo studies using the seaworm. Myxicola infundibulum, Neurotoxicology 1989; 10: 743
   PubMedGoogle Scholar
• Anthony D. C., Boekelheide K., Anderson C. W., Graham D. G. The effect of 3,4-dimethyl substitution on the neurotoxicity of 2,5-hexanedione. II. Dimethyl substitution accelerates pyrrole formation and protein crosslinking. Toxicol. Appl. Pharmacol. 1983; 71: 372
   PubMed Web of Science ®Google Scholar
• Anthony D. C., Boekelheide K., Graham D. G. The effect of 3,4-dimethyl substitution on the neurotoxicity of 2,5-hexanedione. I. Accelerated clinical neuropathy is accompanied by more proximal axonal swellings. Toxicol. Appl. Pharmacol. 1983; 71: 362
   PubMed Web of Science ®Google Scholar
• Anthony D. C., Giangaspero F., Graham D. G. The spatio-temporal pattern of the axonopathy associated with the neurotoxicity of 3,4-dimethyl-2,5-hexanedione in the rat. J. Neuropath. Exp. Neurol. 1983; 42: 548
   PubMedGoogle Scholar
• Graham D. G., Anthony D. C., Szakal-Quin G., Gottfried M. R., Boekelheide K. Covalent crosslinking of neurofilaments in the pathogenesis ofn-hexane neuropathy. Neurotoxicology 1985; 6: 55
   PubMed Web of Science ®Google Scholar
• Gold B. G., Griffin J. W., Price D. L., Hoffman P. N. Primary and secondary changes in axonal transport in neurofibrillary disorders. The Cytoskeleton: A Target for Toxic Agents, T. W. Clarkson, P. R. Sager, T. L. M. Syversen. Plenum Press, New York 1986; 119
   Google Scholar
• Monaco S., Wongmongkolrit T., Shearson C. M., Patton A., Schaetzle B., Autilio-Gambetti L., Gambetti P., Sayre L. M. Giant axonopathy characterized by intermediate location of axonal enlargements and acceleration of neurofilament transport. Brain Res. 1990; 519: 73
   PubMed Web of Science ®Google Scholar
• Center M. B., Szakal-Quin G., Anderson C. W., Anthony D. C., Graham D. G. Evidence that pyrrole formation is a pathogenetic step in gammadiketone neuropathy. Toxicol. Appl. Pharmacol. 1987; 87: 351
   PubMedGoogle Scholar
• Rosenberg C. K., Center M. B., Szakal Q. G., Anthony D. C., Graham D. G. d,l-versus meso-3,4-dimethyl-2,5-hexanedione: a morphometric study of the proximo-distal distribution of axonal swellings in the anterior root of the rat. Toxicol. Appl. Pharmacol. 1987; 87: 363
   PubMedGoogle Scholar
• De Caprio A. P., Fowke J. H. Limited and selective adduction of carbonyl-terminal lysines in the high molecular weight neurofilament proteins by 2,5-hexanedione. in vitro. Brain Res. 1992; 586: 219
   PubMedGoogle Scholar
• Rosenberg C. K., Anthony D. C., Szakal Q. G., Genter M. B., Graham D. G. Hyperbaric oxygen accelerates the neurotoxicity of 2,5-hexanedione. Toxicol. Appl. Pharmacol. 1987; 87: 374
   PubMedGoogle Scholar
• StClair M. B. G., Amarnath V., Moody M. A., Anthony D. C., Anderson C. W., Graham D. G. Pyrrole oxidation and protein cross-linking as necessary steps in the development of γ-diketone neuropathy. Chem. Res. Toxicol 1988; 1: 179
   PubMedGoogle Scholar
• Ansbacher L. E., Bosch E. P., Cancilla P. A. Disulfiram neuropathy: a neurofilamentous distal axonopathy. Neurology 1982; 32: 424
   PubMed Web of Science ®Google Scholar
• Bergouignan F. X., Vital C., Henry P., Eschapasse P. Disulfiram neuropathy. J. Neurol. 1988; 235: 382
   PubMed Web of Science ®Google Scholar
• Bilbao J. M., Briggs S. J., Gray T. A. Filamentous axonopathy in disulfiram neuropathy. Ultrastruc. Pathol. 1984; 7: 295
   PubMed Web of Science ®Google Scholar
• Brugnone F., Marnelli G., Zotti S., Zanella I., De Paris P., Caroldi S., Betta A. Blood concentration of carbon disulfide in “normal” subjects and in alcoholic subjects treated with disulfiram. Br. J. Ind. Med. 1992; 49: 658
   PubMedGoogle Scholar
• Valentine W. M., Amarnath V., Amarnath K., Rirnmele F., Graham D. G. Carbon disulfide-mediated protein cross-linking byN,N-diethyl-dithioearbamate. Chem. Res. Toxicol. 1995; 8: 96
   PubMed Web of Science ®Google Scholar
• Amarnath V., Anthony D. C., Valentine W. M., Graham D. G. The molecular mechanism of the carbon disulfide mediated cross-linking of proteins. Chem. Res. Toxocol. 1991; 4: 148
   PubMedGoogle Scholar
• De Caprio A. P., Olajas E. S., Chen X., Fowke J. H., Zhu M., Bank S. Characterization of isothiocyanates, thioureas, and other lysine adduction products in carbon disulfide-treated peptides and protein. Chem. Res. Toxicol. 1992; 5: 496
   PubMedGoogle Scholar
• Joris S. J., Aspilla K. I., Chakrabarti C. L. Decomposition of monoalkyl dithiocarbmates. Anal. Chem. 1970; 42: 647
   Google Scholar
• Valentine W. M., Graham D. G., Anthony D. C. Covalent cross-linking of erythrocyte spectrin by carbon disulfide. in vivo, Toxicol. Appl. Pharmacol. 1992; 121: 71
   Google Scholar
• Riihimaki V., Kivisto H., Peltonen K., Helpio E., Aitio A. Assessment of exposure to carbon disulfide in viscose production workers from urinary 2-thiothiazolidine-4-carboxylic acid determinations. Am. J. Indust. Med. 1992; 22: 85
   PubMedGoogle Scholar
• Phillips M. Detection of carbon disulfide in breath and air: A possible new risk factor for coronary artery disease. Int. Arch. Occup. Environ. Health 1992; 64: 119
   PubMed Web of Science ®Google Scholar
• Kawai T., Yasugi T., Mizunuma K., Horiguchi S., Uchida Y., Iwani O., Iguchi H., Ideka M. Dose-dependent increase in 2,5-hexanedione in the urine of workers exposed ton-hexane. Int. Arch. Occup. Environ. Health 1991; 63: 285
   PubMed Web of Science ®Google Scholar
• Saito I., Shibata E., Huang J., Hisanaga N., Ono Y., Takeuchi Y. Determination of urinary 2,5-hexanedione concentration by an improved analytical method as an index of exposure ton-hexane. Br. J. Ind. Med. 1991; 48: 568
   PubMedGoogle Scholar
• Cavanagh J. B. personal communication
   Google Scholar
• Anthony D. C., Amarnath V., Simons G. R., Clair M. B. G., Moody M. A., Graham D. G. Accumulation of pyrrole residues as the molecular basis of cumulative neurotoxic dose of 2,5-hexanedione. J. Neuropathol. Exp. Neurol. 1988; 47: 325
   Google Scholar
• Amarnath V., Valentine W. M., Amarnath K., Eng M. A., Graham D. G. The mechanism of nucleophilic substitution of alkylpyrroles in the presence of oxygen. Chem. Res. Toxicol. 1994; 7: 56
   PubMed Web of Science ®Google Scholar
• Pyle S. J., Amarnath V., Graham D. G., Anthony D. C. The role of pyrrole formation in the alteration in neurofilament transport induced during exposure to 2,5-hexanedione. J. Neuropathol. Exp. Neurol. 1992; 51: 451
   PubMed Web of Science ®Google Scholar
• Pyle S. J., Amarnath V., Graham D. G., Anthony D. C. Acceleration of neurofilament transport following 2,5-hexanedione exposure is a persistent response of the axon. J. Neuropathol. Exp. Neurol. 1991; 50: 321
   Google Scholar
• Pyle S. J., Amarnath V., Graham D. G., Anthony D. C. Decreased levels of the high molecular weight subunit of neurofilaments and accelerated neurofilament transport during the recovery phase of 2,5-hexanedione exposure. Cell Motil. Cytoskel 1993; 26: 133
   PubMedGoogle Scholar
• Valentine W. M., Pyle S. J., Anthony D. C., Graham D. G. Covalent cross-linking of neurofilaments by carbon disulfide in vitro. The Toxicologist 1993; 13: 125
   Google Scholar
• Clark A. W., Griffin J. W., Price D. L. The axonal pathology in chronic IDPN intoxication. J. Neuropathol. Exp. Neurol. 1980; 39: 42
   PubMed Web of Science ®Google Scholar
• Griffin J. W., Price D. L. Proximal axonopathies induced by toxic chemicals. Experimental and Clinical Neurotoxicology, P. S. Spencer, H. H. Schaumburg. Williams and Wilkins, Baltimore 1980; 161
   Google Scholar
• Griffin J. W., Price D. L. Demyelination in experimental IDPN and hexacarbon neuropathies: evidence for axonal influence. Lab. Invest. 1981; 45: 130
   PubMedGoogle Scholar
• Moser V. C., Boyes W. K. Prolonged neurobehavioral and visual effects of short-term exposure to 3,3′-iminodipropionitrile (IDPN) in rats. Fundam. Appl. Toxicol. 1993; 21: 277
   PubMedGoogle Scholar
• Denlinger R. H., Anthony D. C., Amarnath V., Graham D. G. Comparison of location, severity, and dose response of proximal axonal lesions induced by 3,3′-iminodiproprionitrile and deuterated analogues. J. Neuropathol. Exp. Neurol. 1992; 51: 569
   PubMedGoogle Scholar