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.

doi:10.1016/0041-008x(83)90023-6

Paper

DOI: 10.1016/0041-008x(83)90023-6

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.

Published Dec 1, 1983 · D. Anthony, Kim Boekelheide, C.William Anderson

Toxicology and applied pharmacology

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Abstract

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Animal Study

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Study Snapshot

The 3,4-dimethyl-2,5-hexanedione compound is 20-30 times more potent and causes more proximal neurofilamentous swellings, suggesting a common mechanism of injury for neurofilament neuropathies.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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References

DOI: 10.1016/0041-008X(83)90024-8

The effect of 3,4-dimethyl substitution on the neurotoxicity of 2,5-hexanedione. II. Dimethyl substitution accelerates pyrrole formation and protein crosslinking.

3,4-dimethyl-2,5-hexanedione, 20-30 times more potent than 2,5-hexanedione, accelerates pyrrole formation and protein crosslinking, potentially explaining neurofilament accumulation in neuropathies.

1983·87citations·D. Anthony et al.·Toxicology and applied pharmacology

Toxicology and applied pharmacology

DOI:

In vitro and in vivo studies of the molecular pathogenesis of n-Hexane neuropathy.

N-hexane neuropathy may be linked to the gamma-diketone 3,4-dimethyl-2,5-hexanedione, which may play a role in neurofilament neuropathies by causing neurofilament-filled swellings in the distal a

1982·33citations·D. Graham et al.·Neurobehavioral toxicology and teratology

Neurobehavioral toxicology and teratology

DOI: 10.1016/0041-008X(82)90389-1

Covalent binding of a neurotoxic n-hexane metabolite: conversion of primary amines to substituted pyrrole adducts by 2,5-hexanedione.

2,5-hexanedione forms substituted pyrrole adducts with primary amines, suggesting pyrrole formation as the probable mode of in vivo tissue binding.

1982·130citations·A. DeCaprio et al.·Toxicology and applied pharmacology

Toxicology and applied pharmacology

DOI: 10.1016/0041-008X(82)90237-X

Studies of the molecular pathogenesis of hexane neuropathy. II. Evidence that pyrrole derivatization of lysyl residues leads to protein crosslinking.

Chronic n-hexane intoxication may cause neurofilament crosslinking through metabolism to 2,5-hexanedione, formation of an imine with lysyl residues, cyclization to form a pyrrole, and covalent crosslinking involving pyr

1982·133citations·D. Graham et al.·Toxicology and applied pharmacology

Toxicology and applied pharmacology

DOI: 10.1126/SCIENCE.6169148

Axonal transport: each major rate component reflects the movement of distinct macromolecular complexes.

Each major rate component of axonal transport in guinea pig retinal ganglion cells represents a distinct macromolecular complex, suggesting that the transport of radiolabeled proteins in the axon reflects the movement of complete subcellular complexes rather than individual proteins.

1981·185citations·M. Tytell et al.·Science

Science

Citations

DOI: 10.3390/toxics9050098

The Role of Protein Adduction in Toxic Neuropathies of Exogenous and Endogenous Origin

Toxic neuropathies, such as solvent-induced neuropathy and metabolic neuropathies, may be linked by metabolites that adduct and cross-link neuroproteins, affecting axonal transport and nerve fiber integrity.

2021·8citations·P. Spencer et al.·Toxics

Toxics

DOI: 10.1177/0192623320910960

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

Chronic exposure to neurotoxic organic solvents triggers peripheral neuropathy due to neuroprotein-reactive -diketone metabolites, potentially impacting other causes of peripheral neuropathy.

2020·7citations·P. Spencer·Toxicologic Pathology

Toxicologic Pathology

DOI: 10.1177/0192623319854326

Toxic Peripheral Neuropathies: Agents and Mechanisms

Toxic peripheral neuropathies are caused by various agents, primarily through modifications, compromised energy or protein biosynthesis, oxidative injury, and disruption of ionic gradients across membranes.

2020·35citations·W. Valentine·Toxicologic Pathology

Toxicologic Pathology

DOI: 10.3109/10408444.2015.1016216

Characterization of the toxicological hazards of hydrocarbon solvents

Hydrocarbon solvents can cause chemical pneumonitis and acute CNS effects when aspirated, and their volatile components can cause ocular and respiratory irritation at exposure levels exceeding occupational recommendations.

2015·66citations·R. H. Mckee et al.·Critical Reviews in Toxicology

Critical Reviews in Toxicology

DOI: 10.1111/joim.12030

Toxic neurofilamentous axonopathies– accumulation of neurofilaments and axonal degeneration

Toxic neurofilamentous axonopathies, caused by various neurotoxic chemicals, involve accumulation of neurofilaments and axonal degeneration, with protein adduct formation as a primary molecular mechanism.

2013·28citations·J. Llorens·Journal of Internal Medicine

Journal of Internal Medicine