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

作者信息

Graham D G, Anthony D C, Boekelheide K, Maschmann N A, Richards R G, Wolfram J W, Shaw B R

出版信息

Toxicol Appl Pharmacol. 1982 Jul;64(3):415-22. doi: 10.1016/0041-008x(82)90237-x.

DOI:10.1016/0041-008x(82)90237-x
PMID:6814014
Abstract
摘要

相似文献

1
Studies of the molecular pathogenesis of hexane neuropathy. II. Evidence that pyrrole derivatization of lysyl residues leads to protein crosslinking.己烷神经病变的分子发病机制研究。II. 赖氨酸残基的吡咯衍生化导致蛋白质交联的证据。
Toxicol Appl Pharmacol. 1982 Jul;64(3):415-22. doi: 10.1016/0041-008x(82)90237-x.
2
Covalent binding of a neurotoxic n-hexane metabolite: conversion of primary amines to substituted pyrrole adducts by 2,5-hexanedione.一种神经毒性正己烷代谢物的共价结合:2,5-己二酮将伯胺转化为取代吡咯加合物。
Toxicol Appl Pharmacol. 1982 Sep 30;65(3):440-50. doi: 10.1016/0041-008x(82)90389-1.
3
n-Hexane neurotoxicity: a mechanism involving pyrrole adduct formation in axonal cytoskeletal protein.正己烷神经毒性:一种涉及轴突细胞骨架蛋白中吡咯加合物形成的机制。
Neurotoxicology. 1987 Spring;8(1):199-210.
4
In vitro and in vivo studies of the molecular pathogenesis of n-Hexane neuropathy.正己烷神经病变分子发病机制的体外和体内研究
Neurobehav Toxicol Teratol. 1982 Nov-Dec;4(6):629-34.
5
Comparative estimation of the neurotoxic risks of N-hexane and N-heptane in rats and humans based on the formation of the metabolites 2,5-hexanedione and 2,5-heptanedione.基于代谢产物2,5 - 己二酮和2,5 - 庚二酮的形成对大鼠和人类中N - 己烷和N - 庚烷神经毒性风险的比较评估。
Adv Exp Med Biol. 1996;387:411-27. doi: 10.1007/978-1-4757-9480-9_50.
6
Molecular mechanism of hexane neuropathy: significant differences in pharmacokinetics between 2.3-, 2.4-, and 2.5-hexanedione.己烷神经病变的分子机制:2,3-、2,4-和2,5-己二酮在药代动力学方面的显著差异。
Ind Health. 1984;22(3):177-87. doi: 10.2486/indhealth.22.177.
7
Pyrrole oxidation and protein cross-linking as necessary steps in the development of gamma-diketone neuropathy.吡咯氧化和蛋白质交联是γ-二酮神经病发展过程中的必要步骤。
Chem Res Toxicol. 1988 May-Jun;1(3):179-85. doi: 10.1021/tx00003a009.
8
Hair pyrrole adducts serve as biomarkers for peripheral nerve impairment induced by 2,5-hexanedione and n-hexane in rats.毛发吡咯加合物可作为 2,5-己二酮和正己烷诱导大鼠周围神经损伤的生物标志物。
PLoS One. 2018 Dec 31;13(12):e0209939. doi: 10.1371/journal.pone.0209939. eCollection 2018.
9
Toxicokinetic study of pyrrole adducts and its potential application for biological monitoring of 2,5-hexanedione subacute exposure.吡咯加合物的毒代动力学研究及其在2,5 -己二酮亚急性暴露生物监测中的潜在应用。
Int Arch Occup Environ Health. 2014 Aug;87(6):655-62. doi: 10.1007/s00420-013-0907-4.
10
The enlarging view of hexacarbon neurotoxicity.六碳神经毒性的放大视图。
Crit Rev Toxicol. 1980 Oct;7(4):279-356. doi: 10.3109/10408448009037489.

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Polygodial and Ophiobolin A Analogues for Covalent Crosslinking of Anticancer Targets.多穗柯因和蛇孢菌素 A 类似物用于抗癌靶点的共价交联。
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2
Neuroprotein Targets of γ-Diketone Metabolites of Aliphatic and Aromatic Solvents That Induce Central-Peripheral Axonopathy.诱导中枢-周围轴突病的脂肪族和芳香族溶剂的γ-二酮代谢物的神经蛋白靶点。
Toxicol Pathol. 2020 Apr;48(3):411-421. doi: 10.1177/0192623320910960. Epub 2020 Mar 12.
3
Pyrrole adducts in globin and plasma of workers exposed to hexane.
工人在暴露于己烷时血红蛋白和血浆中的吡咯加合物。
Int Arch Occup Environ Health. 2019 Aug;92(6):873-881. doi: 10.1007/s00420-019-01430-7. Epub 2019 Apr 6.
4
Wittig derivatization of sesquiterpenoid polygodial leads to cytostatic agents with activity against drug resistant cancer cells and capable of pyrrolylation of primary amines.倍半萜多香树醛的维蒂希衍生化反应可生成对耐药癌细胞具有活性且能够使伯胺发生吡咯化反应的细胞生长抑制剂。
Eur J Med Chem. 2015 Oct 20;103:226-37. doi: 10.1016/j.ejmech.2015.08.047. Epub 2015 Aug 29.
5
Animal models of peripheral neuropathy due to environmental toxicants.环境毒物所致周围神经病的动物模型
ILAR J. 2014;54(3):315-23. doi: 10.1093/ilar/ilt058.
6
Biological exposure indices of pyrrole adducts in serum and urine for hazard assessment of n-hexane exposure.用于正己烷暴露危害评估的血清和尿液中吡咯加合物的生物暴露指数。
PLoS One. 2014 Jan 22;9(1):e86108. doi: 10.1371/journal.pone.0086108. eCollection 2014.
7
Correlation between levels of 2, 5-hexanedione and pyrrole adducts in tissues of rats exposure to n-hexane for 5-days.大鼠经 5 天正己烷染毒后组织中二己酮和吡咯加合物水平的相关性。
PLoS One. 2013 Sep 30;8(9):e76011. doi: 10.1371/journal.pone.0076011. eCollection 2013.
8
Neurofilaments are nonessential to the pathogenesis of toxicant-induced axonal degeneration.神经丝对毒物诱导的轴突变性的发病机制并非必不可少。
J Neurosci. 2001 Apr 1;21(7):2278-87. doi: 10.1523/JNEUROSCI.21-07-02278.2001.
9
Biomarker research in neurotoxicology: the role of mechanistic studies to bridge the gap between the laboratory and epidemiological investigations.神经毒理学中的生物标志物研究:机制研究在弥合实验室与流行病学调查之间差距方面的作用。
Environ Health Perspect. 1996 Mar;104 Suppl 1(Suppl 1):55-67. doi: 10.1289/ehp.96104s155.
10
In vitro binding of [14C]2,5-hexanedione to rat neuronal cytoskeletal proteins.[14C]2,5-己二酮与大鼠神经元细胞骨架蛋白的体外结合
Neurochem Res. 1994 Sep;19(9):1165-73. doi: 10.1007/BF00965151.