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Benzyl alcohol induces a reversible fragmentation of the Golgi apparatus and inhibits membrane trafficking between endosomes and the trans-Golgi network

Authors :
Simm, Roger
Kvalvaag, Audun Sverre
van Deurs, Bo
Lindbäck, Toril
Sandvig, Kirsten
Simm, Roger
Kvalvaag, Audun Sverre
van Deurs, Bo
Lindbäck, Toril
Sandvig, Kirsten
Source :
Simm , R , Kvalvaag , A S , van Deurs , B , Lindbäck , T & Sandvig , K 2017 , ' Benzyl alcohol induces a reversible fragmentation of the Golgi apparatus and inhibits membrane trafficking between endosomes and the trans-Golgi network ' , Experimental Cell Research , vol. 357 , no. 1 , pp. 67-78 .
Publication Year :
2017

Abstract

Benzyl alcohol (BnOH) is widely used as a component of foods, cosmetics, household products and medical products. It is generally considered to be safe for human use, however, it has been connected to a number of adverse effects, including hypersensitivity reactions and neonatal deaths. BnOH is a membrane fluidizing agent that can affect membrane protein activity and cellular processes such as ligand binding to cell surface receptors, endocytosis and degradation of lysosomal cargo. In this study, we examined the effects of BnOH on intracellular transport using Shiga toxin (Stx), diphtheria toxin (DT) and ricin. BnOH caused reduced toxicity of all three toxins at BnOH concentrations that cause membrane fluidization. The reduced toxicity of Stx and ricin was mainly due to inhibition of retrograde transport between endosomes and the trans-Golgi network as BnOH had small effects on cell association and endocytosis of ricin and Stx. Strikingly, BnOH also induced a reversible fragmentation of the Golgi apparatus.

Details

Database :
OAIster
Journal :
Simm , R , Kvalvaag , A S , van Deurs , B , Lindbäck , T & Sandvig , K 2017 , ' Benzyl alcohol induces a reversible fragmentation of the Golgi apparatus and inhibits membrane trafficking between endosomes and the trans-Golgi network ' , Experimental Cell Research , vol. 357 , no. 1 , pp. 67-78 .
Notes :
English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1322702722
Document Type :
Electronic Resource