Next Article in Journal
Deoxynivalenol in the Diet Impairs Bone Mineralization in Broiler Chickens
Previous Article in Journal
Biomonitoring Data for Assessing Aflatoxins and Ochratoxin A Exposure by Italian Feedstuffs Workers
Previous Article in Special Issue
Ricin: An Ancient Story for a Timeless Plant Toxin
Article Menu
Issue 6 (June) cover image

Export Article

Open AccessReview

Intracellular Transport and Cytotoxicity of the Protein Toxin Ricin

1
Department of Medical Biology and Genetics, Faculty of Biology, University of Gdańsk, Wita Stwosza 59, 80-308 Gdańsk, Poland
2
Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, 0379 Oslo, Norway
3
Faculty of Mathematics and Natural Sciences, Department of Biosciences, University of Oslo, 0316 Oslo, Norway
*
Author to whom correspondence should be addressed.
Toxins 2019, 11(6), 350; https://doi.org/10.3390/toxins11060350
Received: 22 May 2019 / Revised: 13 June 2019 / Accepted: 14 June 2019 / Published: 18 June 2019
(This article belongs to the Special Issue Ricin Toxins)
  |  
PDF [2584 KB, uploaded 18 June 2019]
  |  

Abstract

Ricin can be isolated from the seeds of the castor bean plant (Ricinus communis). It belongs to the ribosome-inactivating protein (RIP) family of toxins classified as a bio-threat agent due to its high toxicity, stability and availability. Ricin is a typical A-B toxin consisting of a single enzymatic A subunit (RTA) and a binding B subunit (RTB) joined by a single disulfide bond. RTA possesses an RNA N-glycosidase activity; it cleaves ribosomal RNA leading to the inhibition of protein synthesis. However, the mechanism of ricin-mediated cell death is quite complex, as a growing number of studies demonstrate that the inhibition of protein synthesis is not always correlated with long term ricin toxicity. To exert its cytotoxic effect, ricin A-chain has to be transported to the cytosol of the host cell. This translocation is preceded by endocytic uptake of the toxin and retrograde traffic through the trans-Golgi network (TGN) and the endoplasmic reticulum (ER). In this article, we describe intracellular trafficking of ricin with particular emphasis on host cell factors that facilitate this transport and contribute to ricin cytotoxicity in mammalian and yeast cells. The current understanding of the mechanisms of ricin-mediated cell death is discussed as well. We also comment on recent reports presenting medical applications for ricin and progress associated with the development of vaccines against this toxin. View Full-Text
Keywords: ricin; protein synthesis inhibition; apoptosis ricin; protein synthesis inhibition; apoptosis
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Sowa-Rogozińska, N.; Sominka, H.; Nowakowska-Gołacka, J.; Sandvig, K.; Słomińska-Wojewódzka, M. Intracellular Transport and Cytotoxicity of the Protein Toxin Ricin. Toxins 2019, 11, 350.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Toxins EISSN 2072-6651 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top