What are protective effects of anti-ricin A-chain aptamer?

Ricin, a lectin from the castor bean plant Ricinus communis is considered one of the most potent plant toxins. Ricin poisoning can cause severe tissue damage and inflammation and can result in death. Most accidental exposures occur by ingestion of the seeds of castor beans whereby the toxin is released after the seed coat is damaged. The ingested toxin causes severe gastrointestinal damage with symptoms and death due to multiorgan failure or cardiovascular collapse.

A research article to be published on November 7, 2008 in the World Journal of Gastroenterology addresses this question. The research team was led by Dr. Kam-Meng Tchou-Wong from New York University School of Medicine in United States.

Authors investigated the therapeutic potential of an RNA ligand (aptamer) specific for the catalytic ricin A-chain (RTA), the protective effects of a 31-nucleotide RNA aptamer (31RA), which formed a high affinity complex with RTA, against ricin-induced toxicity in cell-based luciferase translation and cell cytotoxicity assays were evaluated.

They have shown that 31RA RNA aptamer can protect against ricin ribotoxicity in cell-based luciferase and cell cytotoxicity assays. Hence, RNA aptamer that inhibits RTA enzymatic activity represents a novel class of nucleic acid inhibitor that has the potential to be developed as a therapeutic agent for the treatment of ricin intoxication.

In this report, authors utilized a stable cell-based luciferase assay and showed that 31RA aptamer also neutralized the inhibitory effects of ricin on translation inhibition in cell-free and cell-based luciferase assays and ricin-induced cytotoxicity assay. The use of a stably transfected cell-based luciferase assay will facilitate the development of high throughput screening for inhibitors of ricin as potential antidotes for the treatment of ricin intoxication.

Reference: Fan S, Wu F, Martiniuk F, Hale ML, Ellington AD, Tchou-Wong KM. Protective effects of anti-ricin A-chain RNA aptamer against ricin toxicity. World J Gastroenterol 2008; 14(41): 6360-6365
http://www.wjgnet.com/1007-9327/14/6360.asp

Correspondence to: Dr. Kam-Meng Tchou-Wong, Department of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, New York 10987, United States. tchouk02@nyumc.org Telephone: +1-845-7313504 Fax: +1-845-3515472

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.