Biomolecules & Therapeutics  https://doi.org/10.4062/biomolther.2020.062
Fumonisin B1-Induced Toxicity Was Not Exacerbated in Glutathione Peroxidase-1/Catalase Double Knock Out Mice
Taddesse Yayeh1, Ha Ram Jeong2, Yoon Soo Park2, Sohyeon Moon3, Bongjun Sur3, Hwan-Soo Yoo4 and Seikwan Oh3,*
1Department of Veterinary Science, College of Agriculture and Environmental Sciences, Bahir Dar University, Bahir Dar 5501, Ethiopia
2St. Louis College of Pharmacy, St. Louis, MO 63108, USA
3Department of Molecular Medicine, School of Medicine, Ewha Womans University, Seoul 07804, Republic of Korea
4College of Pharmacy, Chungbuk National University, Osong 28160, Republic of Korea
*E-mail: skoh@ewha.ac.kr
Tel: +82-2-6986-6271, Fax: +82-2-6986-7014
Received: April 14, 2020; Revised: June 4, 2020; Accepted: June 8, 2020; Published online: July 7, 2020.
© The Korean Society of Applied Pharmacology. All rights reserved.

Abstract
Fumonisin B1 (FB1) structurally resembles sphingolipids and interferes with their metabolism leading to sphingolipid dysregulation. We questioned if FB1 could exacerbate liver or kidney toxicities in glutathione peroxidase 1 (Gpx1) and catalase (Cat) knockout mice. While higher serum levels of thiobarbituric acid reactive substances (TBARS) and sphinganine (Sa) were measured in Gpx1/Cat knockout mice (Gpx1/Cat KO) than wild type mice after 5 days of FB1 treatment, serum levels of alanine aminotransferase (ALT), sphingosine-1 phosphate (So-1-P), and sphinganine-1 phosphate (Sa-1-P) were found to be relatively low. Although Sa was highly elevated in Gpx1/Cat KO mice and wild mice, lower levels of So and Sa were found in both the kidney and liver tissues of Gpx/Cat KO mice than wild type mice after FB1 treatment. Paradoxically, FB1-induced cellular apoptosis and necrosis were hastened under oxidative stress in Gpx1/Cat KO mice.
Keywords: Fumonisin B1, Catalase, Glutathione peroxidase1, Sphingosine, Sphinganine


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