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Fumonisin B1-Induced Toxicity Was Not Exacerbated in Glutathione Peroxidase-1/Catalase Double Knock Out Mice

  • Yayeh, Taddesse (Department of Veterinary Science, College of Agriculture and Environmental Sciences, Bahir Dar University) ;
  • Jeong, Ha Ram (St. Louis College of Pharmacy) ;
  • Park, Yoon Soo (St. Louis College of Pharmacy) ;
  • Moon, Sohyeon (Department of Molecular Medicine, School of Medicine, Ewha Womans University) ;
  • Sur, Bongjun (Department of Molecular Medicine, School of Medicine, Ewha Womans University) ;
  • Yoo, Hwan-Soo (College of Pharmacy, Chungbuk National University) ;
  • Oh, Seikwan (Department of Molecular Medicine, School of Medicine, Ewha Womans University)
  • Received : 2020.04.14
  • Accepted : 2020.06.08
  • Published : 2021.01.01

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

References

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