1. Fumonisin B1-Induced Toxicity Was Not Exacerbated in Glutathione Peroxidase-1/Catalase Double Knock Out Mice
- Author
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Hwan Soo Yoo, Seikwan Oh, Taddesse Yayeh, Ha Ram Jeong, Bongjun Sur, Sohyeon Moon, and Yoon Soo Park
- Subjects
0301 basic medicine ,medicine.medical_specialty ,GPX1 ,Thiobarbituric acid ,Glutathione peroxidase1 ,medicine.disease_cause ,Biochemistry ,Fumonisin B1 ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Sphingosine ,Internal medicine ,Drug Discovery ,medicine ,TBARS ,Pharmacology ,biology ,Catalase ,Sphinganine ,030104 developmental biology ,Endocrinology ,chemistry ,030220 oncology & carcinogenesis ,Knockout mouse ,Toxicity ,biology.protein ,Molecular Medicine ,Original Article ,Oxidative stress - 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.
- Published
- 2021