Fumonisin B1-Induced Toxicity Was Not Exacerbated in Glutathione Peroxidase-1/Catalase Double Knock Out Mice
| Autor: | Hwan Soo Yoo, Seikwan Oh, Taddesse Yayeh, Ha Ram Jeong, Bongjun Sur, Sohyeon Moon, Yoon Soo Park |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
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 |
| Zdroj: | Biomolecules & Therapeutics |
| ISSN: | 2005-4483 1976-9148 |
| DOI: | 10.4062/biomolther.2020.062 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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