Alterations in Tissue Metabolite Profiles with Amifostine-Prophylaxed Mice Exposed to Gamma Radiation
Autor: | Stephen Y. Wise, Michael Girgis, Thomas M. Seed, Meth Jayatilake, Yaoxiang Li, Oluseyi O. Fatanmi, Amrita K. Cheema, Vijay K. Singh |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Excessive Bleeding Drug mice Endocrinology Diabetes and Metabolism media_common.quotation_subject Metabolite lcsh:QR1-502 Spleen Pharmacology Biochemistry Article lcsh:Microbiology acute radiation syndrome 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine lipidomes amifostine Molecular Biology metabolites media_common Kidney business.industry gamma radiation Acute Radiation Syndrome tissue Amifostine Haematopoiesis 030104 developmental biology medicine.anatomical_structure chemistry 030220 oncology & carcinogenesis biomarker business medicine.drug |
Zdroj: | Metabolites Volume 10 Issue 5 Metabolites, Vol 10, Iss 211, p 211 (2020) |
ISSN: | 2218-1989 |
DOI: | 10.3390/metabo10050211 |
Popis: | Acute exposure to high-dose ionizing irradiation has the potential to severely injure the hematopoietic system and its capacity to produce vital blood cells that innately serve to ward off infections and excessive bleeding. Developing a medical radiation countermeasure that can protect individuals from the damaging effects of irradiation remains a significant, unmet need and an area of great public health interest and concern. Despite significant advancements in the field of radiation countermeasure development to find a nontoxic and effective prophylactic agent for acute radiation syndrome, no such drug has yet been approved by the Food and Drug Administration. This study focuses on examining the metabolic corrections elicited by amifostine, a potent radioprotector, on tissues of vital body organs, such as the heart, spleen, and kidney. Our findings indicate that prophylaxis with this drug offers significant protection against potentially lethal radiation injury, in part, by correction of radiation-induced metabolic pathway perturbations. |
Databáze: | OpenAIRE |
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