Inorganic nitrite alters mitochondrial dynamics without overt changes in cell death and mitochondrial respiration in cardiomyoblasts under hyperglycemia.
Autor: | Anand CR; Department of Biochemistry, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram 695011, Kerala, India., Bhavya B; Department of Biochemistry, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram 695011, Kerala, India., Jayakumar K; Department of Cardiovascular and Thoracic Surgery, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram 695011, Kerala, India. Electronic address: jk@sctimst.ac.in., Harikrishnan VS; Division of Laboratory Animal Sciences, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram 695011, Kerala, India. Electronic address: harikrishnan@sctimst.ac.in., Gopala S; Department of Biochemistry, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram 695011, Kerala, India. Electronic address: srinivasg@sctimst.ac.in. |
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Jazyk: | angličtina |
Zdroj: | Toxicology in vitro : an international journal published in association with BIBRA [Toxicol In Vitro] 2021 Feb; Vol. 70, pp. 105048. Date of Electronic Publication: 2020 Nov 05. |
DOI: | 10.1016/j.tiv.2020.105048 |
Abstrakt: | Inorganic nitrate or nitrite supplementation has been reported to demonstrate positive outcomes in rodent models of obesity and diabetes as well as in type 2 diabetic humans and even included in clinical trials pertaining to cardiovascular diseases in the recent decade. However, there are contrasting data regarding the useful and toxic effects of the anions. The primary scope of this study was to analyze the beneficial/detrimental alterations in redox status, mitochondrial dynamics and function, and cellular fitness in cardiomyoblasts inflicted by nitrite under hyperglycemic conditions compared with normoglycemia. Nitrite supplementation in H9c2 myoblasts under high glucose diminishes the Bcl-x (Copyright © 2020 Elsevier Ltd. All rights reserved.) |
Databáze: | MEDLINE |
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