Anand 2020 Toxicol In Vitro

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Publications in the MiPMap
Anand CR, Bhavya B, Jayakumar K, Harikrishnan VS, Gopala S (2020) Inorganic nitrite alters mitochondrial dynamics without overt changes in cell death and mitochondrial respiration in cardiomyoblasts under hyperglycemia. Toxicol In Vitro 70:105048.

Β» PMID: 33161133 Open Access

Anand CR, Bhavya B, Jayakumar K, Harikrishnan VS, Gopala S (2020) Toxicol In Vitro

Abstract: 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-xL expression and mitochondrial ROS levels without significant initiation of cell death or decline in total ROS levels. Concomitantly, there are tendencies towards lowering of mitochondrial membrane potential, but without noteworthy changes in mitochondrial biogenesis and respiration. The study also revealed that under high glucose stress, nitrite may alter mitochondrial dynamics by Drp1 activation possibly via Akt1-Pim1 axis. Moreover, the study revealed differential effects of Drp1 silencing and/or nitrite under the above glycemic conditions. Overall, the study warrants more research regarding the effects of nitrite therapy in cardiac cells exposed to hyperglycemia. β€’ Keywords: Dynamin related protein1, Hyperglycemia, Mitochondria, Nitrite, Rat cardiac myoblasts β€’ Bioblast editor: Plangger M β€’ O2k-Network Lab: IN Thiruvananthapuram Gopala S

Labels: MiParea: Respiration, Pharmacology;toxicology  Pathology: Diabetes, Obesity 

Organism: Rat  Tissue;cell: Heart  Preparation: Intact cells 

Coupling state: LEAK, ROUTINE, ET  Pathway: ROX  HRR: Oxygraph-2k 


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