Boron inhibits apoptosis in hyperapoptosis condition: Acts by stabilizing the mitochondrial membrane and inhibiting matrix remodeling

• Published in: Biochimica et biophysica acta. General subjects Vol. 1863; no. 1; pp. 144 - 152
• Main Authors: Routray, Indusmita, Ali, Shakir
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.01.2019
• Subjects: abnormal development; apoptosis; boron; Caspase-3; Cell death; Cytochrome c; diabetes; DNA damage; membrane potential; Mitochondria; mitochondrial membrane; neurodegenerative diseases; phosphatidylserines; protective effect; Cytochrome c; Mitochondria; Cell death; Caspase-3
• ISSN: 0304-4165; 1872-8006; 1872-8006
• DOI: 10.1016/j.bbagen.2018.10.007

An abnormally high apoptosis has been associated with a number of clinical conditions including embryonal malformations and various pathologies such as neuronal degeneration and diabetes. In this study, boron is reported to inhibit apoptosis in hyperapoptosis conditions as demonstrated in a model of hyperapoptosis. Boron is a metalloid which is present in food in small amounts and is suggested here to inhibit apoptosis by stabilizing the mitochondrial membrane structure, thus preventing matrix remodeling and the release of cytochrome c, an apoptosis-inducer protein from the mitochondrion. The protective effect was assessed by measuring the changes in mitochondrial membrane potential, the levels of cytochrome c and downstream activation of caspase 3, besides phosphatidylserine exposure on the cell surface and DNA damage. The study has implication in clinical conditions characterized by hyperapoptosis as seen in certain embryonal malformations and various pathologies. •Boron protects the cell in hyperapoptosis condition•It stabilizes the mitochondrial membrane and prevent matrix remodeling, thus inhibiting the release of cytochrome c•Boron is suggested in clinical conditions characterized by hyperapoptosis