Cyclosporin A Inhibits UV-Radiation-Induced Membrane Damage but is Unable to Inhibit Carboxyatractyloside-Induced Permeability Transition

2009 ◽  
Vol 172 (5) ◽  
pp. 575-583 ◽  
Author(s):  
Noemí García ◽  
Cecilia Zazueta ◽  
Mohammed El-Hafidi ◽  
Natalia Pavón ◽  
Eduardo Martínez-Abundis ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Uv Radiation ◽  
Membrane Damage ◽  
Permeability Transition ◽  
Induced Membrane ◽  
Radiation Induced

scholarly journals Regulation of divalent metal ions to the aggregation and membrane damage of human islet amyloid polypeptide oligomers

RSC Advances ◽  
2021 ◽  
Vol 11 (21) ◽  
pp. 12815-12825
Author(s):  
Yajie Wang ◽  
Feihong Meng ◽  
Tong Lu ◽  
Chunyun Wang ◽  
Fei Li
Keyword(s):  
Metal Ions ◽  
Metal Binding ◽  
Membrane Damage ◽  
Islet Amyloid Polypeptide ◽  
Divalent Metal ◽  
Human Islet ◽  
Divalent Metal Ions ◽  
Islet Amyloid ◽  
Induced Membrane ◽  
Human Islet Amyloid Polypeptide

Their is a counteraction between a decrease in the disruptive ability of metal-associated oligomer species and an increase in the quantity of oligomers promoted by the metal binding in the activity of hIAPP induced membrane damage.

scholarly journals Bax-induced Cytochrome C Release from Mitochondria Is Independent of the Permeability Transition Pore but Highly Dependent on Mg2+ Ions

1998 ◽  
Vol 143 (1) ◽  
pp. 217-224 ◽  
Author(s):  
Robert Eskes ◽  
Bruno Antonsson ◽  
Astrid Osen-Sand ◽  
Sylvie Montessuit ◽  
Christoph Richter ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Cyclosporin A ◽  
Mitochondrial Permeability Transition Pore ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Cytochrome C Release ◽  
Mitochondrial Permeability ◽  
Isolated Mitochondria ◽  
Mammalian Homologue

Bcl-2 family members either promote or repress programmed cell death. Bax, a death-promoting member, is a pore-forming, mitochondria-associated protein whose mechanism of action is still unknown. During apoptosis, cytochrome C is released from the mitochondria into the cytosol where it binds to APAF-1, a mammalian homologue of Ced-4, and participates in the activation of caspases. The release of cytochrome C has been postulated to be a consequence of the opening of the mitochondrial permeability transition pore (PTP). We now report that Bax is sufficient to trigger the release of cytochrome C from isolated mitochondria. This pathway is distinct from the previously described calcium-inducible, cyclosporin A–sensitive PTP. Rather, the cytochrome C release induced by Bax is facilitated by Mg2+ and cannot be blocked by PTP inhibitors. These results strongly suggest the existence of two distinct mechanisms leading to cytochrome C release: one stimulated by calcium and inhibited by cyclosporin A, the other Bax dependent, Mg2+ sensitive but cyclosporin insensitive.

Trans Fat Supplementation Increases UV-Radiation-Induced Oxidative Damage on Skin of Mice

Lipids ◽  
2013 ◽  
Vol 48 (10) ◽  
pp. 977-987 ◽  
Author(s):  
R. C. S. Barcelos ◽  
H. J. Segat ◽  
D. M. Benvegnú ◽  
F. Trevizol ◽  
K. Roversi ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Uv Radiation ◽  
Trans Fat ◽  
Fat Supplementation ◽  
Radiation Induced
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