scholarly journals Pivotal Role of Akt Activation in Mitochondrial Protection and Cell Survival by Poly(ADP-ribose)polymerase-1 Inhibition in Oxidative Stress

2005 ◽  
Vol 280 (42) ◽  
pp. 35767-35775 ◽  
Author(s):  
Antal Tapodi ◽  
Balazs Debreceni ◽  
Katalin Hanto ◽  
Zita Bognar ◽  
Istvan Wittmann ◽  
...  
2008 ◽  
Vol 36 (8) ◽  
pp. 2328-2334 ◽  
Author(s):  
Olivier Huet ◽  
Christaine Cherreau ◽  
Carole Nicco ◽  
Laurent Dupic ◽  
Marc Conti ◽  
...  

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 161
Author(s):  
Nikolaos Nenadis ◽  
Efi Samara ◽  
Fani Th. Mantzouridou

In the present work, the role of the carboxyl group of o-dihydroxybenzoic acids (pyrocatechuic, 2,3-diOH-BA and protocatechuic, 3,4-diOH-BA) on the protection against induced oxidative stress in Saccharomyces cerevisiae was examined. Catechol (3,4-diOH-B) was included for comparison. Cell survival, antioxidant enzyme activities, and TBARS level were used to evaluate the efficiency upon the stress induced by H2O2 or cumene hydroperoxide. Theoretical calculation of atomic charge values, dipole moment, and a set of indices relevant to the redox properties of the compounds was also carried out in the liquid phase (water). Irrespective of the oxidant used, 2,3-diOH-BA required by far the lowest concentration (3–5 μM) to facilitate cell survival. The two acids did not activate catalase but reduced superoxide dismutase activity (3,4-diOH-BA>2,3-diOH-BA). TBARS assay showed an antioxidant effect only when H2O2 was used; equal activity for the two acids and inferior to that of 3,4-diOH B. Overall, theoretical and experimental findings suggest that the 2,3-diOH-BA high activity should be governed by metal chelation. In the case of 3,4-diOH BA, radical scavenging increases, and chelation capacity decreases. The lack of carboxyl moiety (3,4-diOH B) adds to radical scavenging, interaction with lipophilic free radicals, and antioxidant enzymes. The present study adds to our knowledge of the antioxidant mechanism of dietary phenols in biological systems.


Oncotarget ◽  
2018 ◽  
Vol 9 (36) ◽  
pp. 24364-24380 ◽  
Author(s):  
Cristiana Angelucci ◽  
Alessio D’Alessio ◽  
Fortunata Iacopino ◽  
Gabriella Proietti ◽  
Alba Di Leone ◽  
...  

2020 ◽  
Vol 222 ◽  
pp. 105450 ◽  
Author(s):  
Michelle Gallo ◽  
David Morse ◽  
Heloisa C. Hollnagel ◽  
Marcelo P. Barros

2013 ◽  
Vol 170 (2) ◽  
pp. 191-197 ◽  
Author(s):  
Mai Ikemura ◽  
Makiya Nishikawa ◽  
Kosuke Kusamori ◽  
Miho Fukuoka ◽  
Fumiyoshi Yamashita ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1871
Author(s):  
Rita Martín-Ramírez ◽  
Rebeca González-Fernández ◽  
Jairo Hernández ◽  
Pablo Martín-Vasallo ◽  
Angela Palumbo ◽  
...  

An excess of oxidative stress (OS) may affect several physiological processes fundamental to reproduction. SIRT1, SIRT6 and SIRT7 are involved in protection stress systems caused by OS, and they can be activated by antioxidants such as celastrol or melatonin. In this study, we evaluate SIRT1, SIRT6 and SIRT7 gene expression in cultured human granulosa-lutein (hGL) cells in response to OS inductors (glucose or peroxynitrite) and/or antioxidants. Our results show that celastrol and melatonin improve cell survival in the presence and absence of OS inductors. In addition, melatonin induced SIRT1, SIRT6 and SIRT7 gene expression while celastrol only induced SIRT7 gene expression. This response was not altered by the addition of OS inductors. Our previous data for cultured hGL cells showed a dual role of celastrol as a free radical scavenger and as a protective agent by regulating gene expression. This study shows a direct effect of celastrol on SIRT7 gene expression. Melatonin may protect from OS in a receptor-mediated manner rather than as a scavenger. In conclusion, our results show increased hGL cells survival with melatonin or celastrol treatment under OS conditions, probably through the regulation of nuclear sirtuins’ gene expression.


2009 ◽  
Vol 185 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Debrah M. Thompson ◽  
Roy Parker

The cellular response to stress conditions involves a decision between survival or cell death when damage is severe. A conserved stress response in eukaryotes involves endonucleolytic cleavage of transfer RNAs (tRNAs). The mechanism and significance of such tRNA cleavage is unknown. We show that in yeast, tRNAs are cleaved by the RNase T2 family member Rny1p, which is released from the vacuole into the cytosol during oxidative stress. Rny1p modulates yeast cell survival during oxidative stress independently of its catalytic ability. This suggests that upon release to the cytosol, Rny1p promotes cell death by direct interactions with downstream components. Thus, detection of Rny1p, and possibly its orthologues, in the cytosol may be a conserved mechanism for assessing cellular damage and determining cell survival, analogous to the role of cytochrome c as a marker for mitochondrial damage.


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