scholarly journals Stress and Cell Death in Yeast Induced by Acetic Acid

10.5772/27726 ◽  
2012 ◽  
Author(s):  
M. J. ◽  
P. Ludovico ◽  
F. Rodrigues ◽  
C. Leo ◽  
M. Crte-Real
Keyword(s):  
Cell Death ◽  
Acetic Acid

scholarly journals Translation machinery reprogramming in programmed cell death in Saccharomyces cerevisiae

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Francesco Monticolo ◽  
Emanuela Palomba ◽  
Maria Luisa Chiusano
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Differential Expression ◽  
Ribosomal Proteins ◽  
Relative Proportion ◽  
Duplication Event ◽  
Genome Duplication Event ◽  
Cell Death Pathway

AbstractProgrammed cell death involves complex molecular pathways in both eukaryotes and prokaryotes. In Escherichia coli, the toxin–antitoxin system (TA-system) has been described as a programmed cell death pathway in which mRNA and ribosome organizations are modified, favoring the production of specific death-related proteins, but also of a minor portion of survival proteins, determining the destiny of the cell population. In the eukaryote Saccharomyces cerevisiae, the ribosome was shown to change its stoichiometry in terms of ribosomal protein content during stress response, affecting the relative proportion between ohnologs, i.e., the couple of paralogs derived by a whole genome duplication event. Here, we confirm the differential expression of ribosomal proteins in yeast also during programmed cell death induced by acetic acid, and we highlight that also in this case pairs of ohnologs are involved. We also show that there are different trends in cytosolic and mitochondrial ribosomal proteins gene expression during the process. Moreover, we show that the exposure to acetic acid induces the differential expression of further genes coding for products related to translation processes and to rRNA post-transcriptional maturation, involving mRNA decapping, affecting translation accuracy, and snoRNA synthesis. Our results suggest that the reprogramming of the overall translation apparatus, including the cytosolic ribosome reorganization, are relevant events in yeast programmed cell death induced by acetic acid.

scholarly journals Effects of acetylsalicylic acid and acetic acid solutions in VX2 carcinoma cells: In vitro analysis

2006 ◽  
Vol 21 (3) ◽  
pp. 151-154 ◽  
Author(s):  
Rogério Saad-Hossne ◽  
René Gamberini Prado ◽  
William Saad Hossne
Keyword(s):  
Cell Death ◽  
Acetic Acid ◽  
Cell Viability ◽  
Acetylsalicylic Acid ◽  
Neoplastic Cell ◽  
Carcinoma Cells ◽  
Acid Solutions ◽  
Vx2 Carcinoma ◽  
Vitro Analysis

PURPOSE: To analyze, in vitro, the effects of acetylsalicylic acid (aspirin) and acetic acid solutions on VX2 carcinoma cells in suspension and to examine the correlation between these effects and neoplastic cell death. METHODS: The VX2 tumor cells (10(7) cells/ml) were incubated in solutions containing differing concentrations (2.5% and 5%) of either acetylsalicylic acid or acetic acid, or in saline solution (controls). Every five minutes, cell viability was tested (using the trypan blue test) and analyzed under light microscopy. RESULTS: Tumor cell viability (in %) decreased progressively and, by 30 minutes, neoplastic cell death had occurred in all solutions. CONCLUSION: Based on this experimental model and the methodology employed, we conclude that these solutions cause neoplastic cell death in vitro.

Cytochrome c Trp65Ser substitution results in inhibition of acetic acid-induced programmed cell death in Saccharomyces cerevisiae

Mitochondrion ◽  
2011 ◽  
Vol 11 (6) ◽  
pp. 987-991 ◽  
Author(s):  
Nicoletta Guaragnella ◽  
Salvatore Passarella ◽  
Ersilia Marra ◽  
Sergio Giannattasio
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Acetic Acid ◽  
Cytochrome C ◽  
Programmed Cell Death

Proteome and metabolome profiling of wild-type and YCA1 -knock-out yeast cells during acetic acid-induced programmed cell death

2015 ◽  
Vol 128 ◽  
pp. 173-188 ◽  
Author(s):  
Valentina Longo ◽  
Maša Ždralević ◽  
Nicoletta Guaragnella ◽  
Sergio Giannattasio ◽  
Lello Zolla ◽  
...  
Keyword(s):  
Cell Death ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Yeast Cells ◽  
Wild Type ◽  
Knock Out ◽  
Metabolome Profiling

scholarly journals Gossypol Acetic Acid Attenuates Cardiac Ischemia/Reperfusion Injury in Rats via an Antiferroptotic Mechanism

Biomolecules ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1667
Author(s):  
Jian-Hong Lin ◽  
Kun-Ta Yang ◽  
Pei-Ching Ting ◽  
Yu-Po Luo ◽  
Ding-Jyun Lin ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Acetic Acid ◽  
Ischemia Reperfusion ◽  
Neonatal Rat ◽  
Mrna Levels ◽  
H9c2 Cells ◽  
Rat Cardiomyocytes ◽  
Protein Levels ◽  
Gossypol Acetic Acid

Myocardial ischemia/reperfusion (I/R) injury has been associated with ferroptosis, which is characterized by an iron-dependent accumulation of lipid peroxide to lethal levels. Gossypol acetic acid (GAA), a natural product taken from the seeds of cotton plants, prevents oxidative stress. However, the effects of GAA on myocardial I/R-induced ferroptosis remain unclear. This study investigated the ability of GAA to attenuate I/R-induced ferroptosis in cardiomyocytes along with the underlying mechanisms in a well-established rat model of myocardial I/R and isolated neonatal rat cardiomyocytes. H9c2 cells and cardiomyocytes were treated with the ferroptosis inducers erastin, RSL3, and Fe-SP. GAA could protect H9c2 cells against ferroptotic cell death caused by these ferroptosis inducers by decreasing the production of malondialdehyde and reactive oxygen species, chelating iron content, and downregulating mRNA levels of Ptgs2. GAA could prevent oxygen-glucose deprivation/reperfusion-induced cell death and lipid peroxidation in the cardiomyocytes. Moreover, GAA significantly attenuated myocardial infarct size, reduced lipid peroxidation, decreased the mRNA levels of the ferroptosis markers Ptgs2 and Acsl4, decreased the protein levels of ACSL4 and NRF2, and increased the protein levels of GPX4 in I/R-induced ex vivo rat hearts. Thus, GAA may play a cytoprotectant role in ferroptosis-induced cardiomyocyte death and myocardial I/R-induced ferroptotic cell death.

scholarly journals Cell wall dynamics modulate acetic acid-induced apoptotic cell death of Saccharomyces cerevisiae

2014 ◽  
Vol 1 (9) ◽  
pp. 303-314 ◽  
Author(s):  
Antonio Rego ◽  
◽  
Ana Duarte ◽  
Flavio Azevedo ◽  
Maria Sousa ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Cell Wall ◽  
Acetic Acid ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

scholarly journals Acid stress adaptation protects Saccharomyces cerevisiae from acetic acid-induced programmed cell death

Gene ◽  
2005 ◽  
Vol 354 ◽  
pp. 93-98 ◽  
Author(s):  
Sergio Giannattasio ◽  
Nicoletta Guaragnella ◽  
Manuela Corte-Real ◽  
Salvatore Passarella ◽  
Ersilia Marra
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Acid Stress ◽  
Stress Adaptation

scholarly journals Gossypol Acetic Acid Prevents Oxidative Stress-Induced Retinal Pigment Epithelial Necrosis by Regulating the FoxO3/Sestrin2 Pathway

2015 ◽  
Vol 35 (11) ◽  
pp. 1952-1963 ◽  
Author(s):  
Jakub Hanus ◽  
Hongmei Zhang ◽  
David H. Chen ◽  
Qinbo Zhou ◽  
Peng Jin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Acetic Acid ◽  
Retinal Pigment Epithelial ◽  
Potent Inhibitor ◽  
Retinal Pigment ◽  
Pigment Epithelial ◽  
Antioxidative Response ◽  
Age Related ◽  
Gossypol Acetic Acid

The late stage of dry age-related macular degeneration (AMD), or geographic atrophy (GA), is characterized by extensive retinal pigment epithelial (RPE) cell death, and a cure is not available currently. We have recently demonstrated that RPE cells die from necrosis in response to oxidative stress, providing a potential novel mechanism for RPE death in AMD. In this study, we screened U.S. Food and Drug Administration-approved natural compounds and identified gossypol acetic acid (GAA) as a potent inhibitor of oxidative stress-induced RPE cell death. GAA induces antioxidative response and inhibits accumulation of excessive reactive oxygen species in cells, through which it prevents the activation of intrinsic necrotic pathway in response to oxidative stress. Sestrin2 (SESN2) is found to mediate GAA function in antioxidative response and RPE survival upon oxidative stress. Moreover, Forkhead box O3 transcription factor (FoxO3) is further found to be required for GAA-mediated SESN2 expression and RPE survival. Mechanistically, GAA promotes FoxO3 nuclear translocation and binding to theSESN2enhancer, which in turn increases its transcriptional activity. Taken together, we have identified GAA as a potent inhibitor of oxidative stress-induced RPE necrosis by regulating the FoxO3/SESN2 pathway. This study may have significant implications in the therapeutics of age-related diseases, especially GA.

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