scholarly journals Impact of Lignocellulose Pretreatment By-Products on S. cerevisiae Strain Ethanol Red Metabolism during Aerobic and An-aerobic Growth

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 806
Author(s):  
Grzegorz Kłosowski ◽  
Dawid Mikulski
Keyword(s):  
Environmental Stress ◽  
Cellular Response ◽  
Stress Factors ◽  
Yeast Cells ◽  
Specific Response ◽  
Anaerobic Conditions ◽  
Fermentation Inhibitors ◽  
Starting Point ◽  
By Products ◽  
Second Generation Ethanol

Understanding the specific response of yeast cells to environmental stress factors is the starting point for selecting the conditions of adaptive culture in order to obtain a yeast line with increased resistance to a given stress factor. The aim of the study was to evaluate the specific cellular response of Saccharomyces cerevisiae strain Ethanol Red to stress caused by toxic by-products generated during the pretreatment of lignocellulose, such as levulinic acid, 5-hydroxymethylfurfural, furfural, ferulic acid, syringaldehyde and vanillin. The presence of 5-hydroxymethylfurfural at the highest analyzed concentration (5704.8 ± 249.3 mg/L) under aerobic conditions induced the overproduction of ergosterol and trehalose. On the other hand, under anaerobic conditions (during the alcoholic fermentation), a decrease in the biosynthesis of these environmental stress indicators was observed. The tested yeast strain was able to completely metabolize 5-hydroxymethylfurfural, furfural, syringaldehyde and vanillin, both under aerobic and anaerobic conditions. Yeast cells reacted to the presence of furan aldehydes by overproducing Hsp60 involved in the control of intracellular protein folding. The results may be helpful in optimizing the process parameters of second-generation ethanol production, in order to reduce the formation and toxic effects of fermentation inhibitors.

Mechanism of inhibition of succinate oxidase by products of oxidation of o-dihydroxycoumarins

1980 ◽  
Vol 45 (2) ◽  
pp. 641-652
Author(s):  
Petr Zbořil
Keyword(s):  
Inhibitory Activity ◽  
Oxidase Activity ◽  
Enzyme Preparation ◽  
Inhibitory Effects ◽  
Anaerobic Conditions ◽  
Long Period ◽  
Mechanism Of Inhibition ◽  
Intermediary Product ◽  
Succinate Oxidase ◽  
By Products

Semiquinone is an intermediary product of the oxidation of daphnetin (7,8-dihydroxycoumarin) and esculetin (6,7-dihydroxycoumarin) by diphenol oxidase; its concentration rapidly decreases. When the oxidation is effected by ferricytochrome c, the concentration of the semiquinone remains practically constant for a long period. Similarly, the ability of the products of daphnetin oxidation by diphenol oxidase to inhibit succinate oxidase activity in mitochondrial fragments rapidly decreases with time; the decrease is considerably slower in the case of cytochrome c. The inhibitory activity of the product decreases with time also during esculetin oxidation by ferricyanide. This indicates that the inhibitory effects must be ascribed predominantly to the semiquinone, the quinone is less efficient. The inhibition of succinate oxidase or succinate dehydrogenase was strongly decreased when the enzyme preparation of Keilin and Hartree was incubated with esculetin and ferricyanide in the presence of KCN or under anaerobic conditions. This demonstrates that the reaction of the inhibitor with the enzyme either involves subsequent oxidations or that the inhibitor preferentially reacts with the oxidized form of the sensitive component of the respiratory chain. The second alternative is very little probable since there is no correlation between the degree of inhibition and the binding of the inhibitor to mitochondrial fragments.

scholarly journals Chemical Modification as a Method of Improving Biocompatibility of Carbon Nonwovens

Materials ◽  
2021 ◽  
Vol 14 (12) ◽  
pp. 3198
Author(s):  
Justyna Frączyk ◽  
Sylwia Magdziarz ◽  
Ewa Stodolak-Zych ◽  
Ewa Dzierzkowska ◽  
Dorota Puchowicz ◽  
...  
Keyword(s):  
Surface Modification ◽  
Cellular Response ◽  
Fiber Surface ◽  
Thermal Conversion ◽  
Cartilage Tissue ◽  
Polar Component ◽  
Nonwoven Fabrics ◽  
Biological Compatibility ◽  
Starting Point

It was shown that carbon nonwoven fabrics obtained from polyacrylonitrile fibers (PAN) by thermal conversion may be modified on the surface in order to improve their biological compatibility and cellular response, which is particularly important in the regeneration of bone or cartilage tissue. Surface functionalization of carbon nonwovens containing C–C double bonds was carried out using in situ generated diazonium salts derived from aromatic amines containing both electron-acceptor and electron-donor substituents. It was shown that the modification method characteristic for materials containing aromatic structures may be successfully applied to the functionalization of carbon materials. The effectiveness of the surface modification of carbon nonwoven fabrics was confirmed by the FTIR method using an ATR device. The proposed approach allows the incorporation of various functional groups on the nonwovens’ surface, which affects the morphology of fibers as well as their physicochemical properties (wettability). The introduction of a carboxyl group on the surface of nonwoven fabrics, in a reaction with 4-aminobenzoic acid, became a starting point for further modifications necessary for the attachment of RGD-type peptides facilitating cell adhesion to the surface of materials. The surface modification reduced the wettability (θ) of the carbon nonwoven by about 50%. The surface free energy (SFE) in the chemically modified and reference nonwovens remained similar, with the surface modification causing an increase in the polar component (ɣp). The modification of the fiber surface was heterogeneous in nature; however, it provided an attractive site of cell–materials interaction by contacting them to the fiber surface, which supports the adhesion process.

scholarly journals Exploring the multiple roles of guardian of the genome: P53

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Wasim Feroz ◽  
Arwah Mohammad Ali Sheikh
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Crucial Role ◽  
Cellular Response ◽  
Genotoxic Stress ◽  
Specific Response ◽  
Main Body ◽  
Repair System ◽  
Tumour Suppression

Abstract Background Cells have evolved balanced mechanisms to protect themselves by initiating a specific response to a variety of stress. The TP53 gene, encoding P53 protein, is one of the many widely studied genes in human cells owing to its multifaceted functions and complex dynamics. The tumour-suppressing activity of P53 plays a principal role in the cellular response to stress. The majority of the human cancer cells exhibit the inactivation of the P53 pathway. In this review, we discuss the recent advancements in P53 research with particular focus on the role of P53 in DNA damage responses, apoptosis, autophagy, and cellular metabolism. We also discussed important P53-reactivation strategies that can play a crucial role in cancer therapy and the role of P53 in various diseases. Main body We used electronic databases like PubMed and Google Scholar for literature search. In response to a variety of cellular stress such as genotoxic stress, ischemic stress, oncogenic expression, P53 acts as a sensor, and suppresses tumour development by promoting cell death or permanent inhibition of cell proliferation. It controls several genes that play a role in the arrest of the cell cycle, cellular senescence, DNA repair system, and apoptosis. P53 plays a crucial role in supporting DNA repair by arresting the cell cycle to purchase time for the repair system to restore genome stability. Apoptosis is essential for maintaining tissue homeostasis and tumour suppression. P53 can induce apoptosis in a genetically unstable cell by interacting with many pro-apoptotic and anti-apoptotic factors. Furthermore, P53 can activate autophagy, which also plays a role in tumour suppression. P53 also regulates many metabolic pathways of glucose, lipid, and amino acid metabolism. Thus under mild metabolic stress, P53 contributes to the cell’s ability to adapt to and survive the stress. Conclusion These multiple levels of regulation enable P53 to perform diversified roles in many cell responses. Understanding the complete function of P53 is still a work in progress because of the inherent complexity involved in between P53 and its target proteins. Further research is required to unravel the mystery of this Guardian of the genome “TP53”.

Sudden infant death syndrome. Review of infant and environmental stress factors on survival

2015 ◽  
Vol 03 (01) ◽  
pp. 005-010
Author(s):  
André Kahn ◽  
José Groswasser ◽  
Patricia Franco ◽  
Sonia Scaillet ◽  
Ineko Kato ◽  
...  
Keyword(s):  
Environmental Stress ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Stress Factors ◽  
Sudden Infant

scholarly journals Effect of Environmental Stress Factors and Recycling on the Lipid Composition of Brewer’s Yeast Mitochondria

2017 ◽  
Vol 66 (9-10) ◽  
pp. 475-480 ◽  
Author(s):  
Gordana Čanadi Jurešić ◽  
◽  
Suzana Popović ◽  
Josip Škara ◽  
Marin Glad ◽  
...  
Keyword(s):  
Environmental Stress ◽  
Lipid Composition ◽  
Stress Factors ◽  
Yeast Mitochondria ◽  
Brewer’S Yeast ◽  
Brewer's Yeast

Environmental Stress Factors in the Treatment of Torture Survivors

1997 ◽  
Vol 12 (S2) ◽  
pp. 138s-138s
Author(s):  
M. Kastrup ◽  
A. Aadamsoo ◽  
L. Subilia ◽  
S. Gluzman ◽  
T. Wenzel
Keyword(s):  
Environmental Stress ◽  
Stress Factors ◽  
Torture Survivors

scholarly journals The environmental stress response causes ribosome loss in aneuploid yeast cells

2020 ◽  
Vol 117 (29) ◽  
pp. 17031-17040 ◽  
Author(s):  
Allegra Terhorst ◽  
Arzu Sandikci ◽  
Abigail Keller ◽  
Charles A. Whittaker ◽  
Maitreya J. Dunham ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Stationary Phase ◽  
Environmental Stress ◽  
Budding Yeast ◽  
Expression Patterns ◽  
Yeast Cells ◽  
Specific Gene ◽  
Environmental Stress Response ◽  
Cellular Stresses

Aneuploidy, a condition characterized by whole chromosome gains and losses, is often associated with significant cellular stress and decreased fitness. However, how cells respond to the aneuploid state has remained controversial. In aneuploid budding yeast, two opposing gene-expression patterns have been reported: the “environmental stress response” (ESR) and the “common aneuploidy gene-expression” (CAGE) signature, in which many ESR genes are oppositely regulated. Here, we investigate this controversy. We show that the CAGE signature is not an aneuploidy-specific gene-expression signature but the result of normalizing the gene-expression profile of actively proliferating aneuploid cells to that of euploid cells grown into stationary phase. Because growth into stationary phase is among the strongest inducers of the ESR, the ESR in aneuploid cells was masked when stationary phase euploid cells were used for normalization in transcriptomic studies. When exponentially growing euploid cells are used in gene-expression comparisons with aneuploid cells, the CAGE signature is no longer evident in aneuploid cells. Instead, aneuploid cells exhibit the ESR. We further show that the ESR causes selective ribosome loss in aneuploid cells, providing an explanation for the decreased cellular density of aneuploid cells. We conclude that aneuploid budding yeast cells mount the ESR, rather than the CAGE signature, in response to aneuploidy-induced cellular stresses, resulting in selective ribosome loss. We propose that the ESR serves two purposes in aneuploid cells: protecting cells from aneuploidy-induced cellular stresses and preventing excessive cellular enlargement during slowed cell cycles by down-regulating translation capacity.

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