Treatment of the budding yeast Saccharomyces cerevisiae with the lipid peroxidation product 4-HNE provokes a temporary cell cycle arrest in G1 phase

Wonisch, Willibald; Kohlwein, Sepp D.; Schaur, Jörg; Tatzber, Franz; Guttenberger, Helmut; Žarković, Neven; Winkler, Rudolf; Esterbauer, Hermann

doi:10.1016/s0891-5849(98)00110-5

Cited by 40 publications

(33 citation statements)

References 23 publications

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“…Selected time points of 2 h and 11 days after incubation in presence of HNE were of interest to us. The ®rst time-point is identical to the generation time of S. cerevisiae and a series of previous studies 3,8,12 used this period to evaluate the biochemical response to HNE in yeast. The second timepoint corresponds to the resumption of proliferation of surviving cells, subsequent to the degeneration and removal of the aldehyde.…”

Section: Resultsmentioning

confidence: 99%

Ultrastructural analysis of HNE‐treated Saccharomyces cerevisiae cells reveals fragmentation of the vacuole and an accumulation of lipids in the cytosol

Wonisch

Zellnig

Kohlwein

et al. 2001

Cell Biochemistry & Function

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Section: Resultsmentioning

confidence: 99%

Ultrastructural analysis of HNE‐treated Saccharomyces cerevisiae cells reveals fragmentation of the vacuole and an accumulation of lipids in the cytosol

Wonisch

Zellnig

Kohlwein

et al. 2001

Cell Biochemistry & Function

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“…At low concentrations (less than 5 mM), HNE has been reported to promote proliferation, 155 and a silent stimulation of antioxidant responses by low levels of HNE (hormesis) can be protective 72 against more drastic assaults such as by carcinogens. 142 At higher concentrations (20-100 mM), HNE causes cell cycle arrest, [120][121][122] disturbs differentiation 156,157 and triggers cell death. The modalities of apoptosis induction pathways are governed by the inherent nature of the cell, prone or not to ROS generation, the level of antioxidant defense and the induction of HNE metabolizing enzymes (summarized in Figure 5).…”

Section: Discussionmentioning

confidence: 99%

“…119,120 In HL60 cells, the way to limit HNE toxicity also seems to be based on the ability to stop cell cycle arrest in G0/G1 via the inhibition of cyclins D1, D2 and A and the hypophosphorylation of retinoblastoma protein (Rb). In 1998, Esterbauer et al 121 showed that treating the budding yeast Saccharomyces cerevisiae with HNE resulted in its temporary arrest in G1 phase. More recently, in prostate PC3 cells, HNE treatment was shown to trigger cell cycle arrest in G2/M, with dephosphorylation of cdc2.…”

Section: Hne Self Limits Apoptosis: Keeping Cool Under Pressurementioning

confidence: 99%

Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance

et al. 2013

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During the last three decades, 4-hydroxy-2-nonenal (HNE), a major a,b-unsaturated aldehyde product of n-6 fatty acid oxidation, has been shown to be involved in a great number of pathologies such as metabolic diseases, neurodegenerative diseases and cancers. These multiple pathologies can be explained by the fact that HNE is a potent modulator of numerous cell processes such as oxidative stress signaling, cell proliferation, transformation or cell death. The main objective of this review is to focus on the different aspects of HNE-induced cell death, with a particular emphasis on apoptosis. HNE is a special apoptotic inducer because of its abilities to form protein adducts and to propagate oxidative stress. It can stimulate intrinsic and extrinsic apoptotic pathways and interact with typical actors such as tumor protein 53, JNK, Fas or mitochondrial regulators. At the same time, due to its oxidant status, it can also induce some cellular defense mechanisms against oxidative stress, thus being involved in its own detoxification. These processes in turn limit the apoptotic potential of HNE. These dualities can imbalance cell fate, either toward cell death or toward survival, depending on the cell type, the metabolic state and the ability to detoxify.

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“…Several practical limitations are related to the low egg numbers and non-synchronous cell divisions in successive batches spawned by females. As shown by Wonisch et al (1998), the yeast Saccharomyces cerevisiae could be one suitable tool for the elucidation of the mode of action of reactive oxylipins, because the genome has been sequenced and culturing of strain STRg6 is easy, which is not the case with copepods, sea urchins or oysters. The identified erg6 mutant, which is susceptible to a broad range of diatomderived oxylipins, can provide a useful model system for further studies on inhibitory mechanisms on the cellular level.…”

Section: Discussionmentioning

confidence: 99%

“…Reactions are not specific and, consequently, the adduct formation induces adverse effects on a broad range of cell functions. The resulting effects include depletion of glutathione (Poot et al, 1987), the inhibition of DNA and protein synthesis (Poot et al, 1988) and induction of cell cycle arrest (Barrera et al, 1991;Wonisch et al, 1998). Fewer studies have been carried out with α,β,γ,δ-unsaturated aldehydes, which are also derived by oxidative transformations of polyunsaturated fatty acids.…”

mentioning

confidence: 99%

Cytotoxicity of diatom-derived oxylipins in organisms belonging to different phyla

Adolph

Bach

Blondel

et al. 2004

Journal of Experimental Biology

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The cytotoxicity of several saturated and unsaturated marine diatom-derived aldehydes and an oxo-acid have been screened in vitro and in vivo against different organisms, such as bacteria, algae, fungi, echinoderms, molluscs and crustaceans. Conjugated unsaturated aldehydes like 2E,4E-decadienal, 2E,4E-octadienal, 5E,7E-9-oxo-nonadienoic acid and 2E-decenal were active against bacteria and fungi and showed weak algicidal activity. By contrast, the saturated aldehyde decanal and the non-conjugated aldehyde 4Z-decenal had either low or no significant biological activity. In assays with oyster haemocytes, 2E,4E-decadienal exhibited a dose-dependent inhibition of cytoskeleton organisation, rate of phagocytosis and oxidative burst and a dose-dependent promotion of apoptosis. A maternal diatom diet that was rich in unsaturated aldehydes induced arrest of cell division and apoptotic cell degradation in copepod embryos and larvae, respectively. This wide spectrum of physiological pathologies reflects the potent cell toxicity of diatom-derived oxylipins, in relation to their non-specific chemical reactivity towards nucleophilic biomolecules. The cytotoxic activity is conserved across six phyla, from bacteria to crustaceans. Deregulation of cell homeostasis is supposed to induce the elimination of damaged cells through apoptosis. However, efficient protection mechanisms possibly exist in unicellular organisms. Experiments with a genetically modified yeast species exhibiting elevated membrane and/or cell wall permeability suggest that this protection can be related to the inability of the oxylipin compounds to enter the cell.

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Treatment of the budding yeast Saccharomyces cerevisiae with the lipid peroxidation product 4-HNE provokes a temporary cell cycle arrest in G1 phase

Cited by 40 publications

References 23 publications

Ultrastructural analysis of HNE‐treated Saccharomyces cerevisiae cells reveals fragmentation of the vacuole and an accumulation of lipids in the cytosol

Ultrastructural analysis of HNE‐treated Saccharomyces cerevisiae cells reveals fragmentation of the vacuole and an accumulation of lipids in the cytosol

Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance

Cytotoxicity of diatom-derived oxylipins in organisms belonging to different phyla

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