Cu,Zn‐superoxide dismutase is necessary for proper function of VDAC in <i>Saccharomyces cerevisiae</i> cells

Karachitos, Andonis; Gałgańska, Hanna; Wojtkowska, Małgorzata; Budzińska, Małgorzata; Stobienia, Olgierd; Bartosz, Grzegorz; Kmita, Hanna

doi:10.1016/j.febslet.2008.12.045

Cited by 24 publications

(18 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…5, the protein carbonylation, which was quantitated after derivatization with 2,4-dinitrophenyl hydrazine, was increased in the Δsod1 cells compared with the wild type cells. This finding supports previously published data that demonstrate oxidative stress in Δsod1 S. cerevisiae cells (e.g., Drakulic et al, 2005;Karachitos et al, 2009;O'Brien et al, 2004). However, the Δsod1 cells treated with the reference substances or the studied extracts contain less carbonylated proteins compared with the untreated cells (see also Table 2).…”

Section: 5supporting

confidence: 93%

“…A more widely distributed copper-and zinc-containing enzyme (CuZnSOD or SOD1) is localized in the cytosol, peroxisomes, lysosomes, and nucleus, as well as the mitochondrial intermembrane space, whereas manganese-containing enzyme (MnSOD or SOD2) is only present in the mitochondrial matrix (O'Brien, Dirmeier, Engle, & Poyton, 2004;Zelko, Mariani, & Folz, 2002). Interestingly, it has been shown that SOD1 is necessary for the proper function of voltage-dependent anion-selective channel (VDAC) (Karachitos et al, 2009), which is regarded as crucial for proper mitochondria function (e.g., Kmita, Stobienia, & Michejda, 1999) and consequently, cell life or death (e.g., Shoshan-Barmatz et al, 2010). Accordingly, it has also been shown that deficient SOD activity may be involved in the etiology of several diseases (e.g., Torsdottir et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of plant extract antioxidative phenolic compounds on energetic status and viability of Saccharomyces cerevisiae cells undergoing oxidative stress

Chanaj-Kaczmarek

Wysocki

Karachitos

et al. 2015

Journal of Functional Foods

Self Cite

View full text Add to dashboard Cite

Section: 5supporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Effects of plant extract antioxidative phenolic compounds on energetic status and viability of Saccharomyces cerevisiae cells undergoing oxidative stress

Chanaj-Kaczmarek

Wysocki

Karachitos

et al. 2015

Journal of Functional Foods

Self Cite

View full text Add to dashboard Cite

“…Thus, in the presence of minocycline the voltage dependence of reconstituted VDAC is weaker although simultaneously the channel is modified to assume lower conductance states that suggests an effect of minocycline on VDAC gating mechanism [39]. Furthermore flickering of VDAC conductance observed in the presence of minocycline might result from VDAC transient blockade/closure [54].…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that VDAC behavior in planar phospholipid membranes made of asolectin is voltage dependent and symmetrical [38][39][40], meaning that the channel closes at about the same rate and to about the same extent depending on the applied potential value but regardless its sign. Thus, VDAC reconstituted into planar phospholipid membranes displays 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Garcia-Martinez EM et al,…”

Section: Minocycline Affects Vdac Conductance and Voltage Dependencementioning

confidence: 99%

Mitochondria and calcium flux as targets of neuroprotection caused by minocycline in cerebellar granule cells

García-Martínez

Sanz-Blasco

Karachitos

et al. 2010

Biochemical Pharmacology

Self Cite

View full text Add to dashboard Cite

This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Garcia-Martinez EM et al., 2 AbstractMinocycline, an antibiotic of the tetracycline family, has attracted considerable interest for its theoretical therapeutic applications in neurodegenerative diseases. However, the mechanism of action underlying its effect remains elusive. Here we have studied the effect of minocycline under excitotoxic conditions. Fluorescence and bioluminescence imaging studies in rat cerebellar granular neuron cultures using fura-2/AM and mitochondria-targeted aequorin revealed that minocycline, at concentrations higher than those shown to block inflammation and inflammation-induced neuronal death, inhibited NMDA-induced cytosolic and mitochondrial rises in Ca 2+ concentrations in a reversible manner. Moreover, minocycline added in the course of NMDA stimulation decreased Ca 2+ intracellular levels, but not when induced by depolarization with a high K + medium. We also found that minocycline, at the same concentrations, partially depolarized mitochondria by about 5-30 mV, prevented mitochondrial Ca 2+ uptake under conditions of environmental stress, and abrogated NMDAinduced reactive oxygen species (ROS) formation. Consistently, minocycline also abrogates the rise in ROS induced by 75 M Ca 2+ in isolated brain mitochondria. In search for the mechanism of mitochondrial depolarization, we found that minocycline markedly inhibited state 3 respiration of rat brain mitochondria, although distinctly increased oxygen uptake in state 4. Minocycline inhibited NADH-cytochrome c reductase and cytochrome c oxidase activities, whereas the activity of succinate-cytochrome c reductase was not modified, suggesting selective inhibition of complex I and IV. Finally, minocycline affected activity of voltage-dependent anion channel (VDAC) as determined in the reconstituted system. Taken together, our results indicate that mitochondria are a critical factor in minocycline-mediated neuroprotection.

show abstract

“…Artificial phospholipid membranes were formed from soybean asolectin (Avanti Polar Lipids, purified by acetone precipitation before use) suspended at concentration of 25 mg/ml in n-decane, across a circular hole (aperture diameter about 250 μm) in the thin wall of Delrin chamber (Warner Instruments) separating two compartments (cis–trans) filled with unbuffered 1M KCl (31, 34, 35). The pH of KCl solution was 6.9.…”

Section: Methodsmentioning

confidence: 99%

The Association of VDAC with Cell Viability of PC12 Model of Huntington’s Disease

et al. 2016

Self Cite

View full text Add to dashboard Cite

It is becoming increasingly apparent that mitochondria dysfunction plays an important role in the pathogenesis of Huntington’s disease (HD), but the underlying mechanism is still elusive. Thus, there is a still need for further studies concerning the upstream events in the mitochondria dysfunction that could contribute to cell death observed in HD. Taking into account the fundamental role of the voltage-dependent anion-selective channel (VDAC) in mitochondria functioning, it is reasonable to consider the channel as a crucial element in HD etiology. Therefore, we applied inducible PC12 cell model of HD to determine the relationship between the effect of expression of wild type and mutant huntingtin (Htt and mHtt, respectively) on cell survival and mitochondria functioning in intact cells under conditions of undergoing cell divisions. Because after 48 h of Htt and mHtt expression differences in mitochondria functioning co-occurred with differences in the cell viability, we decided to estimate the effect of Htt and mHtt expression lasted for 48 h on VDAC functioning. Therefore, we isolated VDAC from the cells and tested the preparations by black lipid membrane system. We observed that the expression of mHtt, but not Htt, resulted in changes of the open state conductance and voltage-dependence when compared to control cells cultured in the absence of the expression. Importantly, for all the VDAC preparations, we observed a dominant quantitative content of VDAC1, and the quantitative relationships between VDAC isoforms were not changed by Htt and mHtt expression. Thus, Htt and mHtt-mediated functional changes of VDAC, being predominantly VDAC1, which occur shortly after these protein appearances in cells, may result in differences concerning mitochondria functioning and viability of cells expressing Htt and mHtt. The assumption is important for better understanding of cytotoxicity as well as cytoprotection mechanisms of potential clinical application.

show abstract

Cu,Zn‐superoxide dismutase is necessary for proper function of VDAC in Saccharomyces cerevisiae cells

Cited by 24 publications

References 34 publications

Effects of plant extract antioxidative phenolic compounds on energetic status and viability of Saccharomyces cerevisiae cells undergoing oxidative stress

Effects of plant extract antioxidative phenolic compounds on energetic status and viability of Saccharomyces cerevisiae cells undergoing oxidative stress

Mitochondria and calcium flux as targets of neuroprotection caused by minocycline in cerebellar granule cells

The Association of VDAC with Cell Viability of PC12 Model of Huntington’s Disease

Contact Info

Product

Resources

About