HOCl-mediated cell death and metabolic dysfunction in the yeast Saccharomyces cerevisiae

King, D. A.; Hannum, Diane M.; Qi, Jian-Shen; Hurst, James K.

doi:10.1016/j.abb.2003.12.012

Cited by 25 publications

(23 citation statements)

References 51 publications

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“…The actual amount of oxidant trapped was ~6×10 7 HOCl/particle, which is just sufficient to overtly kill laboratory strains of bacteria, as determined by cell-free viability assays [142]. An interesting comparison is presented by S. cerevisiae ; ~10-fold greater amounts of HOCl are required to kill this yeast, suggesting that even optimal production of this oxidant within neutrophil phagosomes may be insufficient to account for its fungicidal activity [143]. …”

Section: Direct Detection and Characterization Of Intraphagosomal Reamentioning

confidence: 99%

What really happens in the neutrophil phagosome?

Hurst

2012

Free Radical Biology and Medicine

111

117

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Current viewpoints concerning the bactericidal mechanisms of neutrophils are reviewed from a perspective that emphasizes challenges presented by the inability to duplicate ex vivo the intracellular milieu. Among the challenges considered are the influences of confinement upon substrate availability and reaction dynamics, direct and indirect synergistic interactions between individual toxins, and bacterial responses to stressors. Approaches to gauging relative contributions of various oxidative and nonoxidative toxins within neutrophils using bacteria and bacterial mimics as intrinsic probes are also discussed.

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Section: Direct Detection and Characterization Of Intraphagosomal Reamentioning

confidence: 99%

What really happens in the neutrophil phagosome?

Hurst

2012

Free Radical Biology and Medicine

111

117

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“…These species are secondary disinfecting agents but also contribute to adverse effects in living cells. [26][27][28][29][30][31][32][33][34][35] Penetration of these molecules into the cell is a key issue. Trans-chlorination, i.e.…”

Section: Introductionmentioning

confidence: 99%

Decomposition of N-Chloroglycine in Alkaline Aqueous Solution: Kinetics and Mechanism

Szabó

Baranyai

Somsák

et al. 2015

Chem. Res. Toxicol.

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The decomposition kinetics and mechanism of N-chloroglycine (MCG) was studied under very alkaline conditions ([OH(-)] = 0.01-0.10 M). The absorbance change is consistent with two consecutive first-order processes in the 220-350 nm wavelength range. The first reaction is linearly dependent on [OH(-)] and interpreted by the formation of a carbanion from MCG in an equilibrium step (KOH) and a subsequent loss of chloride ion from this intermediate: kobs1 = KOH k1 = (6.4 ± 0.1) × 10(-2) M(-1) s(-1), I = 1.0 M (NaClO4), and T = 25.0 °C. The second process is assigned to the first-order decomposition of N-oxalylglycine, which is also formed as an intermediate in this system: kobs2 = (1.2 ± 0.1) × 10(-3) s(-1). Systematic (1)H and (13)C NMR measurements were performed in order to identify and follow the concentration changes of the reactant, intermediate, and product. It is confirmed that the decomposition proceeds via the formation of glyoxylate ion and produces N-formylglycine as a final product. This compound is stable for an extended period of time but eventually hydrolyses into formate and glycinate ions. A detailed mechanism is postulated which resolves the controversies found in earlier literature results.

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“…Third, environmental pH affects the kinetics of extracellular enzymes, including virulence factors (Borg-von Zepelin et al 1998). Fourth, environmental pH affects nutrient uptake, as many plasma membrane transporters use the proton gradient, which is not maintained at alkaline pH (King et al 2004). Nutrient solubility is also affected in neutral-alkaline environments, making their uptake more difficult (Howard 1999;Bensen et al 2004;Baek et al 2008).…”

mentioning

confidence: 99%

Mutational Analysis of Candida albicans SNF7 Reveals Genetically Separable Rim101 and ESCRT Functions and Demonstrates Divergence in bro1-Domain Protein Interactions

Wolf

Davis²

2010

Genetics

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The opportunistic pathogen Candida albicans can grow over a wide pH range, which is associated with its ability to colonize and infect distinct host niches. C. albicans growth in neutral-alkaline environments requires proteolytic activation of the transcription factor Rim101. Rim101 activation requires Snf7, a member of the endosomal sorting complex required for transport (ESCRT) pathway. We hypothesized that Snf7 has distinct functions in the Rim101 and ESCRT pathways, which we tested by alanine-scanning mutagenesis. While some snf7 alleles conferred no defects, we identified alleles with solely ESCRTdependent, solely Rim101-dependent, or both Rim101-and ESCRT-dependent defects. Thus, Snf7 function in these two pathways is at least partially separable. Both Rim101-and ESCRT-dependent functions require Snf7 recruitment to the endosomal membrane and alleles that disrupted both pathways were found to localize normally, suggesting a downstream defect. Most alleles that conferred solely Rim101-dependent defects were still able to process Rim101 normally under steady-state conditions. However, these same strains did display a kinetic defect in Rim101 processing. Several alleles with solely Rim101-dependent defects mapped to the C-terminal end of Snf7. Further analyses suggested that these mutations disrupted interactions with bro-domain proteins, Rim20 and Bro1, in overlapping but slightly divergent Snf7 domains.

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HOCl-mediated cell death and metabolic dysfunction in the yeast Saccharomyces cerevisiae

Cited by 25 publications

References 51 publications

What really happens in the neutrophil phagosome?

What really happens in the neutrophil phagosome?

Decomposition of N-Chloroglycine in Alkaline Aqueous Solution: Kinetics and Mechanism

Mutational Analysis of Candida albicans SNF7 Reveals Genetically Separable Rim101 and ESCRT Functions and Demonstrates Divergence in bro1-Domain Protein Interactions

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