PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 4164898

Phosphorylation in hydrogen bacteria.

L Bongers
View original source ↗Export metadata ↓

Abstract

The electron-transport system of cell-free extracts obtained from Hydrogenomonas H-20 has been studied with particular reference to phosphorylation associated with the oxyhydrogen reaction. Cell-free preparations of this organism exhibit oxidative phosphorylation with hydrogen and succinate as electron donors. This activity could be uncoupled with a number of agents. Ratios of phosphorylative activity to oxidative activity observed varied from 0.2 to 0.7. Factors affecting the efficiency of phosphorylation were examined. Inhibitor and spectrophotometric studies indicated that phosphorylation with hydrogen as electron donor occurs exclusively at a site in an abbreviated electron transport chain between H(2) and cytochrome b. The possible occurrence of a cytochrome b oxidase and the requirement for a quinone are discussed, as well as the correlation between the abbreviated pathway and the energy generation by the cell. Evidence is presented which indicates that nicotinamide adenine dinucleotide does not participate in the hydrogen oxidation path which is coupled to adenosine triphosphate formation.

Explore related subjects

Antimycin ACyanidesCytochromesDicumarolDinitrophenolsElectron TransportHydrogenNADOxidative PhosphorylationPseudomonasQuinolinesSuccinatesJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

L Bongers. 1967. Phosphorylation in hydrogen bacteria.. https://doi.org/10.1128/jb.93.5.1615-1623.1967

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Bcl2/bcl-xL inhibitor engenders apoptosis and increases chemosensitivity in mesothelioma.

Mesothelioma is a neoplasm of the pleura that is currently incurable by conventional therapies. Previously, we demonstrated that mesothelioma overexpresses BCL-X(L), an anti-apoptotic member of the BCL-2 family. In addition, we have shown that down regulation of BCL-X(L) using a BCL-X(L) antisense oligonucleotide engenders mesothelioma apoptotic cell death in vitro and in vivo. The purpose of this study is to evaluate the efficacy of bcl2/bcl-x(L) inhibitor, 2-methoxy antimycin A3, in inducing apoptosis and increasing chemo-sensitivity in vitro and in vivo. Several bcl-x(L) high-expression tumor cell lines and one normal human cell line were exposed to 2-methoxy antimycin A3. 2-methoxy antimycin A3 demonstrated significant growth inhibition only in these tumor cell lines, with little effect on normal human cells. Treatment with 2-methoxy antimycin A3 alone resulted in a dramatic increase in the induction of apoptosis in the cancer cells. Apoptosis occurs through decreasing mitochondrial membrane potential and caspase activation. Notably, treatment with 2-methoxy antimycin A3 does not alter BCL-2 family protein expression. Synergistic inhibition of tumor growth by the coadministration of cisplatin and 2-methoxy antimycin A3 was observed in both in vitro and in vivo experiments. Together, these findings indicate that exposure of cancer cells to small molecule Bcl-2/x(L) inhibitors such as 2-methoxy antimycin A3 alone, or in the combination with other chemotherapeutics, may represent a novel therapeutic strategy in treatment of cancer, especially mesothelioma.

Antimycin A↗
PubMed2006

Sensing intracellular oxygen using near-infrared phosphorescent probes and live-cell fluorescence imaging.

The development and application of a methodology for measurement of oxygen within single mammalian cells are presented, which employ novel macromolecular near infrared (NIR) oxygen probes based on new metalloporphyrin dyes. The probes, which display optimal spectral characteristics and sensitivity to oxygen, excellent photostability, and low cytotoxicity and phototoxicity, are loaded into cells by simple transfection procedures and subsequently analyzed by high-resolution fluorescence microscopy. The methodology is demonstrated by sensing intracellular oxygen in different mammalian cell lines, including A549, Jurkat, and HeLa, and monitoring rapid and transient changes in response to mitochondrial uncoupling by valinomycin and inhibition by antimycin A. Furthermore, the effect of ryanodine receptor-mediated Ca(2+) influx on cellular oxygen uptake is shown by substantial changes in the level of intracellular oxygen. The results demonstrate the ability of this technique to measure small, rapid, and transient changes in intracellular oxygen in response to different biological effectors. Moreover, this technique has wide ranging applicability in cell biology and is particularly useful in the study of low oxygen environments (cellular hypoxia), mitochondrial and cellular (dys)function, and for therapeutic areas, such as cardiovascular and neurological research, metabolic diseases, and cancer.

Antimycin A↗
PubMed2006

Inhibition of specific electron transport pathways leads to oxidative stress and decreased Candida albicans proliferation.

Candida parapsilosis mitochondria contain three respiratory chains: the classical respiratory chain (CRC), a secondary parallel chain (PAR) and an "alternative" oxidative pathway (AOX). We report here the existence of similar pathways in C. albicans. To observe the capacity of each pathway to sustain yeast growth, C. albicans cells were cultured in the presence of inhibitors of these pathways. Antimycin A and KCN totally abrogated yeast growth, while rotenone did not prevent proliferation. Furthermore, rotenone promoted only partial respiratory inhibition. Lower concentrations of KCN that promote partial inhibition of respiration did not inhibit yeast growth, while partial inhibition of respiration with antimycin A did. Similarly, AOX inhibitor BHAM decreased O(2) consumption slightly but completely stunted cell growth. Reactive oxygen species production and oxidized glutathione levels were enhanced in cells treated with antimycin A or BHAM, but not rotenone or KCN. These findings suggest that oxidative stress prevents C. albicans growth.

Antimycin A↗