PubMed · 5478368
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F Kreuzer. 1970. Gas diffusion in the tissues.. https://pubmed.ncbi.nlm.nih.gov/5478368/
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Electron transport between the two photosynthetic reaction centres of high plants is mediated by plastoquinone, a rieske iron-sulfur centre, cytochrome f and plastocyanin. Measurements of redox equilibration amongst these have produced confusing results, with apparent equilibrium constants being estimated that are inconsistent with in vitro measurements of redox midpoint potentials of the components concerned. We have critically reexamined methods for deconvoluting cytochrome f absorbance signals in intact leaves. We have determined the decay of cytochrome f+ following light to dark transitions from steady state and compared this with the decay of the oxidised photosystem I primary donor, P700+. Measurements across a wide range of different irradiances and CO2 concentrations were all consistent with cyt f and P700 existing in redox equilibrium, with a potential difference of around 117 mV. These results are discussed in relation to our understanding of the organisation of the photosynthetic electron transport. They also have implications for measurements of PSI electron flux--provided more than about 20% of P700+ is oxidised in the light, then the initial decay in the concentration of P700+ following a light to dark transition provides a good estimate of electron flux through PSI. Where P700 is largely reduced in the light, net reduction of cyt f+ might need to be corrected for.
We have observed an exchange of (18)O in the reactions of CO(2) with peroxynitrite using membrane-inlet mass spectrometry and HPLC negative electrospray ionization mass spectrometry. The exchange appeared on addition of peroxynitrite to a solution containing (18)O-labeled CO(2) in equilibrium with bicarbonate. It was observed as a temporarily enhanced rate of depletion of (18)O from CO(2), a rate that was greater than the rate of (18)O depletion caused by the hydration/dehydration cycle of CO(2). In addition, we detected the appearance of mass peaks attributed to (18)O in product NO(3)(-). As a further measure of the (18)O exchange, there was a redistribution of (18)O such that the ratio of doubly to singly labeled CO(2) could not be described by the binomial expansion. This is not due to the hydration/dehydration cycle of CO(2) but most likely to recycling of CO(2) in the reaction with peroxynitrite. This (18)O exchange associated with the reactions of CO(2) and peroxynitrite may open a new methodology for studying this significant process.
To identify the factors involved in the inhibition of ultrasound (US)-induced free radical production and cell killing by pre-sonication incubation or by high cell density, we used different densities of U937 cells, and with (up to 2 h) or without pre-sonication incubations, the cell suspensions were exposed to 1 MHz US (10% duty factor at 100 Hz pulse rate; intensities 0.1-0.5 W/cm(2) for 1 min). The intensity 0.3 W/cm(2) was used for cell killing experiments and 0.5 W/cm(2) for free radical experiments. Free radical production was determined by electron paramagnetic resonance (EPR)-spin trapping with DMPO while cell killing was determined by assays for lysis, loss of cell viability, apoptosis and necrosis. The results show that at higher cell densities, CO(2) in the medium rapidly increased, with shorter pre-sonication incubation required to attain complete inhibition of both free radical production and cell killing. Cell killing at 0.3 W/cm(2) and free radical production at 0.5 W/cm(2) were both inhibited at 10 million cells/ml without incubation, and at 2 million cells/ml incubated for 2 h before sonication. Level of CO(2) alone could not account for the inhibition; consumption of gases in the medium is also considered in the inhibitory effect of pre-sonication, while suppression of cavitational activities due to the "viscosity effect" is considered a more important factor in the inhibition by high cell density.