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Transient to stationary radon (220Rn) emissions from a phonolitic rock exposed to subvolcanic temperatures.

ABSTRACT: Rock substrates beneath active volcanoes are frequently subjected to temperature changes caused by the input of new magma from the depth and/or the intrusion of magma bodies of variable thickness within the subvolcanic rocks. The primary effect of the influx of hot magma is the heating of surrounding host rocks with the consequent modification of their physical and chemical properties. To assess mobilization in subvolcanic thermal regimes, we have performed radon (220Rn) thermal experiments on a phonolitic lava exposed to temperatures in the range of 100-900°C. Results from these experiments indicate that transient Rn signals are not unequivocally related to substrate deformation caused by tectonic stresses, but rather to the temperature-dependent diffusion of radionuclides through the structural discontinuities of rocks which serve as preferential pathways for gas release. Intense heating/cooling cycles are accompanied by rapid expansion and contraction of minerals. Rapid thermal cycling produced both inter- and intra-crystal microfracturing, as well as the formation of macroscopic faults. The increased number of diffusion paths dramatically intensified Rn migration, leading to much higher emissions than temperature-dependent transient changes. This geochemical behaviour is analogous to positive anomalies recorded on active volcanoes where dyke injections produce thermal stress and deformation in the host rocks. An increased Rn signal far away from the location of a magmatic intrusion is also consistent with microfracturing of subsurface rocks over long distances via thermal stress propagation and the opening of new pathways.

SUBMITTER: Mollo S

PROVIDER: S-EPMC6837235 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Transient to stationary radon (<sup>220</sup>Rn) emissions from a phonolitic rock exposed to subvolcanic temperatures.

Mollo Silvio S Tuccimei Paola P Soligo Michele M Galli Gianfranco G Iezzi Gianluca G Scarlato Piergiorgio P

Royal Society open science 20191030 10

Rock substrates beneath active volcanoes are frequently subjected to temperature changes caused by the input of new magma from the depth and/or the intrusion of magma bodies of variable thickness within the subvolcanic rocks. The primary effect of the influx of hot magma is the heating of surrounding host rocks with the consequent modification of their physical and chemical properties. To assess mobilization in subvolcanic thermal regimes, we have performed radon (<sup>220</sup>Rn) thermal exper ...[more]

PMID: 31824701

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Project description:BackgroundPrevious evaluation by different molecular and physiological assays of Staphylococcus aureus (S. aureus) responses to heat shock exposure yielded a still fragmentary view of the mechanisms determining bacterial survival or death at supra-physiological temperatures. This study analyzed diverse facets of S. aureus heat-shock adjustment by recording global transcriptomic and metabolic responses of bacterial cultures shifted for 10 min from 37 degrees C to a sub-lethal (43 degrees C) or eventually lethal (48 degrees C) temperature. A relevant metabolic model of the combined action of specific stress response mechanisms with more general, energy-regulating metabolic pathways in heat-shocked S. aureus is presented.ResultsWhile S. aureus cultures shifted to 43 degrees C or left at 37 degrees C showed marginal differences in growth and survival rates, bacterial cultures exposed to 48 degrees C showed a rapid growth arrest followed by a subsequent decline in viable counts. The most substantial heat shock-induced changes at both 43 degrees C and 48 degrees C occurred in transcript levels of HrcA- and CtsR-regulated genes, encoding classical chaperones DnaK and GroESL, and some Hsp100/Clp ATPases components, respectively. Other metabolic pathways up-regulated by S. aureus exposure at 48 degrees C included genes encoding several enzymes coping with oxidative stress, and DNA damage, or/and impaired osmotic balance. Some major components of the pentose phosphate cycle and gluconeogenesis were also up-regulated, which reflected depletion of free glucose by bacterial cultures grown in Mueller-Hinton broth prior to heat shock. In contrast, most purine- and pyrimidine-synthesis pathway components and amino acyl-tRNA synthetases were down-regulated at 48 degrees C, as well as arginine deiminase and major fermentative pathway components, such as alcohol, lactate and formate dehydrogenases. Despite the heat-induced, increased requirements for ATP-dependent macromolecular repair mechanisms combined with declining energy sources, intracellular ATP levels remained remarkably constant during heat shock.ConclusionThe sequential loss of replication and viability at 48 degrees C cannot be explained by significant reductions in intracellular ATP levels, but may reflect ATP rerouting for macromolecular repair mechanisms and cell survival. Our metabolic model also suggests that heat-stressed S. aureus should down-regulate the production of potential, DNA-damaging reactive oxygen species that might result from electron transport-generated ATP, involving excessive levels of free heavy metals, in particular iron.

Dataset Information

Transient to stationary radon (220Rn) emissions from a phonolitic rock exposed to subvolcanic temperatures.

Publications

Transient to stationary radon (<sup>220</sup>Rn) emissions from a phonolitic rock exposed to subvolcanic temperatures.

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