Hydrocarbon biodegradation and soil microbial community response to repeated oil exposure

Bioremediation strategies continue to be developed to mitigate the environmental impact of petroleum hydrocarbon contamination. This study investigated the ability of soil microbiota, adapted by prior exposure, to biodegrade petroleum. Soils from Barrow Is. (W. Australia), a class A nature reserve and home to Australia’s largest onshore oil field, were exposed to Barrow production oil (50 ml/kg soil) and incubated (25 °C) for successive phases of 61 and 100 days. Controls in which oil was not added at Phase I or II were concurrently studied and all treatments were amended with the same levels of additional nutrient and water to promote microbial activity. Prior exposure resulted in accelerated biodegradation of most, but not all, hydrocarbon constituents in the production oil. Molecular biodegradation parameters measured using gas chromatography–mass spectrometry (GC–MS) showed that several aromatic constituents were degraded more slowly with increased oil history. The unique structural response of the soil microbial community was reflected by the response of different phospholipid fatty acid (PLFA) sub-classes (e.g. branched saturated fatty acids of odd or even carbon number) measured using a ratio termed Barrow PLFA ratio (B-PLFAr). The corresponding values of a previously proposed hydrocarbon degrading alteration index showed a negative correlation with hydrocarbon exposure, highlighting the site specificity of PLFA-based ratios and microbial community dynamics. B-PLFAr values increased with each Phase I and II addition of production oil. The different hydrocarbon biodegradation rates and responses of PLFA subclasses to the Barrow production oil probably relate to the relative bioavailability of production oil hydrocarbons. These different effects suggest preferred structural and functional microbial responses to anticipated contaminants may potentially be engineered by controlled pre-exposure to the same or closely related substrates. The bioremediation of soils freshly contaminated with petroleum could benefit from the addition of exhaustively bioremediated soils rich in biota primed for the impacting hydrocarbons.

MOLES3: implementing an ISO standards driven data catalogue

ISO19156 Observations and Measurements (O&M) provides a standardised framework for organising information about the collection of information about the environment. Here we describe the implementation of a specialisation of O&M for environmental data, the Metadata Objects for Linking Environmental Sciences (MOLES3). MOLES3 provides support for organising information about data, and for user navigation around data holdings. The implementation described here, “CEDA-MOLES”, also supports data management functions for the Centre for Environmental Data Archival, CEDA. The previous iteration of MOLES (MOLES2) saw active use over five years, being replaced by CEDA-MOLES in late 2014. During that period important lessons were learnt both about the information needed, as well as how to design and maintain the necessary information systems. In this paper we review the problems encountered in MOLES2; how and why CEDA-MOLES was developed and engineered; the migration of information holdings from MOLES2 to CEDA-MOLES; and, finally, provide an early assessment of MOLES3 (as implemented in CEDA-MOLES) and its limitations. Key drivers for the MOLES3 development included the necessity for improved data provenance, for further structured information to support ISO19115 discovery metadata export (for EU INSPIRE compliance), and to provide appropriate fixed landing pages for Digital Object Identifiers (DOIs) in the presence of evolving datasets. Key lessons learned included the importance of minimising information structure in free text fields, and the necessity to support as much agility in the information infrastructure as possible without compromising on maintainability both by those using the systems internally and externally (e.g. citing in to the information infrastructure), and those responsible for the systems themselves. The migration itself needed to ensure continuity of service and traceability of archived assets.

p22phox C242T SNP inhibits inflammatory oxidative damage to endothelial cells and vessels

Background— T NADPH oxidase, by generating reactive oxygen species, is involved in the pathophysiology of many cardiovascular diseases and represents a therapeutic target for the development of novel drugs. A single-nucleotide polymorphism (SNP) C242T of the p22phox subunit of NADPH oxidase has been reported to be negatively associated with coronary heart disease (CHD) and may predict disease prevalence. However, the underlying mechanisms remain unknown. Methods and Results— Using computer molecular modelling we discovered that C242T SNP causes significant structural changes in the extracellular loop of p22phox and reduces its interaction stability with Nox2 subunit. Gene transfection of human pulmonary microvascular endothelial cells showed that C242T p22phox reduced significantly Nox2 expression but had no significant effect on basal endothelial O2.- production or the expression of Nox1 and Nox4. When cells were stimulated with TNFα (or high glucose), C242T p22phox inhibited significantly TNFα-induced Nox2 maturation, O2.- production, MAPK and NFκB activation and inflammation (all p<0.05). These C242T effects were further confirmed using p22phox shRNA engineered HeLa cells and Nox2-/- coronary microvascular endothelial cells. Clinical significance was investigated using saphenous vein segments from non CHD subjects after phlebectomies. TT (C242T) allele was common (prevalence of ~22%) and compared to CC, veins bearing TT allele had significantly lower levels of Nox2 expression and O2.- generation in response to high glucose challenge. Conclusions— C242T SNP causes p22phox structural changes that inhibit endothelial Nox2 activation and oxidative response to TNFα or high glucose stimulation. C242T SNP may represent a natural protective mechanism against inflammatory cardiovascular diseases.