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In situ and laboratory estimations of total O2 intake rates and diffusive O2 fluxes in the eastern South Atlantic Ocean reveal an agreement between O2 intake rates and diffusive O2 uptake rate with a minor difference between both uptakes which is associated with sediment macrofauna. Diffusive O2 intake and O2-penetration depths are associated directly with organic content and inversely with water depth. Laboratory measurements of total O2 uptake rates are lesser than in situ measurements, while that of diffusive uptake rates are greater than in situ measurements.

Multivariate statistical methods were used to analyse the vitality of Scots pines (Pinus sylvestris L.) by means of various biochemical, physiological, and nutritional characteristics, irrespective of tree age and without site-specific information. The vitality model was developed in three steps. First, artificial neural networks were used to select a minimal set of biomarkers as input variables with respect to the output variable circular surface increment (regression problem). In the second step, vitality states were classified by using the selected biomarkers (cluster analysis). Finally, discriminant analysis was applied to assign Scots pines to one of four classified vitality states. Sulfate sulfur (SO42−-S), non-protein-nitrogen (NPN), arginine (Arg), and chlorophylla (Chla) proved to be the best dynamic input variables to reliably determine the vitality of Scots pines. As the results of regression problem solutions showed, the optimized neural network found growth responses to the driving variables that are valid for both young and mature pine stands. However, the sensitivity analysis of the neural network also indicated that of the four variables, sulfate is the least sensitive. Nevertheless, the sulfate response of the network can be successfully used to analyze the specific effects of multiple exposure on the vitality of Scots pines. To summarize final vitality model enables the vitality of Scots pines to be evaluated without reference to tree age or knowing the specific forest conditions. [Copyright &y& Elsevier]

Studies the degradation of 2-trans,5-cis-tetradecadienoyl-coenzyme A, a metabolite of oleic acid, in rat heart mitochondria. Kinetic measurements of metabolite and cofactor formation; Occurrence of oleate beta-oxidation via the classical isomerase-dependent pathway; Effect of NADH on the degradation.

Discusses the control of fatty acid oxidation in the heart with emphasis on the energy-linked regulation of this process. Relationship between the energy-dependent rate of fatty acid oxidation and the intramitochondrial ratio of [acetyl-CoA]:[free CoA]; Effects of coenzymes and fatty acid metabolites on the activities of enzymes of fatty acid oxidation.

Abstract: Age models for the emplacement time of mass flow deposits from the Cape Blanc Debris Flow, the Mauritania Slide Complex and a levee of the Mauritania Canyon were obtained by offshore X-ray fluorescence (XRF) element stratigraphy on five gravity cores, allowing the assessment of slope instability in this part of the NW African continental margin with respect to climate-related sea-level variations during the Quaternary. The Cape Blanc Debris Flow emplaced approximately 155kyr ago whereas deposition of the Mauritania Slide Complex is linked to the rapid sea-level rise at the Pleistocene/Holocene boundary. Turbidites on a levee of the Mauritania Canyon close to the Mauritania Slide Complex occurred at stage boundaries. These findings agree with other studies which show that the NW African continental margin has been unstable over the last Quaternary cycles, and that downslope sediment transport is frequently coupled to periods of climatic changes at stage boundaries. [Copyright &y& Elsevier]

Abstract: The changes in waste management policy caused by the massive generation of waste materials (e.g. construction and demolition waste material, municipal waste incineration products) has led to an increase in the reuse and recycling of waste materials. For environmental risk assessment, test procedures are necessary to examine waste materials before they can be reused. In this article, results of column and lysimeter leaching tests having been applied to inorganic compounds in a reference demolition waste material are presented. The results show a good agreement between the leaching behaviour determined with the lysimeter unit and the column units used in the laboratory. In view of less time and system requirements compared to lysimeter systems, laboratory column units can be considered as a practicable instrument to assess the time-dependent release of inorganic compounds under conditions similar to those encountered in a natural environment. The high concentrations of elements in the seepage water at the initial stage of elution are reflected by the laboratory column leaching tests. In particular, authorities or laboratories might benefit and have an easy-to-use, but nevertheless reliable, method to serve as a basis for decision-making. [Copyright &y& Elsevier]

Human 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10) is a mitochondrial enzyme encoded by the SCHAD gene, which escapes chromosome X inactivation. 17β-HSD10/SCHAD mutations cause a spectrum of clinical conditions, from mild mental retardation to progressive infantile neurodegeneration. 17β-HSD10/SCHAD is essential for the metabolism of isoleucine and branched-chain fatty acids. It can inactivate 17β-estradiol and steroid modulators of GABAA receptors, and convert 5α-androstanediol into 5α-dihydrotestosterone (DHT). Certain malignant prostatic epithelial cells contain high levels of 17β-HSD10, generating 5α-DHT in the absence of testosterone. 17β-HSD10 has an affinity for amyloid-β peptide, and might be linked to the mitochondrial dysfunction seen in Alzheimer''s disease. This versatile enzyme might provide a new drug target for neuronal excitability control and for intervention in Alzheimer''s disease and certain cancers. [Copyright &y& Elsevier]

Presents a study on the crystal structure and reaction mechanism of Escherichia coli 2,4-dienoyl-CoA reductase. Background on the reductase escherichia coli 2,4-dienoyl-CoA, an iron-sulfur flavoenzyme required for the metabolism of unsaturated fatty acids with double bonds at even carbon positions; Reaction initiated by hydride transfer from NADPH to FAD; Inspection of the substrate binding pocket explaining the relative promiscuity of the enzyme.

Abstract: Several mouse models for mitochondrial fatty acid β-oxidation (FAO) defects have been developed. So far, these models have contributed little to our current understanding of the pathophysiology. The objective of this study was to explore differences between murine and human FAO. Using a combination of analytical, biochemical and molecular methods, we compared fibroblasts of long chain acyl-CoA dehydrogenase knockout (LCAD−/−), very long chain acyl-CoA dehydrogenase knockout (VLCAD−/−) and wild type mice with fibroblasts of VLCAD-deficient patients and human controls. We show that in mice, LCAD and VLCAD have overlapping and distinct roles in FAO. The absence of VLCAD is apparently fully compensated, whereas LCAD deficiency is not. LCAD plays an essential role in the oxidation of unsaturated fatty acids such as oleic acid, but seems redundant in the oxidation of saturated fatty acids. In strong contrast, LCAD is neither detectable at the mRNA level nor at the protein level in men, making VLCAD indispensable in FAO. Our findings open new avenues to employ the existing mouse models to study the pathophysiology of human FAO defects. [Copyright &y& Elsevier]

Abstract: The β-oxidation of oleic acid in Saccharomyces cerevisiae (S. cerevisiae) was studied by comparing the growth of wild-type cells on oleic acid or palmitic acid with the growth of mutants that either had a deletion in the YOR180c (DCI1) gene reported to encode Δ3,5,Δ2,4-dienoyl-CoA isomerase (dienoyl-CoA isomerase) or in the PTE1 gene encoding peroxisomal thioesterase 1. Growth of wild-type cells was indistinguishable from that of YOR180c mutant cells on either palmitic acid or oleic acid, whereas the PTE1 mutant grew slower and to a lower density on oleic acid but not on palmitic acid. The identification of 3,5-tetradecadienoic acid in the medium of wild-type cells but not in the medium of the PTE1 mutant proves the operation of the thioesterase-dependent pathway of oleate β-oxidation in S. cerevisiae. Dienoyl-CoA isomerase activity was very low in wild-type cells, fourfold higher in the YOR180c mutant, and not associated with purified Yor180c protein. These observations support the conclusion that the YOR180c gene does not encode dienoyl-CoA isomerase. [Copyright &y& Elsevier]

Abstract: This study of sediments from the Cap Timiris Canyon demonstrates that geochemical data can provide reliable age-depth correlation even of highly turbiditic cores and attempts to improve our understanding of how turbidite emplacement is linked to climatic-related sea-level changes. The canyon incises the continental margin off NW Africa and is an active conduit for turbidity currents. In sediment cores from levee and intrachannel sites turbidites make up 6–42% of sediment columns. Age models were fitted to all studied cores by correlating downcore element data to dated reference cores, once turbidite beds had been removed from the dataset. These age models enabled us to determine turbidite emplacement times. The Cap Timiris Canyon has been active at least over the last 245kyr, with turbidite deposition seemingly linked to stage boundaries and glacial stages. The highly turbiditic core from the intrachannel site postdates to≈15kyr and comprises Holocene and late Pleistocene sediments. Turbidite deposition at this site was associated especially with the rapid sea-level rise at the Pleistocene/Holocene transition. During the Holocene, turbidity current activity decreased but did not cease. [Copyright &y& Elsevier]

Abstract: The steroids allopregnanolone and allotetrahydrodeoxycorticosterone (3α,5α-THDOC) are positive allosteric modulators of GABAA receptors, generated by the reduction of 5α-dihydroprogesterone (5α-DHP) and 5α-DHDOC, respectively, under the catalysis of human type 3 3α-hydroxysteroid dehydrogenase (HSD). However, brain enzymes catalyzing the conversion of such tetrahydrosteroids back to the corresponding 5α-dihydrosteroids remain to be identified. Characterization of human type 10 17β-HSD provides a new insight into its importance for the oxidation of steroid modulators of GABAA receptors. The apparent catalytic efficiency (kcat/Km) of this enzyme for the oxidation of allopregnanolone and 3α,5α-THDOC are 432 and 1381min-1mM-1, respectively. This enzyme has negligible 3-ketosteroid reductase activity for 5α-DHP and 5α-DHDOC even in an acidic environment. Immunoreactivity against 17β-HSD10 was found in a number of neuronal populations. Taken together, evidence suggests that 17β-HSD10 is the brain enzyme capable of catalyzing the oxidation of steroid modulators of GABAA receptors. [Copyright &y& Elsevier]

The degradation of elaidic acid (9-trans-octadecenoic acid), oleic acid, and stearic acid by rat mitochondria was studied to determine whether the presence of a trans double bond in place of a cis double bond or no double bond affects β-oxidation. Rat mitochondria from liver or heart effectively degraded the coenzyme A derivatives of all three fatty acids. However, with elaidoyl-CoA as a substrate, a major metabolite accumulated in the mitochondrial matrix. This metabolite was isolated and identified as 5-trans-tetradecenoyl-CoA. In contrast, little or none of the corresponding metabolites were detected with oleoyl-CoA or stearoyl-CoA as substrates. A kinetic study of long-chain acyl-CoA dehydrogenase (LCAD) and very long-chain acyl-CoA dehydrogenase revealed that 5-trans-tetradecenoyl-CoA is a poorer substrate of LCAD than is 5-cis-tetradecenoylCoA, while both unsaturated acyl-CoAs are poor substrates of very long-chain acyl-CoA dehydrogenase when compared with myristoyl-CoA. Tetradecenoic acid and tetradecenoylcarnitine were detected by gas chromatography/mass spectrometry and tandem mass spectrometry, respectively, when rat liver mitochondria were incubated with elaidoyl-CoA but not when oleoyl-CoA was the substrate. These observations support the conclusion that 5-trans-tetradecenoyl-CoA accumulates in the mitochondrial matrix, because it is less efficiently dehydrogenated by LCAD than is its cis isomer and that the accumulation of this β-oxidation intermediate facilitates its hydrolysis and conversion to 5-trans-tetradecenoylcarnitine thereby permitting a partially degraded fatty acid to escape from mitochondria. Analysis of this compromised but functional process provides insight into the operation of β-oxidation in intact mitochondria. [ABSTRACT FROM AUTHOR]

The degradation of 2-trans,5-cis-tetradecadienoyl-CoA, a metabolite of oleic acid, by the purified complex of fatty acid oxidation from Escherichia coli was studied to determine how much of the metabolite is converted to 3,5-cis-tetradecadienoyl-CoA and thereby diverted from the classical, isomerase-dependent pathway of oleate β-oxidation. Approximately 10% of the 2,5-intermediate was converted to the 3,5-isomer. When the latter compound was allowed to accumulate, it strongly inhibited the flux through the main pathway. Since Δ3,5,Δ2,4-dienoyl-CoA isomerase was not detected in E. coli cells grown on oleate, the 3,5-intermediate cannot be metabolized via the reductase-dependent pathway. However, it was hydrolyzed by a thioesterase, which was most active with 3,5-cis-tetradecadienoyl-CoA as substrate and which was induced by growth of E. coli on oleate. An analysis of fatty acids present in the medium after growth of E. coli on oleate revealed the presence of 3,5-tetradecadienoate, which was not detected after cells were grown on palmitate or glucose. Altogether, these data prompt the conclusion that oleate is mostly degraded via the classical, isomerase-dependent pathway in E. coli but that a small amount of 2-trans,5-cistetradecadienoyl-CoA is diverted from the pathway via conversion to 3,5-cis-tetradecadienoyl-CoA by Δ³,&*Delta;²enoyl-CoA isomerase. The 3,5-intermediate, which would strongly inhibit β-oxidation if allowed to accumulate, is hydrolyzed, and the resultant 3,5-tetradecadienoate is excreted into the growth medium. This study provides evidence for the novel function of a thioesterase in β-oxidation. [ABSTRACT FROM AUTHOR]

In vitro enzyme assays have demonstrated that human type 10 17β-hydroxysteroid dehydrogenase (17β-HSD10) catalyzes the oxidation of 5α-androstane-3α,17β-diol (adiol), an almost inactive androgen, to dihydrotestosterone (DHT) rather than androsterone or androstanedione. To further investigate the role of this steroid-metabolizing enzyme in intact cells, we produced stable transfectants expressing 17β-HSD10 or its catalytically inactive Y168F mutant in human embryonic kidney (HEK) 293 cells. It was found that DHT levels in HEK 293 cells expressing 17β-HSD10, but not its catalytically inactive mutant, will dramatically increase if adiol is added to culture media. Moreover, certain malignant prostatic epithelial cells have more 17β-HSD10 than normal controls, and can generate DHT, the most potent androgen, from adiol. This event might promote prostate cancer growth. Analysis of the 17β-HSD10 sequence shows that this enzyme does not have any ER retention signal or transmembrane segments and has not originated by divergence from a retinol dehydrogenase. The data suggest that the unique mitochondrial location of this HSD [Eur. J. Biochem. 268 (2001) 4899] does not prevent it from oxidizing the 3α-hydroxyl group of a C19 sterol in living cells. The experimental results lead to the conclusion that mitochondrial 17β-HSD10 plays a significant part in a non-classical androgen synthesis pathway along with microsomal retinol dehydrogenases. [Copyright &y& Elsevier]

Gravity driven mass-flow deposits proven by sedimentary and digital echosounder data are indicative for prevailing dynamic sedimentary conditions along the continental margin of the western Argentine Basin. In this study we present geochemical data from a total of 23 gravity cores. Pore-water SO4 is generally depleted within a few meters below the sediment surface by anaerobic oxidation of methane (AOM). The different shapes of SO4 profiles (concave, kink- and s-type) can be consistently explained by sedimentary slides possibly in combination with changes in the CH4 flux from below, thus, mostly representing transient pore-water conditions. Since slides may keep their original sedimentary signature, a combined analysis and numerical modeling of geochemical, physical properties, and hydro acoustic data could be applied in order to reconstruct the sedimentary history. We present first order estimates of the dating of sedimentary events for an area where conventional stratigraphic methods failed to this day. The results of the investigated sites suggest that present day conditions are the result of events that occurred decades to thousands of years ago and promote a persisting mass transport from the shelf into the deep-sea, depositing high amounts of reactive compounds. The high abundance of reactive iron phases in this region maintains low hydrogen sulfide levels in the sediments by a nearly quantitative precipitation of all reduced sulfate by AOM. For the total region we estimate a SO4 (or CH4) flux of 6.6 × 1010 moles per year into the zone of AOM. Projected to the global continental slope and rise area, this may sum up to about 2.6 × 1012 moles per year. Provided that the sulfur is completely fixed in the sediments it is about twice the global value of the recent global sulfur burial in marine sediments of 1.2 × 1012 moles per year as previously estimated. Thus, AOM obviously contributes very significantly to the regulation of global sulfur reservoirs, which is hitherto not sufficiently recognized. This finding may have implications for global geochemical models, as sulfur burial is an important control factor in the development of atmospheric oxygen levels over time. [Copyright &y& Elsevier]

A full-length cDNA of mouse type 10 17β-hydroxysteroid dehydrogenase (17β-HSD10) was cloned from brain, representing the accurate nucleotide sequence information that rendered possible an accurate deduction of the amino acid sequence of the wild-type enzyme. A comparison of sequences and three-dimensional models of this enzyme revealed that structures previously reported by other groups carry either a truncated or mutated amino-terminal sequence. Fusion of the first 11 residues of the wild-type enzyme to the green fluorescent protein directed the reporter protein into mitochondria. Thus, the N-terminus was identified as a mitochondrial targeting signal that accounts for the intracellular localization of the mouse enzyme. This enzyme is normally associated with mitochondria, not with the endoplasmic reticulum as suggested by its trivial name ‘endoplasmic reticulum-associated amyloid-β biding protein (ERAB)’. After its C-terminal region was used to raise rabbit anti-17βHSD10 antibodies, immunogold electron microscopy showed that an abundance of this enzyme could be found in hippocampal synaptic mitochondria of βAPP transgenic mice, but not in normal controls. High levels of this enzyme may disrupt steroid hormone homeostasis in synapses and contribute to synapse loss in the hippocampus of the mouse Alzheimer’s disease model. [Copyright &y& Elsevier]