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Folate supplementation is becoming increasingly popular not only to decrease homocystein, a long with the finding that moderate hyperhomocysteinaemia is a cardiovascular risk factor but also diminish some other risks related to folate depletion. The aim of the study was to investigate whether folic acid supplementation leads to behavioural and electrophysiological changes in rats. Therefore, 30 male Wistar rats were divided to three groups. Each of animal groups was consisted of 10 animals. Folic acid was applied to rats by gavage for 8 weeks. Group I as a control group was taking folic acid-free water by gavage throughout the duration of the experiment. Groups II and III were treated with 2.0 mg/kg/day and 20.0 mg/kg/day of folic acid, respectively. Behavioural effects were evaluated by open field motor activity and by acoustic startle response. Electrophysiological examination was done by recording spontaneous activity and sensory evoked potentials from the visual, somatosensory, as weil as auditory cortex. No significant effects on motor activity or acoustic startle response were observed. Both doses of folic acid shortened the latency of the visual cortical evoked potential (p

Sulfate reduction rates have been studied in surface sediments from 17 stations of the southeast Atlantic continental margin, 15 degrees 38'S-27 degrees 57' S, the area outlying from Angola and Namibia. Depth-integrated sulfate reduction rates were highest at 1300 m. They went down exponentially with greater water depth. Depth-integrated sulfate reduction rates agreed with known patterns of coastal upwelling intensity and correlated well with surface organic carbon concentrations. Lateral downslope transport of organic carbon apparently takes place, based on sulfate reduction rates as a function of depth and compared with sediment trap data. Kinetics of oxygen utilization in surface sediments are much faster than those for anaerobic organic carbon remineralization. The cause is not clear.

A study was undertaken to design, synthesize and identify an inhibitor acting as an irreversible inactivator of the long-chain specific beta-oxidation system in intact liver mitochondria and relate it to the fatty acid degradation of the organelle. It was believed that fatty acid degradation involves a two-enzyme system responsible for the catalysis of a full cycle of beta-oxidation. It was discovered that the thiolase inhibitor in the form 4-bromotiglic acid was most responsive to the chemical inactivation as a result of its vital sulfhydryl group.

A place close to the center of the amino-terminal half of the Escherichia coli multifunctional fatty acid oxidation protein is properly protected all through the enoyl-coenzyme A (CoA) hydratase family. Amino-terminal region of the E. coli multifunctional protein has a common CoA-binding place for various substrates that interact at the active zone with the key residues for either the D- and L-dehydration of 3-hydroxyacyl-CoA or the enoyl-CoA isomerization.

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.

Mitochondrial beta-oxidation degrades 3-phenylpropionic acid (PPA), facilitating the development the principle behind beta-oxidation. The low activity of peroxisomal acyl CoA oxidase, associated with 3-phenylpropionyl-CoA confirmed peroxisomal beta-oxidation of PPA to be a slow process.

The control of fatty acid oxidation in heart is reviewed with special emphasis on the energy-linked regulation of this process. Studies with perfused working hearts and isolated mitochondria have revealed an inverse relationship between the energy-dependent rate of fatty acid oxidation and the intramitochondrial ratio of (acetyl-CoA):(free CoA) at sufficiently high concentrations of fatty acids. Studies with isolated enzymes demonstrated a strong inhibition of 3-ketoacyl-CoA thiolase by acetyl-CoA at low concentrations of free CoA. Together these observations prompted the proposal that the rate of fatty acid oxidation is tuned to the energy demand of heart via the regulation of 3-ketoacyl-CoA thiolase by the (acetyl-CoA):(free CoA) ratio. Evidence in support of this regulatory model has been obtained with isolated rat heart mitochondria in which either the activity of 3-ketoacyl-CoA thiolase was decreased by use of mechanism-based inhibitors or the intramitochondrial ratio of (acetyl-CoA):(free CoA) was adjusted with L-carnitine. Because intermediates of Beta-oxidation normally do not accumulate in mitochondria, it remains unclear how the entry of fatty acyl-CoA into the Beta-oxidation spiral is tuned to the activity of 3-ketoacyl-CoA thiolase. A control of fatty acid oxidation in heart via the regulation of carnitine palmitoyltransferase I by malonyl-CoA has not been established even though malonyl-CoA is present in this tissue and strongly inhibits myocardial carnitine palmitoyltransferase I.

The degradation pathway of unsaturated fatty acids containing double bonds extending from odd-numbered carbon atoms was elucidated. The analysis focused on the degradation pathway of 5-enoyl-CoAs, which are formed during beta-oxidation of these fatty acids. The results showed that 5-enoyl-CoAs are initially dehydrogenated to 2,5-dienoyl-CoAs, which then undergo isomerization to 2,4-dienoyl-CoAs. The isomerized derivatives can then be reduced by the NADPH-dependent 2,4-dienoyl-CoA reductase. This process demonstrates how odd-numbered double bonds can be reductively removed during beta-oxidation.

A novel long-chain acyl-CoA thioesterase, named thioesterase III, that is expressed when Escherichia coli is grown on long-chain fatty acids is described. The newly characterized thioester III, might function in the thioesterase-dependent pathway of [beta]-oxidation oleic acid and other unsaturated fatty acids.

The molecular mechanism of reduction by Escherichia coli NADPH-dependent 2,4-dienoyl-CoA reductase (DCR), an auxiliary enzyme required for [beta]-oxidation of unsaturated fatty acids is described.