Water-soluble Oxidation Products Research Articles

Composition and Properties of Oxidation Products of Heavy Oil Resid Asphaltenes

Asphaltenes of various heavy oil resids are oxidized by aqueous sodium percarbonate solutions at 200°C and 4 MPa pressure. The composition and properties of the obtained products are analyzed. Water-soluble oxidation products in the asphaltene oxidation products comprise 47.4-49.4%. Products of oxidative condensation of asphaltenes enriched with hydroxyl, ether, and carboxyl groups dominate in the composition of water-insoluble oxidation products. The water-soluble oxidation products represent carboxylic acid concentrate. The characteristics of the structural-group composition of the obtained oxidation products are disclosed. The possibility of practical utilization of asphaltene oxidation products as adhesion additives to road asphalt and for removal of phenol from water is demonstrated.

Surface modification of poly(ethylene terephthalate) fibers induced by radio frequency air plasma treatment

The surface chemical and physical modifications of poly(ethylene terephthalate) (PET) fibers induced by radiofrequency air plasma treatments were correlated with the characteristics of the discharge parameters and the chemical composition of the plasma itself, to identify the plasma-induced surface processes prevailing under different operating conditions. Treated polymer surfaces were characterized by water droplet absorption time measurements and XPS analysis, as a function of the aging time in different media, and by AFM analysis. They exhibited a remarkable increase in hydrophilicity, accompanied by extensive etching and by the implantation of both oxygen- and nitrogen-containing polar groups. Etching was mainly a consequence of ion bombardment, yielding low molecular weight, water soluble oxidation products, while surface chemical modifications were mainly due to the action of neutral species on the plasma-activated polymer surface.

ReviewMicrobial Attack on Sulphur-Containing Hydrocarbons: Implications for the Biodesulphurisation of Oils and Coals

The literature covered by this review deals with microbiological attack on organic sulphur-containing hydrocarbons, often represented by the model heterocyclic compound, dibenzothiophene. The objective of most research in this area is to find suitable biocatalysts for removal at the industrial scale of organic sulphur from fossil fuels. Ideally, microbes for desulphurisation should attack the sulphur in hydrocarbons without altering the carbon skeleton or affecting other valuable components of the oil or coal. Organisms able to cleave carbon—sulphur bonds releasing sulphur atoms (as sulphate in aerobic mechanisms or hydrogen sulphide in anaerobic processes) appear to fulfil these requirements. Biodesulphurisation mechanisms which convert sulphur heterocycles into water-soluble oxidation products could cause the loss of the hydrocarbons associated with the sulphur hetero atom from the bulk fuel. Biodesulphurisation is biologically possible and practically attainable at the laboratory scale. The development of microbial processes for removing organic sulphur from oils and coals is as yet unproven and is unlikely to be economic.

Incorporation of chylomicron fatty acids into the developing rat brain.

The developing brain obtains polyunsaturated fatty acids from the circulation, but the mechanism and route of delivery of these fatty acids are undetermined. 14C-labeled chylomicrons were prepared by duodenal infusion of [1-14C]16:0, [1-14C]18:2(n-6), [1-14C]18:3(n-3), or [1-14C]22:6(n-3) into adult donor rats, and were individually injected into hepatectomized 2-wk-old suckling rats. After minor correction for trapped blood in the brain, the incorporation of chylomicron fatty acids after 30 min was nearly half that of a co-injected free fatty acid reference. [1-14C]22:6(n-3)-labeled chylomicrons showed an average 65% greater incorporation than chylomicrons prepared from the other fatty acids. This apparent selectivity may have been partly due to lower oxidation of 22:6(n-3) in the brain compared to the other fatty acids tested, based on recovered water-soluble oxidation products. The bulk of the radioactivity in the brain was found in phospholipid and triacylglycerol, except that animals injected with [1-14C]22:6(n-3) chylomicrons showed considerable incorporation also into the fatty acid fraction instead of triacylglycerol. These data show that chylomicrons may be an important source of fatty acids for the developing rat brain.

Uptake of fatty acids by the developing rat brain.

Polyunsaturated fatty acids are avidly taken up by the developing rat brain. To explore the specificity of this process, [1-14C]labeled 16:0, 18:2n-6, 18:3n-3, and 22:6n-3 each were co-injected with [3H]18:1n-9 into the jugular vein of two-wk-old functionally hepatectomized and sham-operated control rats. The radioactivities present in the brain, liver and serum were assessed 30 min after injection. Uptake of labeled fatty acids into brain lipids steadily increased with increasing degree of unsaturation, with more than twice as much uptake of 22:6n-3 compared to 16:0. Phosphatidylcholine was the principal radioactive species in the brain except for animals injected with [1-14C]22:6n-3, in which more of the label was incorporated into phosphatidylethanolamine. Determination of water-soluble oxidation products in the brain and serum revealed that the greater uptake of the more unsatrated fatty acids did not result from differences in rates of degradation.

Effects of feeding high-fat diets to rats: metabolism of erucic acid (C 22:1 n-9) in the perfused liver and secretion of metabolites to the perfusate.

The liver metabolism of erucic acid, 22:1 n-9, was studied in rat livers perfused with 14-14C-labelled erucic acid for 15 and 60 min, determining the distribution of radioactivity in the perfusate and in the lipids of the liver cell organelles. The rats were adapted to a high-fat diet containing either partially hydrogenated marine oil (PHMO) or palm oil (PO), both adjusted to a 10% content of linoleic acid. The results showed an efficient uptake and metabolism of erucic acid with the secretion to the perfusate medium of labelled free fatty acids other than erucic acid, labelled phospholipids as well as water soluble oxidation products. Only minor amounts of secreted labelled triglycerides were found within 60 min of perfusion. In the liver, labelled lipids accumulated in the endoplasmic reticulum, after 15 min mainly as free fatty acids, after 60 min as triglycerides. The esterification pathway, including the erucic acid given as well as chain-shortened fatty acids, seemed to be preferred under the experimental conditions and with adequate linoleic acid in the diet. A chain shortening of erucic acid probably took place in both peroxisomes and mitochondria shown by the presence of labelled 18:1 and 20:1 in the organelle-bound phospholipids. A chain shortening was found in both dietary groups, and is assumed to be an affect of the adaptation to a high-fat diet rather than an effect of dietary very long chain monoenoic fatty acids. Somewhat higher levels were found in the PHMO group, but the difference in the dietary fat was not a major factor in the liver lipid adaptation.

Oxidation of sulphide minerals—VI Ferrous and ferric iron in the water-soluble oxidation products of iron sulphide minerals

A pseudo-kinetic method has been developed for determining the ferrous and ferric iron in the water-soluble oxidation products of pyrrhotite, pyrite and chalcopyrite, and ores and concentrates containing them. Two determinations are required for each material. In one, the total iron is determined with 1,10-phenanthroline after reduction to Fe(II). In the other, the reduction of Fe(III) is retarded by complexation with fluoride. The difference in the amount of ferrous phenanthranoline complex produced in these two determinations is a function of the original FE(III) concentration and of time.

The Effect of Fatty-acid Autoxidation Products on Blood Coagulation

Polyunsaturated fatty acids were allowed to autoxidise in air over 4 days. The water soluble oxidation products were extracted at daily intervals and tested for their effect on blood coagulation. After 1 day there was slight acceleration of the recalcification and RVV times, but from 2-4 days the extracts became increasingly inhibitory. The P.T. and P.T.T. were also inhibited. In the thrombin generation test the extracts delayed the appearance of thrombin, but the peak thrombin level was increased and its rate of decay was reduced. When added to phospholipid the extracts altered their coagulant activity. The presence of autoxidation products could account for some of the variable results obtained with different preparations of phospholipids.

Stimulation of ketogenesis by dibutyryl cyclic AMP in isolated rat hepatocytes.

The effect of dibutyryl cyclic 3',5'-AMP (dbcAMP) on the oxidation of 1-14Cpalmitate to water-soluble material and ketone bodies was investigated in isolated rat liver cells prepared by perfusion of the liver with collagenase and hyaluronidase. About two-thirds of the label in water-soluble oxidation products was recovered as ketone bodies which were distributed approximately equally between β-hydroxybutyrate and acetoacetate plus acetone. Dibutyryl cAMP (1.0 × 10−3 M) and epinephrine (8 × 10−5 M) both enhanced ketone body formation. Sodium butyrate,which mimics the inhibitory effect of dbcAMP on palmitate oxidation to CO2, had no effect on ketogenesis. The rate of ketogenesis was directly related to the molar ratio of palmitate to albumin. The efficacyof dbcAMP in stimulatingketogenesis also depended upon the molar ratio of plmitate to albumin.Thus, ketone body formation was enhanced by 105, 52, and 13% at molar ratiosof 0.1, 0.4,and 1.6 respectively. Since these results suggest that cyclic AMP modulates...

The Effect of Ionizing Irradiation on the Oxidation of Palmitate-1- 14 C by Thymus and Liver

New Zealand rabbits, fasted for 12 hours, were subjected to 500 rads of whole-body irradiation. K+-palmitate-1-14C oxidation was assayed with the 600 X g supernatant of thymus and liver homogenates, in the presence of ATP, at various time intervals from irradiation. For a period of 24 hours following irradiation, oxidation by liver preparations was not significantly affected. The rate of oxidation by thymus was decreased to less than one-third of the control value within 12 hours from irradiation and, at 24 hours, was almost completely abolished. Increased ATP concentration could increase only to a small extent the oxidation by thymus preparations of irradiated animals. Oxidation by isolated thymus mitochondria was also inhibited by irradiation. Counting of the water-soluble oxidation products of palmitate-1-14C suggests that the inhibition is not due to the impairment of the reactions of the citric acid cycle. The non-esterified fatty acid concentration of thymus was not altered at 12 hours following irradiation. Esterification of K+-palmitate-l-14C into the thymus lipids was not affected 12 hours after irradiation.

The inhibition of certain mitochondrial enzymes by fatty acids oxidized by ultraviolet light or ascorbic acid

1. 1. The relation between lipide oxidation and the activity of succinoxidase, choline oxidase, and aminoxidase of rat liver mitochondria has been examined following ultraviolet irradiation, incubation of mitochondria with ultraviolet-irradiated methyl linolenate and methyl linoleate, and incubation with ascorbic acid. 2. 2. Ultraviolet irradiation of mitochondria produced an oxidation of lipide which was directly proportional to the period of irradiation. Succinoxidase and choline oxidase were inhibited in direct proportion to the extent of lipide oxidation. Incubation of irradiated mitochondria with reduced glutathione gave a partial (< 33 %) restoration of succinoxidase activity. 3. 3. Incubation of mitochondria with ascorbic acid resulted in an inhibition of succinoxidase, choline oxidase, and aminoxidase which was directly proportional to lipide oxidation, as in the case of ultraviolet irradiation. Liver slices incubated with ascorbic acid also showed an increased lipide oxidation and decreased succinoxidase activity. 4. 4. Succinoxidase was inhibited by ultraviolet-irradiated methyl linolenate and its water-soluble oxidation products. The unoxidized ester had little or no effect. Methyl linolenate and methyl linoleate oxidized to the same degree by ultraviolet irradiation had equal inhibitory action on succinoxidase. 5. 5. The results indicate that the effects of ultraviolet light on cells may be mediated in part by the oxidation products of lipide constituents.