Protective effect of estrogens and catecholestrogens against peroxidative membrane damagein vitro

The antioxidant effects of natural estrogens (estrone E₁; 17β-estradiol), synthetic estrogens (17α-ethynylestradiol, EE₂; mestranol, MES; diethylstilbestrol, DES) and catechle-strogens (2-hydroxyestradiol; 4-hydroxyestradiol 4-OHE₂) on lipid peroxidation induced by different means in rat liver microsomes were investigated. The extent of lipid peroxidation was determined by measuring thiobarbituric acid reactive substances. Prooxidants included Fe³⁺/ADP/reduced NADPH, Fe²⁺/ascorbate,tert-butyl hydroperoxide (t-BOOH) and 2,2′-azobis (2-amidinopropane) (AAPH). Estrogens and catecholestrogens decreased lipid peroxidation in all four systems tested. In the iron/ascorbate model it was shown that (i)-OHE₂ and DES had analogous patterns of inhibition, irrespective of the presence of NADPH or the functional integrity of the microsómes, and (ii) the antioxidant activities of E₁, EE₂ and MES were dependent on the assay conditions with the activity being markedley higher when estrogen metabolism was favored. When peroxidation was initiated by the peroxyl radical generator AAPH, the inhibitory effects observed were least pronounced. Our data also showed that, in each of the systems, all inhibitors displayed the same order of inhibitory potency with DES and catecholestrogens being the most potent antioxidants under all experimental conditions used. The present results confirm earlier findings and point toward a link between estrogen metabolism and estrogen antioxidant activity. The data also indicate that estrogens and catecholestrogens interact with the peroxidative process at different levels with their interactions with iron or the metal-derived species being the most important modes of inhibition.     

Promotion of iron-induced rat liver microsomal lipid peroxidation by copper

Although copper has been demonstrated to promote lipid peroxidation in a number of systems, the mechanisms involved have not been fully defined. In this study, the role of copper in modifying lipid peroxidation has been explored in rat hepatic microsomes. In an in vitro system containing reduced glutathione (GSH, 200 μM) and Tris buffer, pH 7,4, cupric sulfate (1–50 μM) potentiated lipid peroxidation induced by ferrous sulfate (10 μM) but was unable to elicit peroxidation in the absence of iron. Higher levels of cupric sulfate (100 μM or greater) were inhibitory. The nature as well as the extent of the peroxidative response of microsomes to cupric sulfate were dependent on glutathione levels in addition to those of iron. Cupric sulfate (100 μM) strongly potentiated ferrous ion-induced lipid peroxidation in the presence of 400–800 μM GSH, while it inhibited peroxidation at lower levels of GSH (0–200 μM) and did not affect ferrous ion-induced peroxidation with glutathione levels of 3–10 mM. The potentiating effect of copper on ferrous ion-induced lipid peroxidation was further explored by investigating: (1) potential GSH-mediated reduction of cupric ions; (2) potential copper/GSH-mediated reduction of ferric ions (formed by oxidation during incubation); and (3) possible promotion of propagation reactions by copper/GSH. Our results indicate that cupric ions are reduced by GSH and thus are converted from an inhibitor to an enhancer of iron-induced lipid peroxidation. Cuprous ions appear to potentiate lipid peroxidation by reduction of ferric ions, rather than by promoting propagation reactions. Iron (in a specific Fe⁺²/Fe⁺³ ratio) is then an effective promoter of initiation reactions.     

Peroxide dependent and independent lipid peroxidation: Site-specific mechanisms of initiation by chelated iron and inhibition by α-tocopherol

Peroxidation of linoleic acid (LA) was catalyzed by Fenton reagent (H₂O₂, and Fe²⁺) in positively charged tetradecyltrimethylammonium bromide (TTAB) micelles, but not in negatively charged sodium dodecylsulfate (SDS) micelles. However, more hydroxyl radicals formedvia the Fenton reaction were trapped byN-t-butyl-α-phenylnitrone (PBN) in SDS micelles than in TTAB micelles. Generation of linoleic acid alkoxy (LO) radicals by Fe²⁺ via reductive cleavage of linoleic acid hydroperoxide (LOOH) resulted in peroxidation of LA and formation of PBN-LO· adducts in SDS micelles, but not in TTAB micelles. This LOOH dependent lipid peroxidation could be catalyzed in TTAB micelles in the presence of a negatively charged iron chelator, nitrilotriacetic acid (NTA). LO radicals formed by the LOOH dependent Fenton reaction were also trapped by PBN at the surface of TTAB micelles in the presence of NTA, but not in its absence. The consumption of a spin probe, 16-(N-oxyl-4,4′-dimethyloxazolidin-2-yl)stearic acid (16-NS) during the LOOH dependent Fenton reaction in the presence of NTA was higher in TTAB micelles of LA than in those of lauric acid (LauA), although the rates and amounts of LO radicals formed in the two types of fatty acid micelles were similar. The rates of 5-NS consumption in LA and LauA micelles were almost the same, and were lower than the rate of 16-NS in LA micelles. NTA-Fe²⁺ initiated peroxidation of LA in TTAB micelles without a lag time in the presence of LOOH, but after a lag period, peroxidation occurred without LOOH. α-Tocopherol inhibited peroxidation of LA catalyzed by Fenton reagent by scavenging OH radicals in TTAB micelles. In contrast, α-tocopherol enhanced free Fe²⁺ induced LOOH dependent lipid peroxidation through the regeneration of Fe²⁺ in SDS micelles. However, it inhibited NTA-Fe²⁺ induced LOOH dependent lipid peroxidation in TTAB micelles. The rate and amount of α-tocopherol oxidized by the Fe²⁺ induced, H₂O₂ dependent Fenton reaction were almost the same in TTAB micelles of LA and LauA. The oxidation of α-tocopherol by the NTA-Fe²⁺ induced, LOOH dependent Fenton reaction was greater and faster in LA micelles than in LauA micelles, although the rates of LO radical production in the two types of micelles were the same. During NTA-Fe²⁺ induced, LOOH dependent lipid peroxidation, α-tocopherol inhibited more effectively the consumption of 16-NS than 5-NS. The results are discussed in relation to the location of iron, the unsaturated bonding region of LA, the OOH group of LOOH, the radical trapping site of PBN, the spin sites of 5-NS and 16-NS, and the phenolic hydroxyl group of α-tocopherol in micelles with different charges. Based on a paper presented at the Symposium on Metals and Lipid Oxidation, held at the AOCS Annual Meeting in Baltimore, MD, April 1990.     

Effect of antioxidants on lipid peroxidation in iron-loaded rats

Indirect evidence has suggested that lipid peroxidation is associated with iron overload in vivo. As a measure of lipid peroxidation, pentane expired in the breath of rats loaded with an accumulated dose of either 100 mg or 186–200 mg of iron injected intraperitoneally as iron dextran was measured over a 7 to 8 week period, and the effect on pentane production of feeding antioxidant-supplemented diets was determined. By the seventh week of feeding the diets, rats fed 0.3% L-ascorbic acid produced 17% less (P=0.03) pentane than did rats fed the basal antioxidant-deficient diet, whereas rats fed 0.004% dl-α-tocopherol acetate produced 92% less (P<0.001). After being fed the basal diet for 7 weeks, iron-loaded rats produced 76±9 pmol pentane/100 g body wt/min. When synthetic antioxidants were added to the diet at a concentration of 0.25%, the order of effectiveness in decreasing pentane production after 1 week was: N,N′-diphenyl-p-phenylenediamine > ethoxyquin > butylated hydroxyanisole > butylated hydroxytoluene > propyl gallate ∼ no antioxidant. After removal of either ethoxyquin or N,N′-diphenyl-p-phenylenediamine from the diets for 1 week, pentane production increased to a high level. The total amount of lipid soluble fluorophores in individual spleens of rats fed N,N′-diphenyl-p-phenylenediamine, ethoxyquin, dl-α-tocopherol acetate, ascorbic acid and no antioxidant were correlated significantly with the corresponding total integrated amount of pentane produced by the individual rats over the 7 to 8 week period. This study has provided some of the most direct evidence to date that lipid peroxidation is associated with iron overload in vivo.     

The antioxidant properties of lycopene concentrate extracted from tomato paste

Lycopene concentrate (LC) containing 50 wt% lycopene was extracted from tomato paste. The antioxidant properties of LC were evaluated by means of chemiluminescence in four models. The four models were superoxide anions generated from pyrogallol autoxidation, hydroxyl radicals from Fenton reaction, singlet oxygens from OH⁻−NaClO−H₂O₂, and lipid peroxidation from 2,2′-azobis(2-amidinopropane)dihydrochloride-induced γ-linolenic acid. LC was an effective scavenger toward superoxide anions, hydroxyl radicals, and singlet oxygens, and also it could effectively reduce lipid peroxidation. The 50% efficient concentrations (EC₅₀) toward superoxide anions, hydroxyl radicals, lipid peroxidation and singlet oxygen were 0.75, 0.05, 0.1, and 1 mg/mL, respectively. In addition, changes of antioxidant behaviors with time were investigated. The time requirements of LC for effectively scavenging superoxide anions, hydroxyl radicals, and inhibiting lipid peroxidation were not higher than 6, 6, and 18 s, respectively.     

Role of lipid structure in the activation of phospholipase A2 by peroxidized phospholipids

The time course of hydrolysis of a mixed phospholipid substrate containing bovine liver 1,2-diacyl-sn-glycero-3-phosphocholine (PC) and 1,2-diacyl-sn-glycero-3-phosphoethanolamine (PE) catalyzed byCrotalus adamanteus phospholipase A₂ was measured before and after peroxidation of the lipid substrate. The rate of hydrolysis was increased after peroxidation by an iron/adenosine diphosphate (ADP) system; the presence of iron/ADP in the assay had a minimal inhibitory effect. The rate of lipid hydrolysis was also increased after the substrate was peroxidized by heat and O₂. Similarly, peroxidation increased the rate of hydrolysis of soy PC liposomes that did not contain PE. In order to minimize interfacial factors that may result in an increase in rate, the lipids were solubilized in Triton X-100. In mixtures of Triton with soy PC in the absence of PE, peroxidation dramatically increased the rate of lipid hydrolysis. In addition, the rate of hydrolysis of the unoxidizable lipid 1-palmitoyl-2-[1-¹⁴C]oleoyl PC incorporated into PC/PE liposomes was unaffected by peroxidation of the host lipid. These data are consistent with the notions that the increase in rate of hydrolysis of peroxidized PC substrates catalyzed by phospholipase A₂ is due largely to a preference for peroxidized phospholipid molecules as substrates and that peroxidation of host lipid does not significantly increase the rate of hydrolysis of nonoxidized lipids.     

Cytoprotective effect of tocopherols in hepatocytes cultured with polyunsaturated fatty acids

When highly unsaturated fatty acids are added to cell cultures, it can become important to include antioxidants in the culture medium to prevent cytotoxic peroxidation. To find an optimal antioxidant for this purpose, the effect of 50 μM α-tocopherol, γ-tocopherol, α-tocopheryl acetate, α-tocopheryl acid succinate, or α-tocopheryl phosphate, or of 1 μMN,N′-diphenyl-1,4-phenylenediamine, was investigated with respect to the agent's ability to prevent lactate dehydrogenase leakage in long-term rat hepatocyte cultures supplemented with 0.5 mM highly unsaturated fatty acids. Formation of thiobarbituric acid reactive substances in the cultures was also measured. α-Tocopheryl acid succinate was found to be the most effective cytoprotective compound, followed byN,N′-diphenyl-1,4-phenylenediamine, α-tocopherol, γ-tocopherol and α-tocopheryl acetate, and α-tocopheryl phosphate was without effect.     

Lipid peroxidation during n−3 fatty acid and vitamin E supplementation in humans

The purpose of this study was to investigate in healthy humans the effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) intake, alone or in combination with dL-α-tocopherol acetate (vitamin E) supplements on lipid peroxidation. Eightly men were randomly assigned in a double-blind fashion to take daily for 6 wk either menhaden oil (6.26 g, n−3 fatty acids) or olive oil supplements with either vitamin E (900 IU) or its placebo. Antioxidant vitamins, phospholipid composition, malondialdehyde (MDA), and lipid peroxides were measured in the plasma at baseline and week 6. At the same time, breath alkane output was measured. Plasma α-tocopherol concentration increased in those receiving vitamin E (P<0.0001). In those supplemented with n−3 fatty acids, EPA and DHA increased in plasma phospholipids (P<0.0001) and plasma MDA and lipid peroxides increased (P<0.001 and P<0.05, respectively). Breath alkane output did not change significantly and vitamin E intake did not prevent the increase in lipid peroxidation during menhaden oil supplementation. The results demonstrate that supplementing the diet with n−3 fatty acids resulted in an increase in lipid peroxidation, as measured by plasma MDA release and lipid peroxide products, which was not suppressed by vitamin E supplementation.     

Glutathione and antioxidants protect microsomes against lipid peroxidation and enzyme inactivation

The study investigated the relationship between lipid peroxidation and enzyme inactivation in rat hepatic microsomes and whether prior inactivation of aldehyde dehydrogenase (ALDH) exacerbated inactivation of other enzymes. In microsomes incubated with 2.5 μM iron as ferric sulfate and 50 μM ascorbate, ALDH, glucose-6-phosphate (G6Pase) and cytochrome P450 (Cyt-P450) levels decreased rapidly and concurrently with increased levels of thiobarbituric acid-reactive substances. Microsomal glutathioneS-transferase and nicotinamide adenine dinucleotide phosphate-cytochromec reductase were little affected during 1 hr of incubation. Addition of reduced glutathione partially protected, andN,N′-diphenyl-p-phenylenediamine and butylated hydroxytoluene completely protected microsomes against inactivation of ALDH, G6Pase and Cyt-P450, as well as lipid peroxidation induced by iron and ascorbate. ALDH was more susceptible than G6Pase to inactivation by iron and ascorbate, and was thus an excellent marker for oxidative stress. Inhibition of ALDH by cyanamide injection of rats exacerbated the inactivation of G6Pase in microsomes incubated with 0.1 mM, but not 25 μM 4-hydroxynonenal (4-HN). 4-HN did not stimulate lipid peroxidation. Thus, 4-HN may play a minor role in microsomal enzyme inactivation. In contrast, lipid, peroxyl radicals play an important role in microsomal enzyme inactivation, as evidenced by the prevention of both lipid peroxidation and enzyme inactivation by chain-breaking antioxidants.     

Natural antioxidants produced in oxidized lipid/amino acid browning reactions

1-Substituted pyrroles (1 and2) and1-substituted 2-(1′-hydroxypropyl)pyrroles (3–5) were produced in reactions between a lipid peroxidation product, 4,5(E)-epoxy-2(E)-heptenal, and the amino acid lysine. The antioxidative activity of compounds1–5 was studied. Oxidative stability was evaluated in refined soybean oil containing compounds1–5, butylated hydroxytoluene (BHT),n-propyl gallate orl-lysine, at concentrations of 50–200 ppm. Oils were either oxidized at 60°C and oxidation products determined by the thiobarbituric acid-reactive substances assay, or they were oxidized at 110°C by the Rancimat method. Although both methods gave similar results, greater differences were observed at 60°C than at 110°C. Addition of compounds1–5,l-lysine, BHT, and propyl gallate significantly (P<0.01) protected the oil against oxidation. The effectiveness order found was:l-lysine << compounds3–4 < compounds1–2 < compound5 ≈ BHT << propyl gallate.     

Involvement of vitamin E and protein thiols in the inhibition of microsomal lipid peroxidation by glutathione

Iron-ascorbate stimulated lipid peroxidation in rat liver microsomes can be inhibited by glutathione (GSH). The role of protein thiols and vitamin E in this process was studied in liver microsomes isolated from rats fed diets either sufficient or deficient in vitamin E and incubated at 37°C unde 100% O₂. Lipid peroxidation was induced by adding 400 μM adenosine 5′-triphosphate, 2.5 to 20 μM FeCl₃, and 450 μM ascorbic acid. One mL of the incubation mixture was removed at defined intervals for the measurement of thiobarbituric acid reactive substances (TBARS), protein thiols and vitamin E. In vitamin E sufficient microsomes, the addition of GSH enhanced the lag time prior to the onset of maximal TBARS accumulation and inhibited the loss of vitamin E. Treatment of these microsomes with the protein thiol oxidant diamide resulted in a 56% loss of protein thiols, but did not significantly change vitamin E levels. However, diamide treatment abolished the GSH-mediated protection against TBARS formation and loss of vitamin E during ascorbate-induced peroxidation. Liver microsomes isolated from rats fed a vitamin E deficient diet contained 40-fold less vitamin E and generated levels of TBARS similar to vitamin E sufficient microsomes at a 4-fold lower concentration of iron. GSH did not affect the lag time prior to the onset of maximal TBARS formation in vitamin E deficient microsomes although total TBARS accumulation was inhibited. Similar to what was previously found in vitamin E sufficient microsomes [Palamanda and Kehrer, (1992)Arch. Biochem. Biophys. 293, 103–109], GSH prevented the loss of protein thiols in vitamin E deficient microsomes. However, GSH did not protect efficiently against the loss of residual vitamin E in deficient microsomes. These data provide support for the concept that GSH protects against microsomal lipid peroxidation by maintaining protein thiols, and consequently vitamin E, in the reduced state. The lack of protection in vitamin E deficient microsomes may be related to the inability of such low levels of vitamin E to inhibit peroxidation.     

Positional distribution of fatty acids in cardiolipin of mitochondria from 21-day-old rats

Pure cardiolipins (1,3-diphosphatidylglycerol) were prepared from mitochondria of heart, liver and kidney from 21-day-old male Wistar rats and submitted toNaja naja venom phospholipase A₂ (EC 3.1.1.4) action. Incubation conditions were controlled carefully, and a complete hydrolysis of cardiolipin to lysocardiolipin {di [1 (1″) acylsn-glycero-3-phosphoryl] 1′, 3′-sn-glycerol} and fatty acids from positions 2 (2″) was obtained in less than two hr practically without side reactions. Cardiolipins from the three organs contained low levels of saturated fatty acids; stearic acid accounted for 0.4–0.7% and palmitic acid for 1.4–3.5% of total fatty acids. These percentages apparently depended on the organ. In all three cases, linoleic acid was the major component, but its percentage varied from 62–78% of total fatty acids. Acyl chains linked to positions 1 (1″) of all three cardiolipin preparations exhibited a similar pattern; they were composed of linoleic acid for 85–89%. This fatty acid also was the main component esterified at position 2 (2″), but its percentage was much more variable: from 39.8% in heart to 51.2% in kidney and 67.8% in liver mitochondria. The remaining acids comprised octadecenoic and polyunsaturated fatty acids with more than 18 carbon atoms in different proportions. As opposed to other phospholipids,cis-vaccenic acid, and not oleic acid, was the main octadecenoic acid present in cardiolipins. Octadecenoic acids were nine- to 10-fold more concentrated at positions 2 (2″) than at positions 1 (1″). The percentage ofcis-vaccenic acid was four- to five-fold higher than that of oleic acid at positions 2 (2″), whereas oleic acid dominated at positions 1 (1″). From results presented in this study and selected literature data, it may be concluded that fatty acids are asymmetrically distributed in cardiolipins of different origins, with linoleic acid showing a definite preference for position 1 (1″).     

Occurrence of wax esters and 1-O-alkyl-2,3-diacylglycerols in goat epididymal sperm plasma membrane

Two unusual lipid classes were detected by thin-layer chromatography in the neutral lipids derived from goat cauda-epididymal sperm plasma membrane. The lipids were identified as wax esters and 1-O-alkyl-2,3-diacylglycerols based on chromatographic properties, identity of their hydrolysis products, and infrared/¹H nuclear magnetic resonance spectral evidence. The membrane containedca. 3 and 5 μg/mg protein of wax esters and alkyldiacylglycerols, respectively. The relative proportions of wax esters and alkyldiacylglycerols in the total neutral lipids were 1.5% and 2.4%, respectively. The lipids contained fatty acids with chain lengths of C₁₄ to C₂₂. The major fatty acids of the wax esters were 14∶0, 16∶0, 16∶1ω7, 18∶0 and 18∶1ω9. The fatty acids in alkyldiacylglycerol were 16∶0, 18∶0, 22∶5ω3 and 22∶6ω3. Alkyldiacylglycerol was particularly rich in docosahexaenoic acid 22∶6ω3) representing 30% of the total fatty acids. The alcohols of wax ester were all saturated with C₂₀–C₂₉ carbon chains. The deacylated products derived from alkyldiacylglycerols were identified as hexadecyl, octadecyl and octadec-9′-enyl glycerol ethers.     

Studies on the reactions of ω-carbethoxy fatty acid sodioesters with brominated compounds

Several ω-carbethoxy fatty acid sodioesters (C₂H₅-O₂ CCHNa(CH₂)_n−1-CO₂C₂H₅ and C₂H₅-O₂CCHNa(CH₂)_n−2-CHNaCO₂ C₂H₅ where n/6, 7, or 8) were condensed with ω-bromoaliphatic esters (Br(CH₂)_zCO₂C₂H₅ where z-5, 8 or 10), α,ω-dibromoalkanes (Br(CH₂)_n′-Br where n′=4, 6 or 8) and α,α′ m- or p-xylene. Tri- and tetraesters and several carbethoxy cycloheptanones which arose mainly from Dieckmann type condensations were isolated. The infrared spectra of the tri- and tetraesters were compared with those of their parent ω-carbethoxy fatty acid ester and additional peaks in the regions ofV _C=O andV _C-O-C were observed. Reactions involving the formation of both the α-sodio and α,α′ salts are also discussed.     

Inhibition by the PAF antagonist WEB 2086 of PAF induced inositol-1,4,5-trisphosphate production in human platelets

Platelet-activating factor (PAF) activates human platelets by binding to a putative PAF receptor which evokes the rapid formation of inositol-1,4,5-trisphosphate (IP₃) by phospholipase C mediated phosphatidylinositol-4,5-bisphosphate (PIP₂) hydrolysis. Stimulation of [³H]inositol-labeled human platelets by PAF (1 nM-1μM) resulted in a concentration-dependent increase of intracellular IP₃, IP₂ and inositolmonophosphate (IP₁). IP₁ levels increased up to three-fold upon maximum stimulation by 100 nM PAF. The EC₅₀ concentration for PAF was 1.2±0.3 nM. Addition of the hetrazepinoic PAF antagonist, WEB 2086, inhibited PAF stimulated hydrolysis of PIP₂ in a dose-dependent manner. WEB 2086 (100 μM) blocked inositol-1,4,5-trisphosphate formation down to baseline levels (IC₅₀=33±12 μM WEB 2086). In thrombin and ADP stimulated platelets, inositol phosphate (IP) generation was not influenced by WEB 2086. It is concluded that WEB 2086 selectively antagonizes PAF-induced increases in IP and does not interfere directly with intracellular signal transduction. Instead, WEB 2086, which has been shown to bind specifically and with high affinity (K_i 15 nM) to human platelets, acts as a competitive antagonist at the PAF receptor level. Based on a paper presented at the Third International Confrence on Platelet-Activating Factor and Structurally Related Alkyl Ether Lipids, Tokyo, Japan, May 1989.     

Syntheses and Crystal Structures of Two Inorganic–Organic Hybrid Frameworks Constructed from Pyridine-2,5-Dicarboxylic Acid

Two novel inorganic–organic hybrid frameworks of [Co(2,5-pydc)(4,4′-bipyo)_0.5(H₂O)₃ · 3H₂O] _n (1) and [Cu_1.5Gd(2,5-pydc)₃(2,2′-bipyo)(H₂O)₄ · 2H₂O] _n (2) (2,5-pydc = pyridine-2,5-dicarboxylic acid; 4,4′-bipyo = 4,4′-bipyridine-N,N′-dioxide; 2,2′-bipyo = 2,2′-bipyridine-N,N′-dioxide) were prepared. Both compounds have been characterized by the elemental analyses, IR spectra, TG analysis and the single crystal diffraction. The salient structural feature for both compounds 1 and 2 is that the 1D chain and the mononuclear fragment are connected by strong hydrogen bond interactions to form 2D structure.     

Synthesis and characterization of polyimides based on isopropylidene-containing bis(ether anhydride)s

Two bis(ether anhydride)s, 4,4′-[1,4-phenylenebis(isopropylidene-1,4-phenyleneoxy)]-diphthalic anhydride (IV _a) and 4,4′-[isopropylidenebis(1,4-phenylene)dioxy]diphthalic anhydride (IV _b), were prepared in three steps starting from the nucleophilic nitrodisplacement reaction of 4-nitrophthalonitrile with α,α ′-bis(4-hydroxyphenyl)-1,4-diisopropylbenzene (I _a) and 4,4′-isopropylidenediphenol (I _b) in N,N-dimethylformamide (DMF) in the presence of potassium carbonate. The bis(ether anhydride)s IV _a and IV _b were polymerized with various aromatic diamines to obtain two series of poly(ether amic acid)s VI _a–g and VII _a–g with inherent viscosities in the range of 0.30∼0.74 and 0.29∼1.01 dL/g, respectively. The poly(ether amic acid)s were converted to poly(ether imide)s VIII _a–g and IX _a–g by thermal cyclodehydration. Most of the poly(ether imide)s could afford flexible and tough films, and they showed high solubility in polar solvents such as N-methyl-2-pyrrolidone (NMP), N,N-dimethylacetamide, and m-cresol. The obtained poly(ether imide) films had tensile strengths of 45∼83 MPa, elongations-to-break of 6∼27%, and initial modulus of 0.6∼1.7 GPa. The T_gs of poly(ether imide)s VIII _a–g and IX _a–g were in the range of 194∼210 and 204∼243 °C, respectively. Thermogravimetric analysis (TG) showed that 10% weight loss temperatures of all the polymers were above 500 °C in both air and nitrogen atomspheres.     

Production and functional characteristics of protein concentrates

Protein concentrates derived from common dry beans (Phaseolus vulgaris L.) may improve world protein resources, reduce on-site preparation time and expense and provide improved nutrition. Several different methods have been studied for the production of these concentrates, including alkali extraction and isoelectric precipitation, ultrafiltration, air-classification and salt extraction under high salt concentrations. Recent studies using solid-solid dry roasting, pin milling and air-classification resulted in the following percent mass fractions: hull/fiber (10%), coarse/starch (70%) and fine/protein (20%). Results indicated that the protein fractions were approximately 45–50% protein, low in raffinose and stachyose and hadtrypsin inhibitor activity reduced to about half of that of raw beans. Nitrogen Solubility Index (NSI) ranged from 33–70% and was associated with the thermal conditions applied during dry roasting. The flours had a bland flavor without the bitter off-flavors which have traditionally limited the use of dry beans in formulated foods. Most minerals and phytic acid tended to be associated with protein flour; however, although iron may have been bound to phytic acid, its absorption by anemic rats was not hindered by the presence of endogenous phytic acid. These flours produced acceptable products when incorporated into cookies, doughnust, quick breads and leavened doughs. Presented at the 78th American Oil Chemists' Society Annual Meeting, May 27–21, 1987, New Orleans, LA.     

Hydrothermal Synthesis of Metal–Organic Coordination Polymers Constructed from Asymmetric Semi-rigid V-shaped Dicarboxylate and Nitrogen-Contained Mixed Ligands

Three new coordination polymers, [Ni(2,4′-oba)(1,10-phen)] _n (1), {[Ni (2,4′-Hoba)₂(4,4′-bipy)(H₂O)₂]·2H₂O} _n (2) and [Zn(2,4′-oba) (4,4′-bipy)] _n (3) (2,4′-H₂oba = 2-(4-carboxyphenoxy)benzoic acid, 1,10- phen = 1,10-phenanthroline, and 4,4′-bipy = 4,4′-bipyridine) have been obtained by hydrothermal synthesis. The framework structures of these polymeric complexes have been determined by single-crystal X-ray diffraction studies. Complex 1 exhibits double-helical chains formed by π–π stacking interactions from the phenyl rings of the 1,10-phen ligands. Complex 2 forms a two-dimensional supramolecular architecture directed by hydrogen bonding. Complex 3 exhibits a three-dimensional structure; Schl?fli symbol of {4⁴·6¹⁰·8}. The luminescent property of compound 3 is discussed.     

Chain-breaking fused heterocyclic antioxidants: Antioxidant activities of 9H-xanthene-2,7-diols and α-tocopherol upon liposomal membranes

We evaluated the antioxidant activities of 9H-xanthene-2,7-diols and α-tocopherol (α-Toc) upon the oxidation of soybean phosphatidylcholine liposomal membranes, induced by 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH) and 2,2′-azobis(2,4-dimethylvaleronitrile (AMVN). The stoichiometric factors of 9H-xanthene-2,7-diols, initiated with water-soluble AAPH and lipid-soluble AMVN, were 1.9–2.7 and 1.2–1.8-fold greater than those of α-Toc, respectively. The consumption profile of the antioxidant confirmed that 9H-xanthene-2,7-diol was completely consumed within the induction period (t _inh) and that the 9H-xanthene-2,7-diol oxidation product was formed. When all oxidation product was depleted, t _inh was terminated, and rapid oxidation occurred. These results suggested that the antioxidant activities of 9H-xanthene-2,7-diol depend not only on the initial hydrogen abstraction from 9H-xanthene-2,7-diol but also on a second hydrogen abstraction from the residual phenolic OH group of the oxidation product. Ascorbic acid (AsA) could not scavenge the radicals by itself in the lipid bilayer. However, when 9H-xanthene-2,7-diol was located in the lipid bilayer, the addition of AsA into the aqueous phase prolonged t _inh and reduced the rate of decay of 9H-xanthene-2,7-diol.