Indicator products: a new tool for lifetime prediction of polymeric materials

The possible correlation between the degree of degradation in the polymer matrix and the release of indicator products was investigated. The degree of degradation was measured by following the molar mass changes by size exclusion chromatography, while indicator products were analyzed by gas chromatography-mass spectrometry. The degree of degradation in polyethylene and polyethylene vinyl acetate matrix after thermooxidation was found to be in correlation with the amount of dicarboxylic acids and lactones formed during aging, while the degree of degradation in photooxidized polyethylene could be predicted from the amount of dicarboxylic acids. The relative amount of lactones compared to the relative amount of dicarboxylic acids increased if the oxidation temperature was increased. However, the total amount of indicator products was in correlation with the remaining number average molar mass and the number of chain scissions caused by oxidation. The amount of butanedioic acid and butyrolactone correlated well with the total amount of dicarboxylic acids and lactones, respectively. Thus, instead of the whole compound classes, butanedioic acid or butyrolactone alone could be used as indicators of oxidation. The detected correlation offers a novel tool for making lifetime predictions and studying the long-term properties of polymeric materials.     

The role of the copper-binding enzyme – laccase – in the biodegradation of polyethylene by the actinomycete Rhodococcus ruber

Polyethylene is considered one of the most durable plastic polymers. Virtually, non-biodegradable polyethylene accumulates in the environment, thus posing an ecological threat to man and wildlife. We have previously isolated a strain of the actinomycete Rhodococcus ruber (designated C208; EC 1.10.3.2.) capable of utilizing and degrading polyethylene. Here, we report the role of the bacterial copper-binding enzyme, laccase, in the oxidation and degradation of polyethylene by this strain. Copper markedly affected the induction and activity of laccase, resulting in polyethylene degradation. mRNA quantification by RT-PCR, revealed a 13-fold increase in laccase mRNA levels, in copper-treated cultures compared with the untreated control. Addition of copper to C208 cultures containing polyethylene enhanced the biodegradation of polyethylene by 75%, as compared with the non-amended control. Furthermore, when an extracellular isoform of laccase collected from the media of copper-induced cells was incubated with polyethylene, reductions of 20% and 15% were obtained in the Average Molecular Weight (Mw) and Average Molecular Number (Mn) with the polymer, respectively. FTIR analysis of similar polyethylene films incubated with the extracellular laccase exhibited an increase in the carbonyl peak, indicating that enzymatic oxidation by laccase plays a major role in the biodegradation of polyethylene.     

Oxidation in ultrahigh molecular weight polyethylene and cross-linked polyethylene acetabular cups tested against roughened femoral heads in a hip joint simulator

This study was aimed at comparing the oxidative degradation of commercial acetabular cups made of cross-linked polyethylene (XLPE) and conventional ultrahigh molecular weight polyethylene (UHMWPE). After testing against deliberately scratched CoCrMo femoral heads in a hip joint simulator, the cups, microtomed parallel to the articulating surface, were analyzed by IR spectroscopy. Due to the potential for artifacts caused by absorbed contaminants, the IR spectra were compared only after hexane extraction; actually, XLPE was found to absorb more serum than UHMWPE. The two sets of unworn acetabular cups showed different oxidation patterns with consequently different distributions of carbonyl species; unworn XLPE was characterized by lower contents of carbonyl species and hydrogen-bonded alcohols and higher contents of trans-vinylene species than unworn UHMWPE. Upon simulator testing, UHMWPE showed more significant changes in oxidation indexes and distribution of carbonyl compounds than XLPE, confirming a better wear behavior for XLPE under the adopted testing conditions.     

In vitro labeling of solid tissues with tritiated thymidine for autoradiographic detection of S-phase nuclei.

In vitro measurement of the thymidine labeling index (TLI) of solid tissues requires hyperbaric oxygenation and is potentiated by blockade of thymidylate synthetase by 5-fluoro-2'-deoxyuridine (FUdR) to favor uptake of tritiated thymidine (3H-TdR). Hyperbaric oxygenation can be achieved in a simple system through injection of oxygen into rubber-stoppered test tubes. Incubations are carried out in Hanks' balanced salt solution in a shaker bath at 37 C for 2 hours; an FUdR concentration of approximately 1 micron is optimal. Autoradiographic exposure for 1 week or less is sufficient for TLI measurements on human tissues. With 3 to 4 atmospheres oxygen tension, incorporation of 3H-TdR is sufficient for TLI measurement throughout slices of tissue cut 1 mm thick or less. Mincing of tissue is not necessary, and the anatomic continuity seen in ordinary histological preparations is preserved. A gradient of labeling intensity is present from the surface to the interior of the tissue, but sufficient intensity of labeling for detection of DNA synthesis can be achieved in the interior of the section. The gradient can be reduced only slightly by prior incubation in 3H-TdR with hyperbaric oxygen at 0 C. The method permits TLI measurements on the same specimens, including needle biopsies, that are used for pathologic diagnosis.     

Blocking of mixed lymphocyte reaction by spleen cells from total lymphoid-irradiated mice involves interruption of the IL-2 pathway.

Treatment with total lymphoid irradiation (TLI) before organ transplantation results in high incidences of donor-specific tolerance. However, the exact mechanism of how TLI induces or maintains tolerance is not known. In many experimental systems of tolerance, lack of IL-2 plays a central role in tolerance induction, as stimulation of immunocompetent cells with Ag in an insufficient IL-2 environment results in tolerance. To examine whether tolerance induction by TLI might involve the IL-2 pathway, we examined how TLI cells affect the ability of immunocompetent cells to produce IL-2 and express IL-2R in the MLR. Responder cells from MLR cultures in which cells from TLI-treated mice were added proliferated 50 to 70% less and produced 68 to 94% less IL-2 bioactivity than responder cells from control cultures. However, coculture of TLI cells into MLR did not alter IL-2R expression on responder cells, as measured by two-color FACS analysis. We found no evidence that TLI cells deleted MLR responder cells. Interestingly, exogenous IL-2 did not restore proliferation of MLR responder cells. These results suggest that TLI may induce tolerance by interrupting the IL-2 pathway in immunocompetent cells. Moreover, that exogenous IL-2 failed to restore immunocompetence suggests that tolerance in the TLI model may be easy to induce and very stable, and provides a rationale for the higher incidences of donor-specific tolerance after TLI treatment.     

Distribution of taurine-like immunoreactivity in the mouse liver during ontogeny and after carbon tetrachloride or phenobarbital intoxication

Summary The ontogenic pattern of development of taurine-like immunoreactivity (TLI) was studied in the mouse liver. The effect on adult mice of carbon tetrachloride or phenobarbital treatment was also examined. Light-microscopically, granules of TLI were first found in the liver from 17-day-old embryos, diffusely distributed throughout the lobules. These positive granules increased with age, were most numerous in the two-week-old mouse, and were notably decreased in the central region of some lobules in the three-week-old mouse. In mature mice, hepatocytes containing TLI-positive granules were distributed unevenly in each liver lobule, and were located predominantly in the peripheral region. Electron-microscopically, TLI was observed in small vesicles in the cytoplasm of hepatocytes and was found mainly in the cisternal lumen of smooth-surfaced endoplasmic reticulum. Some taurine-positive vesicles surrounding the reticulum seemed to associate with the protoplasm. Similar positive vesicles were often located near the bile canaliculi. In carbon tetrachloride-intoxicated mature mice, TLI was no longer limited to the peripheral region of lobules; hepatocytes situated in the central region of lobules also contained intense TLI. In mice injected with a small and repeated dose of phenobarbital, the distribution pattern of TLI was similar to that in the untreated group. However, in mice injected with a large dose of phenobarbital, TLI was markedly increased, especially in the central region of lobules. The results demonstrate that the distribution pattern of TLI in mouse liver changes during development, and that the pattern in mature mice is affected by intoxication with carbon tetrachloride or a toxic dose of phenobarbital.     

Integrated Approach for Polycyclic Aromatic Hydrocarbon Solubilization from the Soil Matrix to Enhance Bioremediation

Polycyclic aromatic hydrocarbons (PAHs) are known to be toxic to living organisms and have been identified as carcinogenic. In this study, a pathway of surfactant flushing, chemical oxidation, and biological treatment is proposed to remediate the soils polluted with the hydrophobic PAHs. Different surfactants such as Tween 80, Brij 35, sodium dodecyl sulfate (SDS), and polyethylene glycol (PEG) 6000 were tested in order to increase the PAH solubilization from the soil matrix. The maximum desorption efficiency of naphthalene and anthracene were found to be 56.5% and 59%, respectively, when Brij and SDS were used. The soluble PAH in the aqueous phase was amended with sodium thiosulfate (3%) to oxidize the PAH into a more bioavailable form. The chemical oxidation with subsequent biodegradation by Pseudomonas aeruginosa exhibited the relatively high PAH degradation rate (1.24 times higher) when compared with chemical oxidation alone. These results display the efficiency of chemical pretreatment of PAH-contaminated soil for improved bioremediation.     

In Vitro Labeling of Solid Tissues with Tritiated Thymidine for Autoradiographic Detection of S-Phase Nuclei

In vitro measurement of the thymidine labeling index (TLI) of solid tissues requires hyperbaric oxygenation and is potentiated by blockade of thymidylate synthetase by 5-fluoro-2' -deoxyuridine (FUdR) to favor uptake of tritiated thymidine (³H-TdR). Hyperbaric oxygenation can be achieved in a simple system through injection of oxygen into rubber-stoppered test tubes. Incubations are carried out in Hanks' balanced salt solution in a shaker bath at 37 C for 4 hours; an FUdR concentration of approximately 1 μM is optimal. Autoradiographic exposure for 1 week or less is sufficient for TLI measurements on human tissues. with 3 to 4 atmospheres oxygen tension, incorporation of ³H-TdR is sufficient for TLI measurement throughout slices of tissue cut 1 mm thick or less. Mincing of tissue is not necessary, and the anatomic continuity seen in ordinary histological preparations is preserved. A gradient of labeling intensity is present from the surface to the interior of the tissue, but sufficient intensity of labeling for detection of DNA synthesis can be achieved in the interior of the section. the gradient can be reduced only slightly by prior incubation in ³H-TdR with hyperbaric oxygen at 0 C. the method permits TLI measurements on the same specimens, including needle biopsies, that are used for pathologic diagnosis.     

Evidence That Ceriporiopsis subvermispora Degrades Nonphenolic Lignin Structures by a One-Electron-Oxidation Mechanism

The white-rot fungus Ceriporiopsis subvermispora is able to degrade nonphenolic lignin structures but appears to lack lignin peroxidase (LiP), which is generally thought to be responsible for these reactions. It is well established that LiP-producing fungi such as Phanerochaete chrysosporium degrade nonphenolic lignin via one-electron oxidation of its aromatic moieties, but little is known about ligninolytic mechanisms in apparent nonproducers of LiP such as C. subvermispora. To address this question, C. subvermispora and P. chrysosporium were grown on cellulose blocks and given two high-molecular-weight, polyethylene glycol-linked model compounds that represent the major nonphenolic arylglycerol-(beta)-aryl ether structure of lignin. The model compounds were designed so that their cleavage via one-electron oxidation would leave diagnostic fragments attached to the polyethylene glycol. One model compound was labeled with (sup13)C at C(inf(alpha)) of its propyl side chain and carried ring alkoxyl substituents that favor C(inf(alpha))-C(inf(beta)) cleavage after one-electron oxidation. The other model compound was labeled with (sup13)C at C(inf(beta)) of its propyl side chain and carried ring alkoxyl substituents that favor C(inf(beta))-O-aryl cleavage after one-electron oxidation. To assess fungal degradation of the models, the high-molecular-weight metabolites derived from them were recovered from the cultures and analyzed by (sup13)C nuclear magnetic resonance spectrometry. The results showed that both C. subvermispora and P. chrysosporium degraded the models by routes indicative of one-electron oxidation. Therefore, the ligninolytic mechanisms of these two fungi are similar. C. subvermispora might use a cryptic LiP to catalyze these C(inf(alpha))-C(inf(beta)) and C(inf(beta))-O-aryl cleavage reactions, but the data are also consistent with the involvement of some other one-electron oxidant.     

Comparison of S-phase fractions measured by flow cytometry and autoradiography in human transplant tumors

The 3H-thymidine labeling index (TLI) and the percentage of cells in the S-phase have been determined by autoradiography and by flow cytometry, (FCM), respectively, in six malignant tumors of human origin transplanted on athymic nude mice. The Dean and Jett model and the graphical model were used to determine the percent of S-phase cells by FCM. Cell cycle analysis was performed using 1) no correction for background; 2) an algebraic function for background correction; and 3) an exponential function for background subtraction. Each of these three data sets was evaluated using both the Dean and Jett model and a graphical model for the evaluation of DNA histograms. The S-phase fractions (SPF) were compared to the corresponding labeling index results. SPF without background correction were 1.54 times higher than the TLI. SPF, after correction using the algebraic model, were 1.29-fold higher than the TLI, whereas SPF obtained after background subtraction according to the exponential model were only 1.05-fold higher than the TLI. Student's t-test revealed significant differences between the mean TLI values (16.25 +/- 9.06) and the mean SPF obtained by FCM without background correction (mean 25.0 +/- 9.36, P less than 0.01), but not between the mean TLI values and the mean SPF percentages after algebraic (mean 21.0 +/- 10.29) and exponential background correction (mean 17.11 +/- 11.59), P greater than 0.05 each. There was no difference between the results obtained using the Dean and Jett model and those obtained using the graphic evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Degradation of ethylene glycol and polyethylene glycols by methanogenic consortia.

Methanogenic enrichments capable of degrading polyethylene glycol and ethylene glycol were obtained from sewage sludge. Ethanol, acetate, methane, and (in the case of polyethylene glycols) ethylene glycol were detected as products. The sequence of product formation suggested that the ethylene oxide unit [HO-(CH2-CH2-O-)xH] was dismutated to acetate and ethanol; ethanol was subsequently oxidized to acetate by a syntrophic association that produced methane. The rates of degradation for ethylene, diethylene, and polyethylene glycol with molecular weights of 400, 1,000, and 20,000, respectively, were inversely related to the number of ethylene oxide monomers per molecule and ranged from 0.84 to 0.13 mM ethylene oxide units degraded per h. The enrichments were shown to best metabolize glycols close to the molecular weight of the substrate on which they were enriched. The anaerobic degradation of polyethylene glycol (molecular weight, 20,000) may be important in the light of the general resistance of polyethylene glycols to aerobic degradation.     

Microbial degradation and deterioration of polyethylene – A review

The ability of microorganisms to use polyethylene as a carbon source has only been recently established. This result has significance both from an environmental point of view, due to the accumulation of millions of tons of waste plastics every year, but also regarding the conservation of integrity for infrastructures incorporating this plastic. A number of microorganisms with the ability to grow on polyethylene have been isolated. The effects of these microorganisms on the physiochemical properties of this polymer have been described; these include changes in crystallinity, molecular weight, topography of samples and the functional groups found on the surface. Although the bio-degradation and bio-deterioration of polyethylene has been demonstrated by several researchers, the enzymes involved and mechanisms associated with these phenomena are still unclear. Nevertheless, it is recognized that both enzymatic and abiotic factors (such UV light) can mediate the initial oxidation of polyethylene chains, and given the chemical similarity between polyethylene and olefins it has been suggested that the metabolic pathways for degradation of hydrocarbons can be used once the size of polyethylene molecules decrease to an acceptable range for enzyme action (typically from 10 to 50 carbons). The long-range structure and morphology of polyethylene have shown important roles, with amorphous regions being more prone to microbial attack than crystalline ones. This review focuses on the recent hypotheses and experimental findings regarding the biodegradation of polyethylene.     

Suppression of pokeweed mitogen-stimulated immunoglobulin production in patients with rheumatoid arthritis after treatment with total lymphoid irradiation

Patients with intractable rheumatoid arthritis (RA) were treated with total lymphoid irradiation (TLI, 2000 rad). We previously reported long-lasting clinical improvement in this group associated with a persistent decrease in circulating Leu-3 (helper subset) T cells and marked impairment of in vitro lymphocyte function. In the present experiments, we studied the mechanisms underlying the decrease in pokeweed mitogen stimulated immunoglobulin (Ig) secretion observed after TLI. Peripheral blood mononuclear cells (PBL) from TLI-treated patients produced 10-fold less Ig (both IgM and IgG) in response to pokeweed mitogen than before radiotherapy. This decrease in Ig production was associated with the presence of suppressor cells in co-culture studies. By using responder cells obtained from normal individuals (allogeneic system), PBL from eight of 12 patients after TLI suppressed Ig synthesis by more than 50%. In contrast, PBL from the same patients before TLI failed to suppress Ig synthesis. Suppression by post-TLI PBL was also demonstrated in an autologous system by using responder cells cryopreserved before TLI. Again, only cells obtained after TLI were suppressive in four of seven patients. PBL with suppressive activity contained suppressor T cells, and the latter cells bore the Leu-2 surface antigen. In 50% of the patients studied, suppressor cells were also found in the non-T fraction and were adherent to plastic. Interestingly, the Leu-2+ cells from TLI-treated patients were no more potent on a cell per cell basis than purified Leu-2+ cells obtained before TLI. Additional experiments suggested that the suppression mediated by T cells after TLI is related to the increased ratio of Leu-2 to Leu-3 cells observed after radiotherapy.     

Opposite effects of total lymphoid irradiation on T cell-dependent and T cell-independent antibody responses

The effect of total lymphoid irradiation (TLI) on the primary antibody response to the dinitrophenylated heterologous protein, keyhole limpet hemocyanin (DNP-KLH), in complete Freund's adjuvant (CFA), and to the trinitrophenylated polysaccharide antigen, Brucella abortus (TNP-BA), was studied in BALB/c mice. The antibody response to both antigens was diminished in comparison with nonirradiated mice when antigens were injected within 3 days after TLI. When the mice were immunized 30 days after completion of TLI the antibody response to DNP-KLH in CFA was still diminished, but the antibody response to TNP-BA was enhanced 5- to 10-fold as compared with that of control animals. The opposite effect of TLI on the two antibody responses was also observed in a syngeneic primary adoptive transfer system.     

Use of total lymphoid irradiation (TLI) in studies of the T cell-dependence of autoantibody production in rheumatoid arthritis

The effect of total lymphoid irradiation (TLI) on T cell-dependent and -independent humoral immune responses was studied in patients with intractable rheumatoid arthritis (RA). The serum levels of several autoantibodies and of antibodies to diphtheria (DT) and tetanus (TT) toxoids and to pneumococcal polysaccharide (PPS; 12 antigenic types) were studied before and after TLI. In addition, the patients were given a booster injection of DT and TT and a single injection of pneumococcal vaccine after radiotherapy. Antibody levels to DT and TT decreased about twofold after TLI and did not rise significantly (p greater than 0.05) after a booster injection. However, there was no reduction in antibody levels to PPS after TLI, and a significant rise in titers was observed after a single vaccination (p less than 0.01). The serum levels of rheumatoid factor (RF), anti-nuclear antibody (ANA), and granulocyte associated IgG rose slightly after TLI. Thus, the autoantibodies and antibodies to polysaccharides appear to be relatively independent of helper T cell function, which is markedly reduced after TLI. On the other hand, antibodies to protein antigens such as DT and TT appear to be more closely dependent upon T helper function in man, as has been reported in rodents. The findings suggest that T cell-independent autoantibody responses alone do not maintain the joint disease activity in RA, because improvement in joint disease after TLI has been reported.     

The effects of total lymphoid irradiation upon corneal vascularization in the rat following chemical cautery

The effect of total lymphoid irradiation (TLI), a form of radiotherapy known to suppress the number of circulating lymphocytes, on corneal neovascularization was assessed in rats. The corneas of TLI-treated rats were cauterized with silver/potassium nitrate one day after delivering gamma irradiation in five equal fractions (10 Gy total dose). Corneal neovascularization was assessed quantitatively by computerized image analysis in corneal flat preparations 4 days after corneal injury following perfusion of the circulation with India ink. TLI reduced the total leukocyte, lymphocyte, neutrophil, and platelet counts below preirradiation levels. The number of circulating lymphocytes was reduced more than neutrophils and platelets. TLI caused a predominance of cytotoxic/suppressor lymphocytes. Tissue examinations 4 days after TLI disclosed an absence of the thymus, as well as a markedly reduced number and size of lymph nodes. TLI rats had less corneal vascularization than nonirradiated controls. Our findings are consistent with the hypothesis that leukocytes play an important role in the pathogenesis of corneal angiogenesis following chemical cautery, but this study does not indicate how TLI suppresses corneal neovascularization.     

Total lymphoid irradiation leads to transient depletion of the mouse thymic medulla and persistent abnormalities among medullary stromal cells

Mice given multiple doses of sublethal irradiation to both the thymus and the peripheral lymphoid tissues showed major transient, and some persistent disruptions in general thymic architecture and in thymic stromal components. At 2 wk after total lymphoid irradiation (TLI), the thymus lacked identifiable medullary regions by immunohistochemical analyses. Medullary stromal cells expression MHC Ag or a medullary epithelial cell Ag, as well as medullary macrophages, were undetectable. Instead, the processes of cortical epithelial cells were observed throughout the entire thymus. Strikingly, thymocyte subsets with mature phenotypes (CD4+CD8- and CD4-CD8+) were present in the apparent absence of a medulla. This early, gross effect was rapidly reversed such that by 1 to 2 mo after TLI, medullary areas with MHC Ag-positive cells were evident. However, abnormalities in a subset of medullary stromal cells appeared to be more persistent. Medullary epithelial cells, identified by the MD1 mAb, were greatly reduced in number and abnormally organized for at least 4 mo after TLI. In addition, macrophages containing endogenous peroxidase activity, normally abundant in medullary regions, were undetectable at all times examined after TLI. Therefore, this irradiation regimen induced both transient and long term effects in the thymus, primarily in medullary regions. These results suggest that TLI may be used as an experimental tool for studying the impact of selective depletion of medullary stromal cells on the development of specific T cell functions.     

Ethanol-induced inhibition of leukotriene degradation by omega-oxidation

omega-Oxidation of leukotrienes is a major pathway in the degradation and inactivation of these proinflammatory mediators. Ethanol inhibited this process in vivo and in vitro. In rat liver in vivo the catabolism of LTE4 to omega-carboxylated leukotrienes was inhibited by 57% by an ethanol dose of 25 mmol/kg body mass administered intragastrically. The site of inhibition was the oxidation of omega-hydroxy-N-acetyl-LTE4 to omega-carboxy-N-acetyl-LTE4 resulting in an accumulation of omega-hydroxy-N-acetyl-LTE4 and of N-acetyl-LTE4. Analogous results were obtained for the oxidative degradation of LTB4 and omega-hydroxy-LTB4 in rat hepatocyte suspensions. Ethanol, at a concentration of 12.5 mmol/l (0.07%; by vol.), caused 68% inhibition of the oxidation of omega-hydroxy-LTB4 by 50% in hepatocyte suspensions. The conversion of omega-hydroxy-LTB4 to omega-carboxy-LTB4 by rat and human liver cytosol was inhibited by ethanol with half maximal concentrations of 100 mumols/l and 300 mumols/l, respectively. Our measurements indicate that direct interference by ethanol of the omega-oxidation of leukotrienes as well as an increased NADH/NAD+ ratio induced by ethanol led to the inhibition of leukotriene degradation. The impairment of leukotriene inactivation in the liver by ethanol may contribute to the development of the inflammatory reaction in acute alcoholic liver disease.     

Effect of steroids and antisteroids on human meningioma cells in primary culture

Human meningiomas are rich in progestin receptors but virtually devoid of oestrogen receptors. We have studied the hormonal sensitivity of meningioma cells in vitro during 8 days of primary culture in the presence of different steroids and antisteroids. On day 8 the thymidine labelling index (TLI) was determined as a measure of cell growth. To date 30 cultures have been established from 39 tissue specimens. 13 cultures had a TLI below 1.0 and their growth were not affected by hormones. The TLI of the other 17 cultures was 3.0 +/- 1.7 (mean +/- SD; range 1.2-7.7). Following culture in the presence of 1 and 10 nM progesterone TLI was 83 +/- 28% (n = 9) and 61 +/- 29% (n = 3) of that of the control cultures respectively. Although in individual cultures occasional differences were found, the overall values are not statistically different from 100. Similarly, 1 nM of oestradiol and testosterone had no effect on the TLI (n = 3). Tamoxifen at 1 nM increased the TLI to 138% in one culture and decreased it to 66% of the control in another. The antiprogestin mifepristone (RU 486) in concentrations of 0.1, 1.0, 10, 100 and 1000 nM decreased the TLI to 72 +/- 30; 54 +/- 20; 55 +/- 20; 59 +/- 18 and 65 +/- 10 respectively (n = 6-15; P less than 0.05 vs control). It is concluded that although a growth promoting effect of progestins on meningioma could not be shown, the therapeutic possibilities of antiprogestins warrant further investigation.     

Limitations of the lignin peroxidase system of the white-rot fungus, Phanerochaete chrysosporium

The lignin peroxidase enzyme system of the white-rot fungus, Phanerochaete chrysosporium was assayed for its capacity to degrade two recalcitrant aliphatic ether compounds, high-molecular-mass polyethylene glycol (PEG 20 000) and methyl tert-butyl ether. Ligninolytic cultures of Phanerochaete chrysosporium were spiked with each ether compound and incubated in reaction vessels. Separate incubations were conducted in which the ether compounds were present as sole carbon source. Other parameters, such as varying the methyl tert-butyl ether concentration and veratryl alcohol additions were tested. No significant degradation of either compound was observed under any of the conditions tested. Implications of these results are discussed with respect to the oxidative limitations of the lignin peroxidase enzyme system and structural features of substrate molecules that may be requisite for oxidation by this system.