Acrylonitrile Treatment Research Articles

Acrylonitrile exposure triggers ovarian inflammation and decreases oocyte quality probably via mitochondrial dysfunction induced apoptosis in mice

Acrylonitrile is an organic chemical synthetic monomer that is widely used in food packaging and manufacturing. Animal studies have reported that acrylonitrile is carcinogenic and toxic, but the effects on the female reproductive function in mammals are unknown. In the present study, we report that acrylonitrile treatment affects ovarian homeostasis in mice, resulting in impaired follicular development. Follicles in acrylonitrile-exposed mice exhibited high levels of inflammation and apoptosis, and acrylonitrile treatment interfered with oocyte development. Transcriptomics analysis showed that acrylonitrile altered the expression of oocyte genes related to apoptosis, oxidative stress, endoplasmic reticulum stress, and autophagy. Further molecular tests revealed that acrylonitrile induced early apoptosis, DNA damage, elevated levels of reactive oxygen species, endoplasmic reticulum abnormalities, and lysosomal aggregation. We also observed disruption of mitochondrial structure and distribution and depolarization of membrane potential. Finally, acrylonitrile treatment in female mice decreased the number and weight of offspring. Altogether, these findings suggest that acrylonitrile impairs the stability of the ovarian internal environment, which in turn affects oocyte development and reduces the number of offspring.

Efficiently degradation of acrylonitrile from aqueous solution by La0.5Ce0.5MO3 (M = Fe, Cu and Co) perovskite-like catalyst: Optimization and reaction pathways

The present study focuses on catalytic degradation of carcinogenic and refractory organic compound (acrylonitrile) with La0.5Ce0.5MO3 (M = Fe, Cu and Co) perovskite-like catalysts synthesized by sol-gel method were examined by catalytic peroxidation process. Various analytical techniques, including XRD, FTIR, BET surface area, XPS, FE-SEM with EDAX and TEM were used for catalyst characterization. During catalytic peroxidation, influence of various operating parameters such as, catalyst dose (250–1250 mg/L), H2O2/ acrylonitrile (0.5–2.5), pH (2–10) and reaction temperature (30–90 °C) was studied and optimized through central composite design (CCD) in response surface methodology (RSM). Maximum acrylonitrile removal of 90.11% was observed at optimum operating conditions (i.e., LCFe catalyst dose 660 mg/L, H2O2/ acrylonitrile molar ratio 1.54, pH 5.4, reaction temperature 56.7 °C and reaction time 3 h). Two-step first order kinetics was performed at optimum operating conditions for the degradation of acrylonitrile at various temperatures and concentrations. To assess the economic viability of catalyst, reusability study was executed over four cycles of experiments at optimum operating conditions. The acrylonitrile removal was gradually dropped from 90.11% to 80.38%, 73.42% and 69.92%, respectively in second, third and fourth cycles. The proposed pathways of acrylonitrile degradation were suggested on the basis of intermediates identified by GC–MS analysis and reactive oxidant species (ROS) study. The operating cost of acrylonitrile treatment from aqueous solution was estimated to be 61.14 $/m3 wastewater by catalytic peroxidation process.

Acrylonitrile induced cell cycle arrest and apoptosis by promoting the formation of reactive oxygen species in human choriocarcinoma cells.

Acrylonitrile (AN), which is widely utilized in the manufacture of plastics, acrylamide, acrylic fibers, and resins, is also one of main components of cigarette smoke (CS). In this study, we examined the effects of AN on the cell viability and apoptosis of JEG-3 and BeWo human choriocarcinoma cancer cell lines. A cell viability assay confirmed that AN decreased the cell proliferation of JEG-3 and BeWo cells in a dose-dependent manner. Additionally, Western blot assay revealed that protein expression of cyclin D and cyclin E decreased, while protein expression of p21 and p27 increased in response to AN treatment for 48 hr. The changes in reactive oxygen species (ROS) levels in JEG-3 and BeWo cells exposed to AN were also measured by a dichlorofluorescein diacetate (DCFH-DA) assay, which revealed that ROS levels increased in response to AN treatment for 48 hr. Moreover, western blot assay confirmed that AN treatment of JEG-3 and BeWo cells for 4 hr promoted the expression of phosphorylated eukaryotic initiation factor 2 alpha protein (p-eIF2α), C/EBP homologous protein (CHOP) and caspase 12, which are known to be involved in ROS-mediated endoplasmic reticulum stress (ER-stress)-related apoptosis. Overall, the protein expression of p53 and Bax (a pro-apoptosis marker) increased, while the expression of Bcl-xl (an anti-apoptotic marker) decreased and the number of apoptotic cells increased in response to AN treatment for 48 hr. Taken together, these results suggest that AN has the potential to induce apoptosis of JEG-3 and BeWo human choriocarcinoma cancer cells by activating ROS.

Resistance of mouse primary microglia and astrocytes to acrylonitrile-induced oxidative stress

Acrylonitrile (ACN) is a widely used chemical in the production of plastics, resin, nitrile, acrylic fibers, synthetic rubber, and acrylamide. ACN is considered a Group 2B possible carcinogen in humans and is known to cause gliomas in rats. These gliomas are predominantly composed of microglia and not astrocytes. Interestingly, ACN treatment does not cause gliomas in mice, suggesting that mouse astrocytes and microglia may be resistant to ACN. We investigated the effects of ACN treatment on primary mouse microglia and astrocytes to investigate their sensitivity to the chemical. Cell viability, ACN uptake, glutathione (GSH) levels and the expression of NF-E2-related factor 2 (Nrf2) were evaluated in primary mouse microglia and astrocytes following ACN treatment. Our results indicate that mouse glial cells are resistant to ACN-induced oxidative stress. Both cell types accumulated ACN; however, there was a minor effect of ACN on cell viability in astrocytes and microglia. Nrf2 and GSH levels were unchanged in ACN-treated as compared to the untreated cells. These observations suggest that primary mouse glial cells are resistant to ACN.

Differential protection of pre- versus post-treatment with curcumin, Trolox, and N-acetylcysteine against acrylonitrile-induced cytotoxicity in primary rat astrocytes

ObjectiveThis study was designed to examine the differential protection of pre- versus post-treatment with three different antioxidants, curcumin (CUR), Trolox, and N-acetylcysteine (NAC), on acrylonitrile (AN)-induced cytotoxicity in primary rat astrocytes. MethodsPrimary astrocyte cultures were treated with CUR, Trolox and NAC for 4h prior to, or following 24h treatment with AN (2.5mM). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), lactate dehydrogenase (LDH) release, lipid peroxidation, glutathione, reactive oxygen species (ROS) and mitochondrial membrane potential were measured to evaluate protection associated with the three antioxidants. Knockdown of Nrf2 expression by liposome transfection with siRNA was used to confirm the role of Nrf2 activation in the protection associated with the three antioxidants. ResultsCompared with AN treatment alone, pre-treatment with CUR at either concentration significantly increased cell viability and mitochondrial membrane potential, and reduced glutathione levels; lipid peroxidation and ROS production were significantly decreased as well. NAC also showed significant efficacy in attenuating AN-induced toxicity at higher concentration. However, pre-treatment with Trolox failed to ameliorate the AN-induced toxicity. When post-treatment with Trolox, this antioxidant led to significant protective effects at both concentrations, while CUR and NAC were efficacious only at the higher concentrations. Knockdown of Nrf2 only abolished the protective effects of CUR pre-treatment on AN-induced cytotoxicity, while the protective effects of NAC and Trolox pre-treatment groups showed no differences between the Nrf2-knockdown and non-knockdown treatments. ConclusionsThe selected antioxidants exert differential cellular protection when administered prior or subsequent to AN-induced cytotoxic events in decreasing cellular viability, antioxidative capacity and mitochondrial function, enhanced cytotoxicity and ROS production. These results suggest that antioxidants should be carefully chosen for their efficacy in preventing or diminishing oxidative damage caused by AN. The differential effect of pre- and post-treatment may be attributed to activation of the Nrf2 signaling pathway.

Differential inflammatory response to acrylonitrile in rat primary astrocytes and microglia

Acrylonitrile (ACN) is extensively used in the production of plastics, resins, nitriles and other commercial products. Chronic low dose exposures to ACN cause glial cell tumors in rats, primarily microglial in origin. Recently it has been determined that astrocytes and microglia respond to ACN-induced oxidative stress differently, which may influence cell-specific activation of inflammatory and carcinogenic pathways. This study was conducted to compare the inflammatory responses of astrocytes and microglia following ACN treatment in vitro to further characterize differential sensitivities and adaptive responses in these cell types. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and p53 levels were measured along with levels of 12 different cytokines and chemokines in primary rat microglia and astrocytes. Additionally levels of cytochrome P450 2E1 (CYP2E1) were measured to evaluate the cells’ ability to metabolize ACN. Results indicate that while both cells upregulate p53 and NF-κB, the cytokines and chemokines produced differ between the cell types. Astrocytes, but not microglia, upregulated CYP2E1 in response to ACN, which may be due to the astrocytes accumulating more ACN than the microglia. Altogether our data implicate the inflammatory response as an important event in ACN-induced neurotoxicity.

Differential response to acrylonitrile toxicity in rat primary astrocytes and microglia

Acrylonitrile (ACN) is a widely used chemical in the production of plastics, resins, nitriles, acrylic fibers, synthetic rubber and acrylamide. While acute high level exposures to ACN are known to be lethal, chronic low dose exposures causes glial cell tumors in rats. Recently, these glial tumors have been characterized as microglial in origin. While effects of ACN on astrocytes, the more numerous glial cell, have been investigated, the effects on microglia are unknown. This study was conducted to compare the responses of astrocytes and microglia to ACN treatment in vitro to address differential sensitivities and adaptive responses to this toxic chemical. Cell viability, ACN uptake, lipid peroxidation byproducts (F2-isoprostanes), glutathione (GSH) levels and expression of NF-E2-related factor 2 (Nrf2) were evaluated in primary rat microglia and astrocytes following ACN treatment. Results indicate that microglia are more sensitive to ACN than astrocytes, accumulating less ACN while demonstrating higher F2-isoprostane levels. GSH levels were up-regulated in both cell types, as a protective mechanism against ACN-induced oxidative stress, while Nrf2 levels were only induced in microglia. Our data suggest that microglia and astrocytes exhibit different sensitivities and responses to ACN, which are linked to the intracellular thiol status inherent to each of these cell types.

The chemical modification of tropical wood polymer composites

Wood polymer composites were manufactured from several types of tropical wood species by impregnating the woods with acrylonitrile monomer solution. The physical and mechanical properties of wood polymer composites were then investigated in this study. The vacuum-pressure method was employed to impregnate wood samples with monomer and in situ polymerization. Acrylonitrile reacted and incorporated with wood, which was confirmed through Fourier transform infrared spectroscopy and scanning electron microscopy test analysis. The mechanical properties of wood samples in terms of modulus of elasticity and compressive modulus were found to be improved on acrylonitrile treatment. Besides, the fabricated wood polymer composite samples had lower water absorption and higher surface hardness (Shore D) value as compared to their corresponding raw one. For wood polymer composites, a significant improvement was found in physical and mechanical properties compared to the raw woods.

Studies on Performance of Acrylonitrile-Pretreated Bamboo-Reinforced Thermosetting Resin Composites

The present study investigates the effect of acrylonitrile treatment of bamboo mats on bamboo-reinforced epoxy and polyester resin composites. Acrylonitrile treatment has been done for 1 and 5 h. The tensile strength and modulus of the composites have been improved with both the resins after acrylonitrile treatment (cyanoethylation) of fibers. Moisture regain decreases significantly on cyanoethylation. Acrylonitrile-pretreated bamboo-reinforced polyester composite decreases the water uptake drastically from 75 to 14%.

Zinc, Copper, Iron, and Selenium Levels in Brain and Liver of Mice Exposed to Acrylonitrile

The mechanism of toxicity of acrylonitrile (AN) has not been fully defined. The research described herein was undertaken to investigate the possible effects of AN on the levels of metallic elements in liver and brain of mice. Thirty-two mice were randomly assigned to four separate groups and treated intraperitoneal (i.p.) once daily for 1 week. Mice in the control group received normal saline, and mice in the three exposure groups received 5, 10, or 20 mg AN/kg b.w. Samples of brain and liver were collected immediately after decapitation. Tissue levels of trace elements (zinc, copper, iron) were determined with flame atomic absorption spectrophotometer or double channel atomic fluorescence absorption spectrophotometer (selenium). Mean brain weights of AN-treated mice were increased as a function of dose compared to controls, but there was no significant change in the ratio of liver/body weight in the four groups. While mean brain zinc decreased as a function of AN dosage, mean liver zinc of the low-dose group significantly increased (p < 0.05); mean liver copper in the medium-dose AN group was significantly higher compared to controls (p < 0.05); however, mean brain copper was increased, but the difference did not attain statistical significance in the three AN groups when compared with the controls (p > 0.05). Mean brain iron levels were significantly decreased in the middle-dose AN group (p < 0.05), but there were no consistent changes in liver iron. Tissue levels of selenium in brain and liver were similar for the control and AN treatment groups. AN induces significant and differential changes in the levels of zinc, copper, and iron in brain and liver. These changes likely play a pivotal role in mediating AN toxicity, most likely via changes in cellular redox status.

Acrylonitrile‐induced oxidative DNA damage in rat astrocytes

Chronic administration of acrylonitrile results in a dose-related increase in astrocytomas in rat brain, but the mechanism of acrylonitrile carcinogenicity is not fully understood. The potential of acrylonitrile or its metabolites to induce direct DNA damage as a mechanism for acrylonitrile carcinogenicity has been questioned, and recent studies indicate that the mechanism involves the induction of oxidative stress in rat brain. The present study examined the ability of acrylonitrile to induce DNA damage in the DI TNC1 rat astrocyte cell line using the alkaline Comet assay. Oxidized DNA damage also was evaluated using formamidopyrimidine DNA glycosylase treatment in the modified Comet assay. No increase in direct DNA damage was seen in astrocytes exposed to sublethal concentrations of acrylonitrile (0-1.0 mM) for 24 hr. However, acrylonitrile treatment resulted in a concentration-related increase in oxidative DNA damage after 24 hr. Antioxidant supplementation in the culture media (alpha-tocopherol, (-)-epigallocathechin-3 gallate, or trolox) reduced acrylonitrile-induced oxidative DNA damage. Depletion of glutathione using 0.1 mM DL-buthionine-[S,R]-sulfoximine increased acrylonitrile-induced oxidative DNA damage (22-46%), while cotreatment of acrylonitrile with 2.5 mM L-2-oxothiazolidine-4-carboxylic acid, a precursor for glutathione biosynthesis, significantly reduced acrylonitrile-induced oxidative DNA damage (7-47%). Cotreatment of acrylonitrile with 0.5 mM 1-aminobenzotriazole, a suicidal inhibitor of cytochrome P450, prevented the oxidative DNA damage produced by acrylonitrile. Cyanide (0.1-0.5 mM) increased oxidative DNA damage (44-160%) in astrocytes. These studies demonstrate that while acrylonitrile does not directly damage astrocyte DNA, it does increase oxidative DNA damage. The oxidative DNA damage following acrylonitrile exposure appears to arise mainly through the P450 metabolic pathway; moreover, glutathione depletion may contribute to the induction of oxidative DNA damage by acrylonitrile.

Effect of fiber surface treatment on the properties of biocomposites from nonwoven industrial hemp fiber mats and unsaturated polyester resin

AbstractBiocomposites were made with nonwoven hemp mats and unsaturated polyester resin (UPE). The hemp fiber volume fraction was optimized by mechanical testing. The effect of four surface treatments of industrial hemp fibers on mechanical and thermal properties of biocomposites was studied. The treatments done were alkali treatment, silane treatment, UPE (matrix) treatment, and acrylonitrile treatment. Bending strength, modulus of elasticity, tensile strength, tensile modulus, impact strength, storage modulus, loss modulus, and tan δ were evaluated and compared for all composites. The mechanical as well as thermal properties of the biocomposites improved after surface treatments. The properties of the above biocomposites were also compared with E‐glass–mat composite. To achieve balance in properties, a hybrid composite of industrial hemp and glass fibers was made. © 2005 Wiley Periodicals, Inc. J Appl Polym Sci 99: 1055–1068, 2006

Effects of acrylonitrile on the activities of antioxidant enzymes and levels of lipid peroxidation in rat testes

To explore the mechanism of male reproductive toxicity induced by acrylonitrile (ACN). Male Sprague-Dawley rats were daily administrated ACN by intraperitoneal injection 5 times a week for 13 weeks at the dose of 0, 7.5, 15.0 and 30.0 mg/kg body weight, respectively. The rats were sacrificed and testes were removed at the end of 4, 8, 13 or 15 weeks, respectively. The activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and glutathione S-transferase (GST) and the levels of glutathione (GSH) and malonaldehyde (MDA) were detected in testes. Following ACN treatment of 4 weeks, the levels of GSH in ACN 15.0 mg/kg and 30.0 mg/kg group were (7.44 +/- 0.77) mg/g pro and (6.95 +/- 0.77) mg/g pro respectively, and the activity of GSH-Px was (70.89 +/- 4.01) U/mg pro in 30.0 mg/kg group, all of which were significantly higher than the control group (P < 0.05, P < 0.01). After 8 weeks, the levels of GSH decreased to (2.50 +/- 0.94) mg/g pro in ACN 30.0 mg/kg group (P < 0.01); the activities of SOD increased to (102.08 +/- 16.08) NU/mg pro and (113.30 +/- 17.20) NU/mg pro in ACN 15.0 mg/kg and 30.0 mg/kg group (P < 0.01). After 13 weeks, the levels of GSH declined in ACN 15.0 mg/kg and 30.0 mg/kg group, and the activities of GST decreased in ACN 30.0 mg/kg group, and of GSH-Px decreased in both doses group. However, the level of MDA [(0.68 +/- 0.16) nmol/mg pro] were significantly higher in 30.0 mg/kg group than that in control group [(0.38 +/- 0.12) nmol/mg pro] (P < 0.01). 2 weeks after stopping ACN treatment, the level of GSH restored to normal but the levels of MDA or the activity of GSH-Px in 30.0 mg/kg group were still higher or lower respectively than those of control (P < 0.05). ACN may impair the balance of antioxidant system, thus induce lipid peroxidation damage to rat testes.

Acrylonitrile produces transient cochlear function loss and potentiates permanent noise-induced hearing loss.

There is growing evidence that agents that produce oxidative stress in the cochlea have significant ototoxic potential by themselves and can potentiate noise-induced hearing loss as well. Acrylonitrile (ACN) metabolism entails conjugation with glutathione, resulting in rapid and pronounced depletion of this important antioxidant in many organs including brain, liver, and kidney. ACN metabolism also results in cyanide (CN) formation through a secondary oxidative pathway. The results of two physiological experiments are reported here. First, the acute effects of ACN (50 mg/kg sc) on auditory sensitivity are assessed using a within subject study. In the second study, persistent effects of ACN alone (50 mg/kg, sc and 2 x 50 mg/kg, sc) and ACN in combination with noise exposure (8 h, 108 dB octave-band noise) are evaluated using threshold sensitivity as the dependent measure. Auditory threshold shift and absolute thresholds were determined using the compound action potential (CAP) amplitude. Acute ACN administration produces a loss in auditory threshold sensitivity that reached a maximum 10-20 min following sc injection. Auditory thresholds returned to control levels 75-100 min following exposure. In the study of permanent auditory threshold shifts, ACN plus noise increased auditory threshold impairment relative to rats receiving noise only when thresholds were assessed 3 weeks following exposure. ACN by itself did not produce permanent threshold impairment 3 weeks following administration. Assays were undertaken in separate groups of rats to track the elevation in blood CN and the depletion of total glutathione in cochlea, brain, and liver following ACN treatment. Systemic blood CN levels were not significantly elevated until 60-120 min following injection, and cochlear glutathione levels showed significant depletion as little as 15 min after injection and remained depressed for about 4 h. The results confirm the prediction that ACN is acutely ototoxic and can enhance noise-induced hearing loss.

Two-year toxicity and oncogenicity study with acrylonitrile incorporated in the drinking water of rats

Sprague–Dawley rats (80 per sex per control and 48 per sex in each treatment group) were given drinking water formulated to contain 0, 35, 100, or 300 ppm acrylonitrile (AN) for up to 2-years. An additional ten rats per sex per group were added for a 1-year interim necropsy. The equivalent doses of AN consumed were 0, 3.4, 8.5, and 21.3 mg/kg per day for males and 0, 4.4, 10.8, and 25.0 for females. Rats were closely monitored clinically with body weight, feed and water consumption measured at numerous intervals. Hematology, clinical chemistry, and urinalysis were evaluated six times. All rats were necropsied when moribund, found dead, or at scheduled termination, with extensive histopathology of all rats. Numerous adverse toxic and oncogenic effects were observed in both sexes of all AN treatment groups. Decreased water consumption, feed consumption, and concomitant body weight suppression occurred within days of study initiation and persisted throughout the study in all treatment groups. An early onset of Zymbal gland tumors in high dose male and female rats, and in the mammary gland of all treated groups of females, was detected in-life. Hematology, clinical chemistry, and urinalysis, repeatedly evaluated, were without significant biological effects, except for an increased urine specific gravity due to the rats lower water intake. Organ weights at study termination were not significantly affected. Mortality was high in all female treated groups, with no surviving male or female 300 ppm rats during the last 2 months of the study. The most significant findings in this study were detected following gross and microscopic examination of an extensive list of tissues from all rats in the study. Nontumorous and tumorous lesions were found at an increased and/or decreased rate in a number of tissues of both sexes at all treatment levels. The primary nontumorous histopathologic effects of AN exposure occurred in the forestomach and the central nervous system of rats of both sexes and involved all treatment groups. A statistically significant increased incidence of tumors in one or more dose levels of either sex occurred in the central nervous system, Zymbal gland, forestomach, tongue, small instestine, and mammary gland. A no-observed-effect level (NOEL) was not identified in this study for toxicity or oncogenicity in either sex.

Induction of oxidative stress and oxidative damage in rat glial cells by acrylonitrile.

Chronic treatment of rats with acrylonitrile (ACN) resulted in a dose-related increase in glial cell tumors (astrocytomas). While the exact mechanism(s) for ACN-induced carcinogenicity remains unresolved, non-genotoxic and possibly tumor promotion modes of action appear to be involved in the induction of glial tumors. Recent studies have shown that ACN induced oxidative stress selectively in rat brain in a dose-responsive manner. The present study examined the ability of ACN to induce oxidative stress in a rat glial cell line, a target tissue, and in cultured rat hepatocytes, a non-target tissue of ACN carcinogenicity. Glial cells and hepatocytes were treated for 1, 4 and 24 h with sublethal concentrations of ACN. ACN induced an increase in oxidative DNA damage, as evidenced by increased production of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) in glial cells but not in rat hepatocytes. Hydroxyl radical formation following ACN treatment was also selectively increased in glial cells. Following 1 and 4 h of ACN exposure, the levels of the non-enzymatic antioxidant glutathione, as well as the activities of the enzymatic antioxidants catalase and superoxide dismutase were significantly decreased in the rat glial cells. Lipid peroxidation and the activity of glutathione peroxidase were not affected by ACN treatment in rat glial cells. No changes in any of these biomarkers of oxidative stress were observed in hepatocytes treated with ACN. These data indicate that ACN selectively induced oxidative stress in rat glial cells.

Restoration of Hydrophilicity of Field-Opened Cotton Fibers by Cyanoethylation Treatment.

Field-opened American cotton fibers were treated with acrylonitrile after impregnation with aqueous sodium hydroxide. By this treatment the water absorbency and the amount of bound water as determined by DSC were increased and approached those of never-dried cotton. As for tensile strength, the increase in dry strength was higher than that of wet strength. On DSC cooling curves peak II, ascribable to freezable bound water, was observed as a small shoulder for field-opened and mercerized cotton fibers. However, this peak disappeared after the acrylonitrile treatment. Those treated fibers showed a nearly circular cross-sectional shape. Lumen and convolution could hardly be observed.

Epoxidation of acrylonitrile by rat and human cytochromes P450.

The cytochromes P450 (P450) involved in the epoxidation of the rat carcinogen acrylonitrile (ACN) to the mutagen 2-cyanoethylene oxide (CEO) have been investigated in hepatic microsomes from F-344 rats and humans. Induction of P450 2E1 by acetone treatment increased the Vmax for rat microsomal CEO formation 5-fold, while ACN treatment had little effect. Treatment with beta-naphthoflavone, dexamethasone, and phenobarbital had little effect upon Vmax but increased the KM 3- to 5-fold. The P450 ligand 1-phenylimidazole and substrate ethanol were potent inhibitors of ACN epoxidation after all treatments. 2-(Diethylamino)ethyl 2,2-diphenylvalerate (SKF 525A; 0.1 mM) was not an effective inhibitor with microsomes from untreated or acetone-treated rats, but inhibited approximately 50% following dexamethasone or phenobarbital treatment. Antibodies to P450 2E1 inhibited > 85% of the ACN epoxidation activity in microsomes from untreated or beta-naphthoflavone- or acetone-treated rats, but only produced 40% and 60% inhibition following dexamethasone or phenobarbital treatments, respectively. These results indicate that P450 2E1 is the major catalyst of ACN epoxidation in untreated rats and that other forms of P450 can also epoxidize ACN. Diethyldithiocarbamate (0.1 mM) was a potent irreversible inhibitor of ACN epoxidation after all of the induction treatments, indicating that it is not specific for P450 2E1. Chlorzoxazone (2 mM) produced 75-90% inhibition after all of the induction treatments, indicating that it interacts with several rodent P450 isoforms in addition to 2E1. Human hepatic microsomes (n = 6) epoxidized ACN with Vmax'S ranging from 129 to 315 pmol of CEO formed/(min.mg of protein) and KM's from 12 to 18 microM.(ABSTRACT TRUNCATED AT 250 WORDS)

Chemical modification of cotton fiber by alkali‐swelling and substitution reactions—acetylation, cyanoethylation, benzoylation, and oleoylation

AbstractBy impregnating cotton fiber with alkaline swelling agents and reacting with some chemical agents which can be substituted for the hydroxyl groups on cellulose molecules in the presence of alkali, highly accessible or decrystallized cotton fibers can be obtained. As the effective substitution reactions, acetylation by acetic anhydride and cyanoethylation by acrylonitrile were applied. The cotton fibers modified by these chemical treatments showed no decrease of tensile strength, and had moisture regain higher than the untreated cotton though the degrees of substitution were as high as 20–30 mol %. The resistance to heat or acid and the soil removal were improved. Dyeability for direct dye was increased, and dyeability for disperse or cationic dye was also given. Benzoylation and oleoylation were also investigated. Crease recovery of the cotton fabrics was somewhat improved and dyeability for disperse dye was given. The cotton fabrics oleoylated after decrystallizing by alkali–acrylonitrile treatment had moisture regain almost the same as the untreated cotton, while high water repellency was given.

Occurrence of "stress"-proteins in yeast after heat-shock, acrylonitrile treatment and during the stationary growth phase.

The response of yeast cells to different kinds of "stress" is not identical. Cells of the stationary growth phase synthesize three new proteins of molecular weights 68, 27 and 24 kD, compared with cells of the exponential growth phase, while heat-shocked cells exhibit new proteins of 100, 90, 84, 70 and 24 kD. After treatment with acrylonitrile two new proteins with molecular weights of 70 and 46 kD appear. However, all three kinds of "stress" lead to the induction of a ribonuclease.