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At least 19 recordsLinked to original sources
PubMed1984

Determination of ethylene oxide, ethylene chlorohydrin, and ethylene glycol in aqueous solutions and ethylene oxide residues in associated plastics.

A gas chromatographic (GC) method was developed for the determination of ethylene oxide and its two reaction products, ethylene chlorohydrin and ethylene glycol, in aqueous ophthalmic solutions. Propylene oxide was used as an internal standard. All three components were determined in one isothermal chromatographic analysis in less than 15 min. An extraction method for the determination of ethylene oxide residues in plastic components was also developed, and certain plastics with different ethylene oxide retention characteristics were identified.

Chlorohydrins↗
PubMed1992

Pharmacokinetics of ethylene in man; body burden with ethylene oxide and hydroxyethylation of hemoglobin due to endogenous and environmental ethylene.

The inhalation pharmacokinetics and the endogenous production of ethylene has been determined in healthy volunteers with respect to the formation of the carcinogen ethylene oxide. Ethylene showed a low degree of accumulation in the body determined in six subjects, the thermodynamic partition coefficient "body/air" being 0.53 +/- 0.23 (mean +/- SD) and the accumulation factor "body/air" at steady-state being 0.33 +/- 0.13 (mean +/- SD). The rate of metabolism was directly proportional to the exposure concentration. Only 2% of ethylene inhaled was metabolized to ethylene oxide, whereas 98% of ethylene was exhaled unchanged. The rate of the endogenous production of ethylene was 32 +/- 12 nmol/h (mean +/- SD), as calculated from exhalation data from 14 subjects. The resulting body burden was 0.44 +/- 0.19 nmol/kg (mean +/- SD). By analyzing published data on ethylene oxide in man its half-life was estimated to be 42 min. Using the pharmacokinetic parameters of ethylene and ethylene oxide, the body burden of ethylene oxide due to the sum of the exposure to environmental ethylene of about 15 ppb and to endogenous ethylene exposure of 0.44 nmol/kg was predicted to be 0.25 nmol/kg. In the blood of five non-smokers and one smoker the hemoglobin adduct resulting from the reaction of ethylene oxide with the N-terminal valine, N-(2-hydroxyethyl)valine, was quantified by gas chromatography/mass spectrometry. The value of 20 +/- 5 pmol/g Hb (mean +/- SD) found in the non-smokers corroborated the steady-state level of 18 +/- 3 pmol/g Hb (mean +/- SD) calculated from the pharmacokinetic approach.

Adult↗
PubMedDate not supplied

Rapid gas chromatographic determination of ethylene oxide, ethylene chlorohydrin, and ethylene glycol residues in rubber catheters.

Isothermal gas chromatography with flame ionization detection was used to determine residual ethylene oxide (EtO), ethylene chlorohydrin, and ethylene glycol in soft rubber catheters that had been sterilized with EtO. Catheter samples were extracted by shaking with carbon disulfide, and the extract was analyzed on a 3% Carbowax 20M on 80-100 mesh Chromosorb 101 column, using nitrogen as the carrier gas. Ten replicate injections of a mixed standards solution gave coefficients of variation of 1.91, 1.23, and 4.74% for EtO, ethylene chlorohydrin, and ethylene glycol, respectively. A linear response was obtained with concentrations ranging from 1.0 to 7.9 micrograms EtO, 14.0 to 88.0 micrograms ethylene chlorohydrin, and 31.0 to 98.5 micrograms ethylene glycol. The proposed method detected as little as 0.5, 5.0, and 16.5 ng EtO, ethylene chlorohydrin, and ethylene glycol, respectively.

Catheterization↗
PubMed1981

[Carcinogenic activity of ethylene oxide and its reaction products 2-chloroethanol, 2-bromoethanol, ethylene glycol and diethylene glycol. I. Carcinogenicity of ethylene oxide in comparison with 1,2-propylene oxide after subcutaneous administration in mice (author's transl)].

Ethylene oxide is an important initial product for a number of organic compounds and, in addition, is used in the medical field for sterilization. The aim of our experiments was to test ethylene oxide and, as a comparative substance, 1,2-propylene oxide in respect to their cancerogenic effectiveness in animal experiments. Ethylene oxide was administered subcutaneously in three dosages (1.0; 0.3 and 0.1 mg single dosage per mouse) once per week to groups of 100 female NMRI mice respectively. In the case of 1,2-propylene oxide, four dosages were used (2.5; 1.0; 0.3 and 0.1 mg single dosage per mouse). The vehicle was tricaprylin. Administrations were carried out over a period of 95 weeks. The mean total dosage per mouse in the case of ethylene oxide amounted to 64.4; 22.7, and 7.3 mg and, in the case of propylene oxide, to 165.4; 72.8; 21.7 and 6.8 mg. Both substances induced local tumours depending upon the dosage. There were mostly fibrosarcomas. In the case of the groups treated with ethylene oxide the frequency was between 11 and 5% and in the case of the groups treated with 1,2-propylene oxide this was between 16 and 2%. The cancerogenic effect of ethylene oxide and 1,2-propylene oxide determined in animal experiments could, therefore, be confirmed statistically. On the basis of the results presented in this paper, new aspects have arisen for the medical evaluation of ethylene oxide residues in the field of manufacturing and use and in respect to the TLV.

Animals↗
PubMed1998

Nuclear events in ethylene signaling: a transcriptional cascade mediated by ETHYLENE-INSENSITIVE3 and ETHYLENE-RESPONSE-FACTOR1.

Response to the gaseous plant hormone ethylene in Arabidopsis requires the EIN3/EIL family of nuclear proteins. The biochemical function(s) of EIN3/EIL proteins, however, has remained unknown. In this study, we show that EIN3 and EILs comprise a family of novel sequence-specific DNA-binding proteins that regulate gene expression by binding directly to a primary ethylene response element (PERE) related to the tomato E4-element. Moreover, we identified an immediate target of EIN3, ETHYLENE-RESPONSE-FACTOR1 (ERF1), which contains this element in its promoter. EIN3 is necessary and sufficient for ERF1 expression, and, like EIN3-overexpression in transgenic plants, constitutive expression of ERF1 results in the activation of a variety of ethylene response genes and phenotypes. Evidence is also provided that ERF1 acts downstream of EIN3 and all other components of the ethylene signaling pathway. The results demonstrate that the nuclear proteins EIN3 and ERF1 act sequentially in a cascade of transcriptional regulation initiated by ethylene gas.

Amino Acid Sequence↗
PubMed1987

[Carcinogenic activity of ethylene oxide and its reaction products 2-chloroethanol, 2-bromoethanol, ethylene glycol and diethylene glycol. III. Research on ethylene glycol and diethylene glycol for carcinogenic effects].

Ethylene glycol and diethylene glycol were each administered once weekly subcutaneously to groups of 100 female NMRI mice at 3 dosages (30; 10 und 3 mg single dose per mouse). Tricaprylin was used as solvent. The mean total dosage per mouse was 2110.5; 707.0 and 196.2 mg for ethylene glycol and 2029.8; 671.7 and 213.3 mg for diethylene glycol. Neither ethylene glycol nor diethylene glycol induced tumors at the injection site or away from the point of administration.

Animals↗
PubMed1979

Determination of ethylene oxide, ethylene chlorohydrin, and ethylene glycol residues in ophthalmic solutions at proposed concentration limits.

A GLC method was developed for the determination of ethylene oxide and its two reaction products, ethylene chlorohydrin and ethylene glycol, in ophthalmic solutions at the levels recently proposed by the Food and Drug Administration. The method requires no extractions, sample preparations, or elaborate trapping and concentrating techniques. All three components can be chromatographed on the same spiral glass column packed with a porous polymer absorbent.

Chlorohydrins↗
PubMed2000

Ethylene promotes ethylene biosynthesis during pea seed germination by positive feedback regulation of 1-aminocyclo-propane-1-carboxylic acid oxidase.

Increased ethylene evolution accompanies seed germination of many species including Pisum sativum L., but only a little is known about the regulation of the ethylene biosynthetic pathway in different seed tissues. Biosynthesis of the direct ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC), the expression of ACC oxidase (ACO), and ethylene production were investigated in the cotyledons and embryonic axis of germinating pea seeds. An early onset and sequential induction of ACC biosynthesis, accumulation of Ps-ACO1 mRNA and of ACO activity, and ethylene production were localized almost exclusively in the embryonic axis. Maximal levels of ACC, Ps-ACO1 mRNA, ACO enzyme activity and ethylene evolution were found when radicle emergence was just complete. Treatment of germinating seeds with ethylene alone or in combination with the inhibitor of ethylene action 2,5-norbornadiene showed that endogenous ethylene regulates its own biosynthesis through a positive feedback loop that enhances ACO expression. Accumulation of Ps-ACO1 mRNA and of ACO enzyme activity in the embryonic axis during the late phase of germination required ethylene, whereas Ps-ACS1 mRNA levels and overall ACC contents were not induced by ethylene treatment. Ethylene did not induce ACO in the embryonic axis during the early phase of germination. Ethylene-independent signalling pathways regulate the spatial and temporal pattern of ethylene biosynthesis, whereas the ethylene signalling pathway regulates high-level ACO expression in the embryonic axis, and thereby enhances ethylene evolution during seed germination.

Amino Acid Oxidoreductases↗
PubMed2002

Loss-of-function mutations in the ethylene receptor ETR1 cause enhanced sensitivity and exaggerated response to ethylene in Arabidopsis.

Ethylene signaling in Arabidopsis begins at a family of five ethylene receptors that regulate activity of a downstream mitogen-activated protein kinase kinase kinase, CTR1. Triple and quadruple loss-of-function ethylene receptor mutants display a constitutive ethylene response phenotype, indicating they function as negative regulators in this pathway. No ethylene-related phenotype has been described for single loss-of-function receptor mutants, although it was reported that etr1 loss-of-function mutants display a growth defect limiting plant size. In actuality, this apparent growth defect results from enhanced responsiveness to ethylene; a phenotype manifested in all tissues tested. The phenotype displayed by etr1 loss-of-function mutants was rescued by treatment with an inhibitor of ethylene perception, indicating that it is ethylene dependent. Identification of an ethylene-dependent phenotype for a loss-of-function receptor mutant gave a unique opportunity for genetic and biochemical analysis of upstream events in ethylene signaling, including demonstration that the dominant ethylene-insensitive phenotype of etr2-1 is partially dependent on ETR1. This work demonstrates that mutational loss of the ethylene receptor ETR1 alters responsiveness to ethylene in Arabidopsis and that enhanced ethylene response in Arabidopsis not only results in increased sensitivity but exaggeration of response.

Alkenes↗
PubMed1999

The relationship between ethylene binding and dominant insensitivity conferred by mutant forms of the ETR1 ethylene receptor.

Ethylene responses in Arabidopsis are mediated by a small family of receptors, including the ETR1 gene product. Specific mutations in the N-terminal ethylene-binding domain of any family member lead to dominant ethylene insensitivity. To investigate the mechanism of ethylene insensitivity, we examined the effects of mutations on the ethylene-binding activity of the ETR1 protein expressed in yeast. The etr1-1 and etr1-4 mutations completely eliminated ethylene binding, while the etr1-3 mutation severely reduced binding. Additional site-directed mutations that disrupted ethylene binding in yeast also conferred dominant ethylene insensitivity when the mutated genes were transferred into wild-type Arabidopsis plants. By contrast, the etr1-2 mutation did not disrupt ethylene binding in yeast. These results indicate that dominant ethylene insensitivity may be conferred by mutations that disrupt ethylene binding or that uncouple ethylene binding from signal output by the receptor. Increased dosage of wild-type alleles in triploid lines led to the partial recovery of ethylene sensitivity, indicating that dominant ethylene insensitivity may involve either interactions between wild-type and mutant receptors or competition between mutant and wild-type receptors for downstream effectors.

Alleles↗
PubMed2002

Ozone-induced ethylene production is dependent on salicylic acid, and both salicylic acid and ethylene act in concert to regulate ozone-induced cell death.

Ethylene is known to influence plant defense responses including cell death in response to both biotic and abiotic stress factors. However, whether ethylene acts alone or in conjunction with other signaling pathways is not clearly understood. Ethylene overproducer mutants, eto1 and eto3, produced high levels of ethylene and developed necrotic lesions in response to an acute O3 exposure that does not induce lesions in O3-tolerant wild-type Col-0 plants. Treatment of plants with ethylene inhibitors completely blocked O3-induced ethylene production and partially attenuated O3-induced cell death. Analyses of the responses of molecular markers of specific signaling pathways indicated a relationship between salicylic acid (SA)- and ethylene-signaling pathways and O3 sensitivity. Both eto1 and eto3 plants constitutively accumulated threefold higher levels of total SA and exhibited a rapid increase in free SA and ethylene levels prior to lesion formation in response to O3 exposure. SA pre-treatments increased O3 sensitivity of Col-0, suggesting that constitutive high SA levels prime leaf tissue to exhibit increased magnitude of O3-induced cell death. NahG and npr1 plants compromised in SA signaling failed to produce ethylene in response to O3 and other stress factors suggesting that SA is required for stress-induced ethylene production. Furthermore, NahG expression in the dominant eto3 mutant attenuated ethylene-dependent PR4 expression and rescued the O3-induced HR (hypersensitive response) cell death phenotype exhibited by eto3 plants. Our results suggest that both SA and ethylene act in concert to influence cell death in O3-sensitive genotypes, and that O3-induced ethylene production is dependent on SA.

Arabidopsis↗
PubMed2002

Ethylene emission and responsiveness to applied ethylene vary among Poa species that inherently differ in leaf elongation rates.

A plant's ability to produce and respond to ethylene is essential for its vegetative growth. We studied whole-shoot ethylene emission and leaf growth responses to applied ethylene in four Poa spp. that differ inherently in leaf elongation rate and whole-plant relative growth rate. Compared with the fast-growing Poa annua and Poa trivialis, the shoots of the slow-growing species Poa alpina and Poa compressa emitted daily 30% to 50% less ethylene, and their leaf elongation rate was more strongly inhibited when ethylene concentration was increased up to 1 microL L(-1). To our surprise, however, low ethylene concentrations (0.02-0.03 microL L(-1)) promoted leaf growth in the two slow-growing species; at the same concentrations, leaf elongation rate of the two fast-growing species was only slightly inhibited. All responses were observed within 20 min after ethylene applications. Although ethylene generally inhibits growth, our results show that in some species, it may actually stimulate growth. Moreover, in the two slow-growing Poa spp., both growth stimulation and inhibition occurred in a narrow ethylene concentration range, and this effect was associated with a much lower ethylene emission. These findings suggest that the regulation of ethylene production rates and perception of the gas may be more crucial during leaf expansion of these species under non-stressful conditions and that endogenous ethylene concentrations are not large enough to saturate leaf growth responses. In the two fast-growing species, a comparatively higher ethylene endogenous concentration may conversely be present and sufficiently high to saturate leaf elongation responses, invariably leading to growth inhibition.

Dose-Response Relationship, Drug↗
PubMed1980

[The toxic effect of ethylene chlorohydrin and ethylene glycol on experimental animals and human cell cultures (author's transl)].

Ethylene chlorohydrin (2-chlorethanol) and ethylene glycol can originate as by-products during ethylene oxide sterilization. We studied the effect of these subsdtances upon human HeLa cells as well as the conjunctiva and the epithelium of the external genitalia of 35 rabbits. - We found ethylene chlorohydrin to be considerably more toxic than ethylene glycol. 2-chloroethanol did not cause any reactions at our cell cultures in dilutions of 1:100 after 4 h action upon the cells and 24 h observation time. In our experimental animals this concentration had only minimal irritating effects at the external genitalia. Ethylene glycol produced cellular damages in dilutions of 1:10 after 5 d only. Our experimental animals showed no reactions to these concentrations. At the conjunctiva of rabbits dilutions of 1:100 ethylene chlorohydrin and 1:10 ethylene glycol had no effect. After application of 2-chloroethanol 1:100 to the external genitalia minimal irritations were observed. Ethylene glycol in dilutions of 1:5 caused irritations of the conjunctiva and the genitalia of our rabbits. Ethylene chlorohydrin- and ethylene glycol concentrations which had a damaging effect upon our cell cultures of our experimental animals were many times higher than those which might be expected to originate during ethylene oxide sterilization.

Animals↗