PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ETHYLENE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

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↗
PubMed2006

Ethylene sensing and gene activation in Botrytis cinerea: a missing link in ethylene regulation of fungus-plant interactions?

Ethylene production by infected plants is an early resistance response leading to activation of plant defense pathways. However, plant pathogens also are capable of producing ethylene, and ethylene might have an effect not only on the plant but on the pathogen as well. Therefore, ethylene may play a dual role in fungus-plant interactions by affecting the plant as well as the pathogen. To address this question, we studied the effects of ethylene on the gray mold fungus Botrytis cinerea and the disease it causes on Nicotiana benthamiana plants. Exposure of B. cinerea to ethylene inhibited mycelium growth in vitro and caused transcriptional changes in a large number of fungal genes. A screen of fungal signaling mutants revealed a Galpha null mutant (deltabcg1) which was ethylene insensitive, overproduced ethylene in vitro, and showed considerable transcriptional changes in response to ethylene compared with the wild type. Aminoethoxyvinylglycine (AVG)-treated, ethylene-nonproducing N. benthamiana plants developed much larger necroses than ethylene-producing plants, whereas addition of ethylene to AVG-treated leaves restricted disease spreading. Ethylene also affected fungal gene expression in planta. Expression of a putative pathogenicity fungal gene, bcspl1, was enhanced 24 h after inoculation in ethylene-producing plants but only 48 h after inoculation in ethylene-nonproducing plants. Our results show that the responses of B. cinerea to ethylene are partly mediated by a G protein signaling pathway, and that ethylene-induced plant resistance might involve effects of plant ethylene on both the plant and the fungus.

Amino Acid Sequence↗
PubMed1982

Effects of exogenous ethylene on ethylene production in citrus leaf tissue.

Exogenous ethylene stimulated ethylene production in intact citrus (Citrus sinensis L. Osbeck cv. "Washington Navel") leaves and leaf discs following a 24-hour exposure. Studies with leaf discs showed that ethylene production decreased when ethylene was removed by aeration. The extent of stimulation was dependent upon the concentration of exogenous ethylene (1-10 microliters per liter). Silver ion blocked the autocatalytic effect of ethylene at concentrations of 0.5 millimolar and lower, but increased ethylene production at higher concentrations. The stimulating effect of ethylene resulted from the enhancement of both 1-aminocyclopropane-1-carboxylic acid (ACC) formation and the conversion of ACC to ethylene. Whereas autocatalysis was evident following 24 hours incubation, autoinhibition of wound- and mannitol-induced ethylene production was observed during the first 24-hour incubation. Ethylene treatment during this period resulted in a marked decrease in ACC levels and ethylene production rates. Furthermore, in leaf discs treated for 24 hours with ethylene, ethylene production rates increased greatly during the first 2 hours after removal of exogenous ethylene by aeration. This increase was eliminated if the discs were transferred to propylene instead of air, indicating that the autocatalytic effect of ethylene is counteracted by its autoinhibitory effect. It is suggested that autocatalysis involves increased synthesis of ACC synthase and the enzyme responsible for the conversion of ACC to ethylene, whereas autoinhibition involves suppression of the activity of these two enzymes.

Journal Article↗
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↗
PubMed1985

Promotion by Ethylene of the Capability to Convert 1-Aminocyclopropane-1-carboxylic Acid to Ethylene in Preclimacteric Tomato and Cantaloupe Fruits.

The intact fruits of preclimacteric tomato (Lycopersicon esculentum Mill) or cantaloupe (Cucumis melo L.) produced very little ethylene and had low capability of converting 1-aminocyclopropane-1-carboxylic acid (ACC) to ethylene. When these unripe tomato or cantaloupe fruits were treated with ethylene for 16 hours there was no increase in ACC content or in ethylene production rate, but the tissue's capability to convert ACC to ethylene increased markedly. Such an effect was also observed in fruits of tomato mutants rin and nor, which do not undergo ripening and the climacteric increase in ethylene production during the senescence. The development of this ethylene-forming capability induced by ethylene increased with increasing ethylene concentration (from 0.1 to 100 microliters per liter) and duration (1 to 24 hours); when ethylene was removed this capability remained high for sometime (more than 24 hours). Norbornadiene, a competitive inhibitor of ethylene action, effectively eliminated the promotive effect of ethylene in tomato fruit. These data indicate that the development of the capability to convert ACC to ethylene in preclimacteric tomato and cantaloupe fruits are sensitive to ethylene treatment and that when these fruits are exposed to exogenous ethylene, the increase in ethylene-forming enzyme precedes the increase in ACC synthase.

Journal Article↗
PubMed1988

Ethylene-induced gene expression in carnation petals : relationship to autocatalytic ethylene production and senescence.

Exposure of carnation (Dianthus caryophyllus L.) flowers to ethylene evokes the developmental program of petal senescence. The temporal relationship of several aspects of this developmental program following treatment with ethylene was investigated. Exposure of mature, presenescent flowers to 7.5 microliters per liter ethylene for at least 6 hours induced petal in-rolling and premature senescence. Autocatalytic ethylene production was induced in petals following treatment with ethylene for 12 or more hours. A number of changes in mRNA populations were noted in response to ethylene, as determined by in vitro translation of petal polyadenylated RNA. At least 6 mRNAs accumulated following ethylene exposure. The molecular weights of their in vitro translation products were 81, 58, 42, 38, 35, and 25 kilodaltons. Significant increases in abundance of most mRNAs were observed 3 hours following ethylene exposure. Ethylene exposure resulted in decreased abundance of another group of mRNAs. Treatment of flowers with competitive inhibitors of ethylene action largely prevented the induction of these ethylene responses in petals. An increase in flower age was accompanied by an increase in the capacity for ethylene to induce petal in-rolling, autocatalytic ethylene production, and changes in mRNA populations suggesting that these responses are regulated by both sensitivity to ethylene and ethylene concentration. These results indicate that changes in petal physiology resulting from exposure to ethylene may be the result of rapid changes in gene expression.

Journal Article↗
PubMed2006

Transcriptional regulation of ethylene receptor and CTR genes involved in ethylene-induced flower opening in cut rose (Rosa hybrida) cv. Samantha.

In this work, the effect of ethylene on flower opening of cut rose (Rosa hybrida) cv. Samantha was studied. However, although ethylene hastened the process of flower opening, 1-MCP (1-methylcyclopropene), an ethylene action inhibitor, impeded it. Ethylene promoted ethylene production in petals, but 1-MCP did not inhibit this process. Of the four ethylene biosynthetic genes tested, Rh-ACS1 and Rh-ACS2 were undetectable; Rh-ACS3 and Rh-ACO1 expression was enhanced by ethylene slightly and greatly, respectively. However, their mRNA amounts were not inhibited by 1-MCP compared with controls. Expression of seven signalling component genes was also studied, including three ethylene receptors (Rh-ETR1, Rh-ETR3, and Rh-ETR5), two CTRs (Rh-CTR1 and Rh-CTR2), and two transcription factors (Rh-EIN3-1 and Rh-EIN3-2). Transcripts of Rh-ETR5, Rh-EIN3-1, and Rh-EIN3-2 were accumulated in a constitutive manner and had no or little response to ethylene or 1-MCP, while transcript levels of Rh-ETR1 and Rh-CTR1 were substantially elevated by ethylene, and those of Rh-ETR3 and Rh-CTR2 were greatly enhanced by ethylene; 1-MCP reduced all the four genes to levels much less than those in control flowers. These results show that ethylene triggers physiological responses related to flower opening in cut rose cv. Samantha, and that continued ethylene perception results in flower opening. Ethylene may regulate flower opening mainly through expression of two ethylene receptor genes (Rh-ETR1 and Rh-ETR3) and two CTR (Rh-CTR1 and Rh-CTR2) genes.

Cyclopropanes↗
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↗