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At least 19 recordsLinked to original sources
PubMed2006

The atmospheric photolysis of E-2-hexenal, Z-3-hexenal and E,E-2,4-hexadienal.

The atmospheric photolysis of E-2-hexenal, Z-3-hexenal and E,E-2,4-hexadienal has been investigated at the large outdoor European Photoreactor (EUPHORE) in Valencia, Spain. E-2-Hexenal and E,E-2,4-hexadienal were found to undergo rapid isomerization to produce Z-2-hexenal and a ketene-type compound (probably E-hexa-1,3-dien-1-one), respectively. Both isomerization processes were reversible with formation of the reactant slightly favoured. Values of j(E-2-hexenal)/j(NO(2)) = (1.80 +/- 0.18) x 10(-2) and j(E,E-2,4-hexadienal)/j(NO(2)) = (2.60 +/- 0.26) x 10(-2) were determined. The gas phase UV absorption cross-sections of E-2-hexenal and E,E-2,4-hexadienal were measured and used to derive effective quantum yields for photoisomerization of 0.36 +/- 0.04 for E-2-hexenal and 0.23 +/- 0.03 for E,E-2,4-hexadienal. Although photolysis appears to be an important atmospheric degradation pathway for E-2-hexenal and E,E-2,4-hexadienal, the reversible nature of the photolytic process means that gas phase reactions with OH and NO(3) radicals are ultimately responsible for the atmospheric removal of these compounds. Atmospheric photolysis of Z-3-hexenal produced CO, with a molar yield of 0.34 +/- 0.03, and 2-pentenal via a Norrish type I process. A value of j(Z-3-hexenal)/j(NO(2)) = (0.4 +/- 0.04) x 10(-2) was determined. The results suggest that photolysis is likely to be a minor atmospheric removal process for Z-3-hexenal.

Aldehydes↗
PubMed2000

An approach to cancer risk assessment for the food constituent 2-hexenal on the basis of 1,N2-propanodeoxyguanosine adducts of 2-hexenal in vivo.

2-Hexenal is formed by plants, and humans are regularly exposed to this mutagenic/genotoxic compound via vegetable foods. 2-Hexenal has not been tested for carcinogenicity, but it forms exocyclic 1,N2-propanodeoxyguanosine adducts like other carcinogenic alpha,beta-unsaturated carbonyl compounds. To quantify the respective DNA adducts as an approach to a theoretical cancer risk assessment, we used a newly developed 32P-postlabelling technique based on nuclease P1 enrichment, allowing a detection limit of 3 adducts per 10(8) nucleotides. Adduct levels were measured at different doses and the covalent binding index (CBI) was found to be dose-dependent. This can be explained by glutathione depletion at higher doses. The CBI at low doses was 0.06. A negligible cancer risk of 1-5 per 10(7) lives was estimated on the basis of TD50 values calculated from the correlation between CBI and TD50 of Lutz and on the daily intake of 2-hexenal via vegetable foods, fruit juices and black tea. A risk of 1.6-8.5 per 10(6) lives was estimated for the hypothetical case of glutathione depletion, e.g. due to consuming special medicaments. In every case, the benefit from eating fruit and vegetables is clearly higher than a possible low and unavoidable cancer risk. Utilization of 2-hexenal as a flavouring agent or as a fungicide, breeding fungus-resistant plants or technological gene construction of fungus resistance may lead to a high hypothetical cancer risk of 2-6 per 10(4) lives under certain circumstances which are avoidable and deserves special case-by-case consideration.

Administration, Oral↗
PubMed1998

Stereochemistry of the biotransformation of 1-hexene and 2-methyl-1-hexene with rat liver microsomes and purified P450s of rats and humans.

The epoxidation of 1-hexene (1a) and 2-methyl-1-hexene (1b), two hydrocarbons present in the ambient air as pollutants, is catalyzed by some human and rat P450 enzymes. The enantioselectivities of these processes, when the reactions were carried out using rat and human liver microsomal preparations, were modest and dependent on both P450 composition and substrate concentrations. Various P450 isoforms (rat P450 2B1 and human P450 2C10 and 2A6) catalyzed the double bond oxidation of 1a and 1b with different product enantioselectivities. In the case of 1a, a moderately enantioselective hydroxylation at the allylic C(3) with the formation of 1-hexen-3-ol (4a) by microsomes from control or preinduced rats was also observed. The oxidation of this metabolite was, in turn, catalyzed by rat liver microsomes and mainly by rat P450 2C11, leading exclusively to the formation of 1-hexen-3-one, with no double bond epoxidation being observed. The stereochemical course of the microsomal epoxide hydrolase-catalyzed hydrolysis of the epoxy alcohols, threo-(+/-)- and erythro-(+/-)-1, 2-epoxyhexan-3-ol, theoretically expected to be formed from 4a, has been investigated.

Alkenes↗
PubMed1989

Effects of the pyrrolizidine alkaloid senecionine and the alkenals trans-4-OH-hexenal and trans-2-hexenal on intracellular calcium compartmentation in isolated hepatocytes.

The pyrrolizidine alkaloid senecionine has been shown to produce an increase in cytosolic free Ca2+ concentration in isolated hepatocytes that correlated with an increase in cellular toxicity. The cytotoxicity was greater in the absence of extracellular Ca2+ than in its presence, suggesting that alterations in intracellular Ca2+ distribution, and not an influx of extracellular Ca2+, were responsible for the senecionine-induced hepatotoxicity. The effect of senecionine, as well as the effects of trans-4-OH-2-hexenal (t-4HH), a microsomal metabolite of senecionine, and a related alkenal, trans-2-hexenal, on the sequestration of Ca2+ in mitochondrial and extramitochondrial compartments were examined in isolated hepatocytes. Each of the test compounds elicited a decrease in the available extramitochondrial Ca2+ stores that was inhibited by pretreatment with the thiol group reducing agent, dithiothreitol. Senecionine and t-4HH decreased the level of Ca2+ sequestered in the mitochondrial compartment of hepatocytes. The presence of a pyridine nucleotide reducing agent, beta-hydroxybutyrate, inhibited this reduction. These results suggest that both senecionine and t-4HH inhibit the sequestration of Ca2+ in extramitochondrial and mitochondrial compartments possibly by inactivating free sulfhydryl groups and oxidizing pyridine nucleotides respectively.

Aldehydes↗
PubMed2005

Cytotoxicities, cell cycle and caspase evaluations of 1,6-diaryl-3(Z)-hexen-1,5-diynes, 2-(6-aryl-3(Z)-hexen-1,5-diynyl)anilines and their derivatives.

Compounds 3, 6-7, 9-10, 15-17, and 20-21 showed growth inhibition effects on a full panel of 60 human cancer cell lines, and most of the average IC50 values of the indicated analogues were from < 0.01 to 96.6 microM, in which analogues 16 and 17 revealed the highest cytotoxic activity with the cancer cell lines at 10(-7) M concentration range. During the cell cycle analysis, a moderate to high apoptotic progress induction was shown by 3, 9, 16-17, and 20 compared with the control, which 2-(6-(2-thienyl)-3(Z)-hexen-1,5-diynyl)aniline 16 showed the highest apoptotic effect. Structures 16-17 displayed a significant G2/M phase arrest in the cell growth cycle compared with other derivatives, which the proportions of the G2/M phase cells were accumulated to 71.5% and 82.6%, respectively. Moreover, the colorimetric assay of 16-17 also provided advanced evidence to the relationship between the compounds and the caspase-3 enzyme, which was one of the major promoters of apoptotic effect.

Alkynes↗
PubMedDate not supplied

[Use of synthetic steroids, inhibitors of microsomal enzymes, for retention of hexenal in the body and for prolongation of hexenal anesthesia under experimental conditions].

17alpha-hydroxydeoxycorticosterone and its acetate derivative inhibited the activity of rat liver microsomal enzymes. The inhibitory effect of steroids was not accompanied by induction of the enzyme synthesis, which was characteristic for the other known inhibitors of mixed function oxydases (SKF 525-A, DPEA, MPDK). These properties of the steroids suggested their use for prolongation of the effect of drugs, which are inactivated by microsomal enzymes. The suggestion was tested using hexobarbital as an example. The transformation of hexobarbital in vitro by the rat liver microsomal enzymes was completely inhibited by the equimolar amount of the steroid acetate. Treatment of rats with the steroid acetate almost doubled the life-time of the hexobarbital in rat blood and resulted in the 1.5-fold increase of the sleeping time. The most effective dose of the steroid acetate was 5 mg per 100 g of body weight, the drug being injected 15 min before hexobarbital administration.

Anesthesia, General↗
PubMedDate not supplied

(E)-2-hexenal-induced DNA damage and formation of cyclic 1,N2-(1,3-propano)-2'-deoxyguanosine adducts in mammalian cells.

(E)-2-Hexenal (hexenal), a natural flavor compound, acts as directly genotoxic agent and forms cyclic 1,N2-propano adducts with deoxyguanosine. Formation of this adduct in isolated DNA and in cells was studied with a modified 32P-postlabeling procedure including HPLC separation, nuclease P1 enrichment, two-dimensional TLC of adducted nucleotide bisphosphates on PEI-cellulose, and quantification of adduct spots by liquid scintillation counting. Adduct formation with the more reactive crotonaldehyde was included for comparison. Synthesized adducted dG-3'-phosphates served as external standards for identification and quantification. In calf thymus DNA, hexenal (0.2 mM) shows a time dependent formation of adducts, yielding 1.55 pmol/mumol of DNA at 5 h incubation. With crotonaldehyde (0.2 mM) the adduct rate was about 10-fold higher. Hexenal also generated 1,N2-propano-dG adducts in the human lymphoblastoid Namalva cell line (0.2 mM, 1 h, 86 fmol/mumol of DNA) and in primary rat colon mucosa cells (0.4 mM, 30 min, 50 fmol/mumol of DNA). In primary colon mucosa cells from rats and humans, hexenal and crotonaldehyde (0.4 mM, 30 min) induced DNA damage, detected by single cell microgel electrophoresis (comet assay). In primary rat gastric mucosa cells, hexenal was only weakly active, inducing detectable DNA damage in 20% of cells at 0.8 mM concentration. In contrast, primary mucosa cells from rat esophagus were as sensitive as colon cells. After single oral application of hexenal to rats (up to 320 mg/kg body wt) DNA damage was not detectable in gastrointestinal mucosa. Analysis of hexenal in selected flavored foods revealed concentrations up to 14 ppm (0.14 mM) that are comparable to its natural occurrence in some fruits and vegetables (up to 30 ppm). Thus, the concentration range selected for the toxicological studies described here clearly is relevant: Hexenal, at concentrations found in food, exerts genotoxic effects in cells from rat and human gastrointestinal tract.

Aldehydes↗
PubMed2006

Activity of trans-2-hexenal against Penicillium expansum in 'Conference' pears.

AIMS: To investigate the effects of trans-2-hexenal on blue mould disease, patulin content and fruit quality in 'Conference' pears. METHODS AND RESULTS: Fruits, wounded and inoculated with Penicillium expansum or non-inoculated, were exposed to trans-2-hexenal vapour treatment (12.5 microl l(-1)) at 20 degrees C. A greater reduction of decay was obtained by treatment application 24 or 48 h after inoculation, in contrast trans-2-hexenal application 2 h after inoculation was ineffective. Fruit storage temperature (-1 degrees C) after treatment did not affect the antifungal activity. Although 2-h exposure to trans-2-hexenal was effective in reducing blue mould, an exposure of at least 8 h was required to reduce fruit patulin content. Treatments did not affect fruit physical-chemical characteristics. After 6 days at 20 degrees C following exposure, trans-2-hexenal residue in treated fruits was less than the natural content of the compound in unripe fruits. CONCLUSIONS: trans-2-Hexenal treatment is effective in the reduction of blue mould infections and patulin content in Conference pears when applied 24-48 h after pathogen inoculation. SIGNIFICANCE AND IMPACT OF THE STUDY: trans-2-Hexenal could be a natural alternative to fungicides in the control of P. expansum infections. Further work is needed to study the methods and conditions avoiding the persistence of off-odours and off-flavours in pears after their exposure to trans-2-hexenal vapours.

Aldehydes↗
PubMed1995

Genotoxic effects of the alpha, beta-unsaturated aldehydes 2-trans-butenal, 2-trans-hexenal and 2-trans, 6-cis-nonadienal.

The genotoxic effects of the 2-alkenals crotonaldehyde, 2-trans-hexenal and 2-trans-6-cis-nonadienal were studied by cytogenetic methods, analyzing frequencies of sister-chromatid-exchanges, numerical and structural chromosome aberrations and micronucleus induction in human blood lymphocytes and cells of the permanent Namalva line. Crotonaldehyde and hexenal were tested in concentrations of 5 microM to 250 microM and nonadienal from 5 microM to 70 microM. Significant dose-related increases of sister-chromatid-exchanges and micronuclei were found for all three compounds. Structural chromosomal aberrations were significantly increased only by crotonaldehyde, but not by hexenal and nonadienal. In contrast numerical chromosome aberrations were not induced by crotonaldehyde whereas hexenal and nonadienal were potent inducers of aneuploidy. The micronuclei were classified by using a centromere-specific DNA probe in a fluorescence in situ hybridization assay. Hexenal and nonadienal increased the percentage of centromere-positive micronuclei, nonadienal being considerably more potent than hexenal. From these results it was concluded that crotonaldehyde acts more as a clastogen whereas hexenal and nonadienal preferentially show aneugenic effects.

Aldehydes↗
PubMed2006

LC/MS/MS method for the quantitation of trans-2-hexenal-derived exocyclic 1,N(2)-propanodeoxyguanosine in DNA.

trans-2-Hexenal is an alpha,beta-unsaturated aldehyde to which humans are exposed daily in small amounts. Hexenal has demonstrated mutagenicity and genotoxicity in vitro and reacts with deoxyguanosine to form diastereomeric hexenal-derived exocyclic 1,N(2)-propanodeoxyguanosine (Hex-PdG) adducts. A highly sensitive and specific method for the measurement of Hex-PdG in DNA has not previously been available. An LC/MS/MS assay for the quantitation of Hex-PdG, using [(13)C4(15)N2]Hex-PdG as an internal standard, was developed, to assess binding of hexenal to DNA. Samples were purified prior to analysis by centrifuge filtration and solid phase extraction and analyzed by LC/MS/MS in the selected reaction monitoring (SRM) mode (SRM m/z 366.2 --> 250.2 for Hex-PdG; SRM m/z 372.2 --> 256.2 for [(13)C4(15)N2]Hex-PdG). Recovery of standards was 89% or greater, and quantitation was unaffected by the addition of increasing concentrations of calf thymus DNA (ctDNA). The limit of quantitation, determined in samples of 200 microg of ctDNA spiked with analyte standard, was 0.015 fmol/microg DNA, which corresponds to approximately 5 Hex-PdG/10(9) unmodified nucleotides. Hex-PdG was detected in ctDNA treated with 0.021 microM, 0.21 microM, or 2.1 mM hexenal but not in untreated DNA. Furthermore, Hex-PdG was not detected in DNA exposed to reactive oxygen species-mediated deoxyribose attack and lipid peroxidation, which resulted in a significant increase in the malondialdehyde-derived pyrimido[1,2-a]purin-10(3H)one. Hex-PdG was not detected in DNA of untreated rat liver, but Hex-PdG in hexenal-treated calf thymus DNA was quantifiable when spiked into the rat liver DNA at 0.035 or 0.35 fmol/microg DNA. These data indicate that Hex-PdG is formed following hexenal treatment and that this method is suitable for in vitro or in vivo assessment of Hex-PdG formation.

Aldehydes↗
PubMed1999

Detection of 1,N2-propanodeoxyguanosine adducts of 2-hexenal in organs of Fischer 344 rats by a 32P-post-labeling technique.

2-Hexenal is an alpha,beta-unsaturated carbonyl compound which is mutagenic, genotoxic and forms cyclic 1,N2-propanodeoxyguanosine adducts like similar propenals for which carcinogenicity was shown, e.g. acrolein or crotonaldehyde. Since humans have a permanent intake of 2-hexenal via vegetarian food this genotoxic compound is considered to play a role in human carcinogenicity. The data base is, however, presently not sufficient for a cancer risk assessment. To date no long term carcinogenicity study on 2-hexenal has been published. Detection of respective DNA adducts of this substance in animals or humans could allow cancer risk assessment. Therefore, we have developed a 32P-post-labeling technique based on nuclease P1 enrichment and TLC separation of the labeled adducts. The respective adducts are stable over a wide pH range from pH 4 to pH 11 and relatively stable against nuclease P1. The detection limit was 0.03 adducts per 10(6) nucleotides and the recovery was 10%. With this method we have shown in vivo formation of 1,N 2-propanodeoxyguanosine adducts of 2-hexenal for the first time and found the respective DNA adducts in different organs of Fischer 344 rats after gavage of 500, 200 and 50 mg 2-hexenal/kg body wt. No adducts could be detected in the organs of untreated rats. There is a clear dependence of the adduct level and the CBI (covalent binding index) on the dose. The CBI of 2-hexenal calculated on the basis of our adduct levels is extremely low (0.06). Since intake of 2-hexenal via fruit and vegetables is very low the cancer risk from 2-hexenal intake via food must also be considered as very low according to a first raw estimation on the basis of CBI and intake. The situation deserves, however, a more precise risk assessment in the future.

Aldehydes↗
PubMed2006

Characterization of a BAHD acyltransferase responsible for producing the green leaf volatile (Z)-3-hexen-1-yl acetate in Arabidopsis thaliana.

Green-leaf volatiles are commonly emitted from mechanically and herbivore-damaged plants. Derived from the lipoxygenase pathway, these compounds may serve as attractants to predators and parasitoids of herbivores, prevent the spread of bacteria and fungi, and induce several important plant defense pathways. In Arabidopsis thaliana, the major volatile released upon mechanical wounding of the leaves is the GLV ester, (Z)-3-hexen-1-yl acetate. We have characterized a member of the BAHD acyltransferase gene family At3g03480 which catalyzes the formation of (Z)-3-hexen-1-yl acetate from acetyl-CoA and (Z)-3-hexen-1-ol. The encoded acetyl CoA:(Z)-3-hexen-1-ol acetyltransferase (CHAT) has the ability to accept several medium-chain-length aliphatic and benzyl-derived alcohols, but has highest catalytic efficiency with (Z)-3-hexen-1-ol. The highest expression of CHAT occurs in the leaves and stems. Upon mechanical damage, the (Z)-3-hexen-1-yl acetate emission peaked after 5 min and declined to pre-damage levels after 90 min. However, CHAT gene transcript levels increased much more slowly with the highest levels detected between 3 and 6 h after wounding. An increase in CHAT enzyme activity in vitro followed the transcript increase, with levels peaking between 10 and 12 h after wounding. Plants expressing either an RNAi cassette for the CHAT gene or plants harboring a T-DNA insertion in the CHAT coding region had greatly reduced (Z)-3-hexen-1-yl acetate emission, showing that the CHAT enzyme is responsible for the in planta production of this ester.

Acetates↗
PubMed2003

Cardiac toxic effects of trans-2-hexenal are mediated by induction of cardiomyocyte apoptotic pathways.

Aldehydes are ubiquitous pollutants with well-indicated but ill-defined cardiovascular toxicity. To investigate the direct toxic effects of environmental aldehyde exposure on the myocardium, 8-wk-old male ICR (Institute of Cancer Research) strain mice were gavage fed trans-2-hexenal (0.1, 1, 10, or 50 mg/kg/wk) or corn oil (vehicle) for 4 wk, during which cardiac function, myocardial morphology, cardiomyocyte apoptosis, and the cytochrome cmediated caspase activation apoptotic pathway were determined. Quantification by enzyme-linked immunosorbent assay (ELISA) revealed that aldehyde- protein adducts increase in mouse hearts following hexenal treatment, whereas echocardiographic analysis displayed a significant impairment of basal left-ventricular contractile function. Both histological analysis and TUNEL (terminal deoxynucleotidyl transferase-mediated nick-end labeling) staining indicated condensed nuclei and a significant increase in cardiomyocyte apoptosis in these mice, but immunohistochemistry-based confocal microscope revealed no marked myofibril disarray. Release of cytochrome c from mitochondria into the cytosol, concomitant with activation of caspase-3 and -9, was also found in hexenal-treated groups. In addition, isolated cardiac mitochondria formed hexenal-protein adducts when treated with hexenal, providing indirect evidence that the cardiac mitochondrion is one of primary subcellular targets of aldehyde toxins. These findings suggest that trans-2-hexenal exposure results in direct cardiac toxicity through, at least in part, induction of mitochondrial cytochrome c release-mediated apoptosis in cardiomyocytes, indicating that the cardiac mitochondrion is one of principal subcellular targets of aldehyde toxins.

Actinin↗
PubMed1999

Cancer risk assessment for crotonaldehyde and 2-hexenal: an approach.

Crotonaldehyde and 2-hexenal are bifunctional compounds that form 1,N2-propanodeoxyguanosine adducts and are mutagenic and genotoxic; crotonaldehyde is carcinogenic. Analysis of the mutations resulting from crotonaldehyde-induced DNA damage revealed the importance of deoxyguanosine adducts. Humans are exposed ubiquitously to these compounds by various routes. The highest daily intake of crotonaldehyde is assumed to be derived from cigarette smoke (31-169 micrograms/kg body weight), and the highest intake of 2-hexenal is probably from fruit and vegetables (31-165 micrograms/kg body weight per day). Because these compounds are suspected to play on important role in carcinogenicity, we developed sensitive 32P-postlabelling techniques for DNA adducts of crotonaldehyde and hexenal, in order to improve estimates of cancer risk. The respective standards were also synthesized and characterized spectroscopically. We report here the results of the 32P-postlabelling, e.g. the stability of the adducts in respect of nuclease P1 treatment, their labelling efficiencies, thin-layer chromatography of adduct spots and the recoveries and detection limits. In untreated male Fischer 344 rats, neither crotonaldehyde nor 2-hexenal adducts were detected, but crotonaldehyde adducts were found in the tissues of rats given single doses of 200 or 300 mg/kg body weight and in the livers of rats after repeated doses of 1 or 10 mg/kg body weight. The adduct levels were higher 20 h after gavage than after 12 h. The adducts persist to a certain extent. 2-Hexenal adducts were detected in tissues of male Fischer 344 rats after gavage with single doses of 50, 200 or 500 mg/kg body weight. The highest adduct levels were measured 48 h after gavage, but no adducts were found 8 h after gavage. Two approaches for cancer risk estimation are discussed. One is based on the correlation between the covalent binding index, calculated from adduct levels, and the median toxic dose (TD50) (Lutz, 1986) and showed a cancer risk of 1 per 10(7) lives for hexenal, assuming dietary intakes of 31-165 micrograms/kg body weight per day. The other is based on a cancer incidence of 0.07 at a dose of crotonaldehyde of 4.2 mg/kg body weight per day assessed from the study of Chung et al. (1986), which can be interpreted as a risk of 5.8-18 new cases per 10(4) smokers, assuming a consumption of 30 cigarettes per day. The latter approach may, however, lead to an overestimate of the cancer risk associated with exposure to crotonaldehyde; the estimate based on our binding studies resulted in a 20-fold lower estimate of the carcinogenic risk of crotonaldehyde.

Adenosine Triphosphate↗