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Epoxygenated Fatty Acids Inhibit Retinal Vascular Inflammation.
Capozzi ME, Hammer SS, McCollum GW, Penn JS
(2016) Sci Rep 6: 39211
MeSH Terms: 8,11,14-Eicosatrienoic Acid, Adamantane, Animals, Cells, Cultured, Disease Models, Animal, Down-Regulation, Endothelial Cells, Epoxy Compounds, Fatty Acids, Unsaturated, Humans, Intercellular Adhesion Molecule-1, Lauric Acids, Male, Mice, Retinal Vasculitis, Retinal Vessels, Tumor Necrosis Factor-alpha, Vascular Cell Adhesion Molecule-1
Show Abstract · Added April 10, 2019
The objective of the present study was to assess the effect of elevating epoxygenated fatty acids on retinal vascular inflammation. To stimulate inflammation we utilized TNFα, a potent pro-inflammatory mediator that is elevated in the serum and vitreous of diabetic patients. In TNFα-stimulated primary human retinal microvascular endothelial cells, total levels of epoxyeicosatrienoic acids (EETs), but not epoxydocosapentaenoic acids (EDPs), were significantly decreased. Exogenous addition of 11,12-EET or 19,20-EDP when combined with 12-(3-adamantane-1-yl-ureido)-dodecanoic acid (AUDA), an inhibitor of epoxide hydrolysis, inhibited VCAM-1 and ICAM-1 expression and protein levels; conversely the diol product of 19,20-EDP hydrolysis, 19,20-DHDP, induced VCAM1 and ICAM1 expression. 11,12-EET and 19,20-EDP also inhibited leukocyte adherence to human retinal microvascular endothelial cell monolayers and leukostasis in an acute mouse model of retinal inflammation. Our results indicate that this inhibition may be mediated through an indirect effect on NFκB activation. This is the first study demonstrating a direct comparison of EET and EDP on vascular inflammatory endpoints, and we have confirmed a comparable efficacy from each isomer, suggesting a similar mechanism of action. Taken together, these data establish that epoxygenated fatty acid elevation will inhibit early pathology related to TNFα-induced inflammation in retinal vascular diseases.
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MeSH Terms
Standard Reticle Slide To Objectively Evaluate Spatial Resolution and Instrument Performance in Imaging Mass Spectrometry.
Zubair F, Prentice BM, Norris JL, Laibinis PE, Caprioli RM
(2016) Anal Chem 88: 7302-11
MeSH Terms: Dimethylpolysiloxanes, Epoxy Compounds, Gentian Violet, Ions, Microscopy, Atomic Force, Polymers, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Show Abstract · Added August 17, 2016
Spatial resolution is a key parameter in imaging mass spectrometry (IMS). Aside from being a primary determinant in overall image quality, spatial resolution has important consequences on the acquisition time of the IMS experiment and the resulting file size. Hardware and software modifications during instrumentation development can dramatically affect the spatial resolution achievable using a given imaging mass spectrometer. As such, an accurate and objective method to determine the working spatial resolution is needed to guide instrument development and ensure quality IMS results. We have used lithographic and self-assembly techniques to fabricate a pattern of crystal violet as a standard reticle slide for assessing spatial resolution in matrix-assisted laser desorption/ionization (MALDI) IMS experiments. The reticle is used to evaluate spatial resolution under user-defined instrumental conditions. Edgespread analysis measures the beam diameter for a Gaussian profile and line scans measure an "effective" spatial resolution that is a convolution of beam optics and sampling frequency. The patterned crystal violet reticle was also used to diagnose issues with IMS instrumentation such as intermittent losses of pixel data.
1 Communities
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7 MeSH Terms
Polymerase Bypass of N(6)-Deoxyadenosine Adducts Derived from Epoxide Metabolites of 1,3-Butadiene.
Kotapati S, Wickramaratne S, Esades A, Boldry EJ, Quirk Dorr D, Pence MG, Guengerich FP, Tretyakova NY
(2015) Chem Res Toxicol 28: 1496-507
MeSH Terms: Butadienes, Chromatography, High Pressure Liquid, DNA, DNA Adducts, DNA Primers, DNA Replication, DNA-Directed DNA Polymerase, Deoxyadenosines, Epoxy Compounds, Humans, Kinetics, Oligodeoxyribonucleotides, Spectrometry, Mass, Electrospray Ionization
Show Abstract · Added March 14, 2018
N(6)-(2-Hydroxy-3-buten-1-yl)-2'-deoxyadenosine (N(6)-HB-dA I) and N(6),N(6)-(2,3-dihydroxybutan-1,4-diyl)-2'-deoxyadenosine (N(6),N(6)-DHB-dA) are exocyclic DNA adducts formed upon alkylation of the N(6) position of adenine in DNA by epoxide metabolites of 1,3-butadiene (BD), a common industrial and environmental chemical classified as a human and animal carcinogen. Since the N(6)-H atom of adenine is required for Watson-Crick hydrogen bonding with thymine, N(6)-alkylation can prevent adenine from normal pairing with thymine, potentially compromising the accuracy of DNA replication. To evaluate the ability of BD-derived N(6)-alkyladenine lesions to induce mutations, synthetic oligodeoxynucleotides containing site-specific (S)-N(6)-HB-dA I and (R,R)-N(6),N(6)-DHB-dA adducts were subjected to in vitro translesion synthesis in the presence of human DNA polymerases β, η, ι, and κ. While (S)-N(6)-HB-dA I was readily bypassed by all four enzymes, only polymerases η and κ were able to carry out DNA synthesis past (R,R)-N(6),N(6)-DHB-dA. Steady-state kinetic analyses indicated that all four DNA polymerases preferentially incorporated the correct base (T) opposite (S)-N(6)-HB-dA I. In contrast, hPol β was completely blocked by (R,R)-N(6),N(6)-DHB-dA, while hPol η and κ inserted A, G, C, or T opposite the adduct with similar frequency. HPLC-ESI-MS/MS analysis of primer extension products confirmed that while translesion synthesis past (S)-N(6)-HB-dA I was mostly error-free, replication of DNA containing (R,R)-N(6),N(6)-DHB-dA induced significant numbers of A, C, and G insertions and small deletions. These results indicate that singly substituted (S)-N(6)-HB-dA I lesions are not miscoding, but that exocyclic (R,R)-N(6),N(6)-DHB-dA adducts are strongly mispairing, probably due to their inability to form stable Watson-Crick pairs with dT.
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13 MeSH Terms
Oxidative Transformation of Demethoxy- and Bisdemethoxycurcumin: Products, Mechanism of Formation, and Poisoning of Human Topoisomerase IIα.
Gordon ON, Luis PB, Ashley RE, Osheroff N, Schneider C
(2015) Chem Res Toxicol 28: 989-96
MeSH Terms: Antigens, Neoplasm, Curcuma, Curcumin, DNA Cleavage, DNA Topoisomerases, Type II, DNA-Binding Proteins, Epoxy Compounds, Humans, Oxidation-Reduction, Plant Extracts
Show Abstract · Added October 9, 2015
Extracts from the rhizome of the turmeric plant are widely consumed as anti-inflammatory dietary supplements. Turmeric extract contains the three curcuminoids, curcumin (≈80% relative abundance), demethoxycurcumin (DMC; ≈15%), and bisdemethoxycurcumin (BDMC; ≈5%). A distinct feature of pure curcumin is its instability at physiological pH, resulting in rapid autoxidation to a bicyclopentadione within 10-15 min. Here, we describe oxidative transformation of turmeric extract, DMC, and BDMC and the identification of their oxidation products using LC-MS and NMR analyses. DMC autoxidized over the course of 24 h to the expected bicyclopentadione diastereomers. BDMC was resistant to autoxidation, and oxidative transformation required catalysis by horseradish peroxidase and H2O2 or potassium ferricyanide. The product of BDMC oxidation was a stable spiroepoxide that was equivalent to a reaction intermediate in the autoxidation of curcumin. The ability of DMC and BDMC to poison recombinant human topoisomerase IIα was significantly increased in the presence of potassium ferricyanide, indicating that oxidative transformation was required to achieve full DNA cleavage activity. DMC and BDMC are less prone to autoxidation than curcumin and contribute to the enhanced stability of turmeric extract at physiological pH. Their oxidative metabolites may contribute to the biological effects of turmeric extract.
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10 MeSH Terms
Lipoxygenase-catalyzed transformation of epoxy fatty acids to hydroxy-endoperoxides: a potential P450 and lipoxygenase interaction.
Teder T, Boeglin WE, Brash AR
(2014) J Lipid Res 55: 2587-96
MeSH Terms: 8,11,14-Eicosatrienoic Acid, Animals, Arachidonate 12-Lipoxygenase, Arachidonate 15-Lipoxygenase, Biocatalysis, Blood Platelets, Chromatography, High Pressure Liquid, Eicosanoids, Epoxy Compounds, Gas Chromatography-Mass Spectrometry, Humans, Hydroxylation, Linolenic Acids, Lipid Peroxides, Lipoxygenase, Mice, Molecular Structure, Nuclear Magnetic Resonance, Biomolecular, Oxidation-Reduction, Recombinant Proteins, Soybean Proteins, Spectrometry, Mass, Electrospray Ionization, Stereoisomerism
Show Abstract · Added January 21, 2015
Herein, we characterize a generally applicable transformation of fatty acid epoxides by lipoxygenase (LOX) enzymes that results in the formation of a five-membered endoperoxide ring in the end product. We demonstrated this transformation using soybean LOX-1 in the metabolism of 15,16-epoxy-α-linolenic acid, and murine platelet-type 12-LOX and human 15-LOX-1 in the metabolism of 14,15-epoxyeicosatrienoic acid (14,15-EET). A detailed examination of the transformation of the two enantiomers of 15,16-epoxy-α-linolenic acid by soybean LOX-1 revealed that the expected primary product, a 13S-hydroperoxy-15,16-epoxide, underwent a nonenzymatic transformation in buffer into a new derivative that was purified by HPLC and identified by UV, LC-MS, and ¹H-NMR as a 13,15-endoperoxy-16-hydroxy-octadeca-9,11-dienoic acid. The configuration of the endoperoxide (cis or trans side chains) depended on the steric relationship of the new hydroperoxy moiety to the enantiomeric configuration of the fatty acid epoxide. The reaction mechanism involves intramolecular nucleophilic substitution (SNi) between the hydroperoxy (nucleophile) and epoxy group (electrophile). Equivalent transformations were documented in metabolism of the enantiomers of 14,15-EET by the two mammalian LOX enzymes, 15-LOX-1 and platelet-type 12-LOX. We conclude that this type of transformation could occur naturally with the co-occurrence of LOX and cytochrome P450 or peroxygenase enzymes, and it could also contribute to the complexity of products formed in the autoxidation reactions of polyunsaturated fatty acids.
Copyright © 2014 by the American Society for Biochemistry and Molecular Biology, Inc.
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23 MeSH Terms
Major groove orientation of the (2S)-N(6)-(2-hydroxy-3-buten-1-yl)-2'-deoxyadenosine DNA adduct induced by 1,2-epoxy-3-butene.
Kowal EA, Wickramaratne S, Kotapati S, Turo M, Tretyakova N, Stone MP
(2014) Chem Res Toxicol 27: 1675-86
MeSH Terms: Alkylation, Butadienes, DNA, DNA Adducts, Deoxyadenosines, Epoxy Compounds, Humans, Molecular Dynamics Simulation, Nuclear Magnetic Resonance, Biomolecular, Nucleic Acid Conformation, Nucleic Acid Denaturation, Oligodeoxyribonucleotides, Stereoisomerism, Transition Temperature, ras Proteins
Show Abstract · Added January 20, 2015
1,3-Butadiene (BD) is an environmental and occupational toxicant classified as a human carcinogen. It is oxidized by cytochrome P450 monooxygenases to 1,2-epoxy-3-butene (EB), which alkylates DNA. BD exposures lead to large numbers of mutations at A:T base pairs even though alkylation of guanines is more prevalent, suggesting that one or more adenine adducts of BD play a role in BD-mediated genotoxicity. However, the etiology of BD-mediated genotoxicity at adenine remains poorly understood. EB alkylates the N(6) exocyclic nitrogen of adenine to form N(6)-(hydroxy-3-buten-1-yl)-2'-dA ((2S)-N(6)-HB-dA) adducts ( Tretyakova , N. , Lin , Y. , Sangaiah , R. , Upton , P. B. , and Swenberg , J. A. ( 1997 ) Carcinogenesis 18 , 137 - 147 ). The structure of the (2S)-N(6)-HB-dA adduct has been determined in the 5'-d(C(1)G(2)G(3)A(4)C(5)Y(6)A(7)G(8)A(9)A(10)G(11))-3':5'-d(C(12)T(13)T(14)C(15)T(16)T(17)G(18)T(19) C(20)C(21)G(22))-3' duplex [Y = (2S)-N(6)-HB-dA] containing codon 61 (underlined) of the human N-ras protooncogene, from NMR spectroscopy. The (2S)-N(6)-HB-dA adduct was positioned in the major groove, such that the butadiene moiety was oriented in the 3' direction. At the Cα carbon, the methylene protons of the modified nucleobase Y(6) faced the 5' direction, which placed the Cβ carbon in the 3' direction. The Cβ hydroxyl group faced toward the solvent, as did carbons Cγ and Cδ. The Cβ hydroxyl group did not form hydrogen bonds with either T(16) O(4) or T(17) O(4). The (2S)-N(6)-HB-dA nucleoside maintained the anti conformation about the glycosyl bond, and the modified base retained Watson-Crick base pairing with the complementary base (T(17)). The adduct perturbed stacking interactions at base pairs C(5):G(18), Y(6):T(17), and A(7):T(16) such that the Y(6) base did not stack with its 5' neighbor C(5), but it did with its 3' neighbor A(7). The complementary thymine T(17) stacked well with both 5' and 3' neighbors T(16) and G(18). The presence of the (2S)-N(6)-HB-dA resulted in a 5 °C reduction in the Tm of the duplex, which is attributed to less favorable stacking interactions and adduct accommodation in the major groove.
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15 MeSH Terms
Structures of exocyclic R,R- and S,S-N(6),N(6)-(2,3-dihydroxybutan-1,4-diyl)-2'-deoxyadenosine adducts induced by 1,2,3,4-diepoxybutane.
Kowal EA, Seneviratne U, Wickramaratne S, Doherty KE, Cao X, Tretyakova N, Stone MP
(2014) Chem Res Toxicol 27: 805-17
MeSH Terms: Air Pollutants, Base Sequence, Carcinogens, DNA Adducts, Deoxyadenosines, Epoxy Compounds, Humans, Models, Molecular, Nuclear Magnetic Resonance, Biomolecular, Tobacco Smoke Pollution
Show Abstract · Added May 29, 2014
1,3-Butadiene (BD) is an industrial and environmental chemical present in urban air and cigarette smoke, and is classified as a human carcinogen. It is oxidized by cytochrome P450 to form 1,2,3,4-diepoxybutane (DEB); DEB bis-alkylates the N(6) position of adenine in DNA. Two enantiomers of bis-N(6)-dA adducts of DEB have been identified: R,R-N(6),N(6)-(2,3-dihydroxybutan-1,4-diyl)-2'-deoxyadenosine (R,R-DHB-dA), and S,S-N(6),N(6)-(2,3-dihydroxybutan-1,4-diyl)-2'-deoxyadenosine (S,S-DHB-dA) [ Seneviratne , U. , Antsypovich , S. , Dorr , D. Q. , Dissanayake , T. , Kotapati , S. , and Tretyakova , N. ( 2010 ) Chem. Res. Toxicol. 23 , 1556 -1567 ]. Herein, the R,R-DHB-dA and S,S-DHB-dA adducts have been incorporated into the 5'-d(C(1)G(2)G(3)A(4)C(5)X(6)A(7)G(8)A(9)A(10)G(11))-3':5'-d(C(12)T(13)T(14)C(15)T(16)T(17)G(18)T(19)C(20)C(21)G(22))-3' duplex [X(6) = R,R-DHB-dA (R(6)) or S,S-DHB-dA (S(6))]. The structures of the duplexes were determined by molecular dynamics calculations, which were restrained by experimental distances obtained from NMR data. Both the R,R- and S,S-DHB-dA adducts are positioned in the major groove of DNA. In both instances, the bulky 3,4-dihydroxypyrrolidine rings are accommodated by an out-of-plane rotation about the C6-N(6) bond of the bis-alkylated adenine. In both instances, the directionality of the dihydroxypyrrolidine ring is evidenced by the pattern of NOEs between the 3,4-dihydroxypyrrolidine protons and DNA. Also in both instances, the anti conformation of the glycosyl bond is maintained, which combined with the out-of-plane rotation about the C6-N(6) bond, allows the complementary thymine, T(17), to remain stacked within the duplex, and form one hydrogen bond with the modified base, between the imine nitrogen of the modified base and the T(17) N3H imino proton. The loss of the second Watson-Crick hydrogen bonding interaction at the lesion sites correlates with the lower thermal stabilities of the R,R- and S,S-DHB-dA duplexes, as compared to the corresponding unmodified duplex. The reduced base stacking at the adduct sites may also contribute to the thermal instability.
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10 MeSH Terms
In vivo roles of conjugation with glutathione and O6-alkylguanine DNA-alkyltransferase in the mutagenicity of the bis-electrophiles 1,2-dibromoethane and 1,2,3,4-diepoxybutane in mice.
Cho SH, Guengerich FP
(2013) Chem Res Toxicol 26: 1765-74
MeSH Terms: Animals, Butadienes, Buthionine Sulfoximine, Chromatography, High Pressure Liquid, DNA Adducts, DNA Mutational Analysis, Epoxy Compounds, Ethylene Dibromide, Glutathione, Glutathione Transferase, Guanine, Liver, Male, Mice, Mice, Transgenic, Mutagenicity Tests, Mutation, Mutation Rate, O(6)-Methylguanine-DNA Methyltransferase, Spectrometry, Mass, Electrospray Ionization
Show Abstract · Added March 7, 2014
Several studies with bacteria and in vitro mammalian systems have provided evidence of the roles of two thiol-based conjugation systems, glutathione (GSH) transferase and O(6)-alkylguanine DNA-alkyltransferase (AGT), in the bioactivation of the bis-electrophiles 1,2-dibromoethane and 1,2,3,4-diepoxybutane (DEB), the latter an oxidation product of 1,3-butadiene. The in vivo relevance of these conjugation reactions to biological activity in mammals has not been addressed, particularly with DEB. In this work, we used transgenic Big Blue mice, utilizing the cII gene, to examine the effects of manipulation of conjugation pathways on liver mutations arising from dibromoethane and DEB in vivo. Treatment of the mice with butathionine sulfoxime (BSO) prior to dibromoethane lowered hepatic GSH levels, dibromoethane-GSH DNA adduct levels (N(7)-guanyl), and the cII mutation frequency. Administration of O(6)-benzylguanine (O(6)-BzGua), an inhibitor of AGT, did not change the mutation frequency. Depletion of GSH (BSO) and AGT (O(6)-BzGua) lowered the mutation frequency induced by DEB, and BSO lowered the levels of GSH-DEB N(7)-guanyl and N(6)-adenyl DNA adducts. Our results provide evidence that the GSH conjugation pathway is a major in vivo factor in dibromoethane genotoxicity; both GSH conjugation and AGT conjugation are major factors in the genotoxicity of DEB. The latter findings are considered to be relevant to the carcinogenicity of 1,3-butadiene.
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20 MeSH Terms
Isolation and characterization of two geometric allene oxide isomers synthesized from 9S-hydroperoxylinoleic acid by cytochrome P450 CYP74C3: stereochemical assignment of natural fatty acid allene oxides.
Brash AR, Boeglin WE, Stec DF, Voehler M, Schneider C, Cha JK
(2013) J Biol Chem 288: 20797-806
MeSH Terms: Chromatography, High Pressure Liquid, Chromatography, Reverse-Phase, Cyclization, Cyclopentanes, Cytochrome P-450 Enzyme System, Epoxy Compounds, Flax, Linoleic Acids, Magnetic Resonance Spectroscopy, Molecular Conformation, Oxylipins, Stereoisomerism
Show Abstract · Added March 7, 2014
Specialized cytochromes P450 or catalase-related hemoproteins transform fatty acid hydroperoxides to allene oxides, highly reactive epoxides leading to cyclopentenones and other products. The stereochemistry of the natural allene oxides is incompletely defined, as are the structural features required for their cyclization. We investigated the transformation of 9S-hydroperoxylinoleic acid with the allene oxide synthase CYP74C3, a reported reaction that unexpectedly produces an allene oxide-derived cyclopentenone. Using biphasic reaction conditions at 0 °C, we isolated the initial products and separated two allene oxide isomers by HPLC at -15 °C. One matched previously described allene oxides in its UV spectrum (λmax 236 nm) and NMR spectrum (defining a 9,10-epoxy-octadec-10,12Z-dienoate). The second was a novel stereoisomer (UV λmax 239 nm) with distinctive NMR chemical shifts. Comparison of NOE interactions of the epoxy proton at C9 in the two allene oxides (and the equivalent NOE experiment in 12,13-epoxy allene oxides) allowed assignment at the isomeric C10 epoxy-ene carbon as Z in the new isomer and the E configuration in all previously characterized allene oxides. The novel 10Z isomer spontaneously formed a cis-cyclopentenone at room temperature in hexane. These results explain the origin of the cyclopentenone, provide insights into the mechanisms of allene oxide cyclization, and define the double bond geometry in naturally occurring allene oxides.
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12 MeSH Terms
Replication past the butadiene diepoxide-derived DNA adduct S-[4-(N(6)-deoxyadenosinyl)-2,3-dihydroxybutyl]glutathione by DNA polymerases.
Cho SH, Guengerich FP
(2013) Chem Res Toxicol 26: 1005-13
MeSH Terms: Adenosine, Chromatography, High Pressure Liquid, DNA Adducts, DNA-Directed DNA Polymerase, Epoxy Compounds, Glutathione, Humans, Kinetics, Molecular Structure, Tandem Mass Spectrometry
Show Abstract · Added March 7, 2014
1,2,3,4-Diepoxybutane (DEB), a metabolite of the carcinogen butadiene, has been shown to cause glutathione (GSH)-dependent base substitution mutations, especially A:T to G:C mutations in Salmonella typhimurium TA1535 [Cho, S. H., et al. (2010) Chem. Res. Toxicol. 23, 1544] and Escherichia coli TRG8 cells [Cho, S. H., and Guengerich, F. P. (2012) Chem. Res. Toxicol. 25, 1522]. We previously identified S-[4-(N(6)-deoxyadenosinyl)-2,3-dihydroxybutyl]GSH [N(6)dA-(OH)2butyl-GSH] as a major adduct in the reaction of S-(2-hydroxy-3,4-epoxybutyl)glutathione (DEB-GSH conjugate) with nucleosides and calf thymus DNA and in vivo in livers of mice and rats treated with DEB [Cho, S. H., and Guengerich, F. P. (2012) Chem. Res. Toxicol. 25, 706]. For investigation of the miscoding potential of the major DEB-GSH conjugate-derived DNA adduct [N(6)dA-(OH)2butyl-GSH] and the effect of GSH conjugation on replication of DEB, extension studies were performed in duplex DNA substrates containing the site-specifically incorporated N(6)dA-(OH)2butyl-GSH adduct, N(6)-(2,3,4-trihydroxybutyl)deoxyadenosine adduct (N(6)dA-butanetriol), or unmodified deoxyadenosine (dA) by human DNA polymerases (Pol) η, ι, and κ, bacteriophage polymerase T7, and Sulfolobus solfataricus polymerase Dpo4. Although dTTP incorporation was the most preferred addition opposite the N(6)dA-(OH)2butyl-GSH adduct, N(6)dA-butanetriol adduct, or unmodified dA for all polymerases, the dCTP misincorporation frequency opposite N(6)dA-(OH)2butyl-GSH was significantly higher than that opposite the N(6)dA-butanetriol adduct or unmodified dA with Pol κ or Pol T7. LC-MS/MS analysis of full-length primer extension products confirmed that Pol κ or Pol T7 incorporated the incorrect base C opposite the N(6)dA-(OH)2butyl-GSH lesion. These results indicate the relevance of GSH-containing adducts for the A:T to G:C mutations produced by DEB.
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10 MeSH Terms