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1.  Novel Organotin(IV) Schiff Base Complexes with Histidine Derivatives: Synthesis, Characterization, and Biological Activity 
Five novel tin Schiff base complexes with histidine analogues (derived from the condensation reaction between L-histidine and 3,5-di-tert-butyl-2-hydroxybenzaldehyde) have been synthesized and characterized. Characterization has been completed by IR and high-resolution mass spectroscopy, 1D and 2D solution NMR (1H, 13C  and 119Sn), as well as solid state 119Sn NMR. The spectroscopic evidence shows two types of structures: a trigonal bipyramidal stereochemistry with the tin atom coordinated to five donating atoms (two oxygen atoms, one nitrogen atom, and two carbon atoms belonging to the alkyl moieties), where one molecule of ligand is coordinated in a three dentate fashion. The second structure is spectroscopically described as a tetrahedral tin complex with four donating atoms (one oxygen atom coordinated to the metal and three carbon atoms belonging to the alkyl or aryl substituents), with one molecule of ligand attached. The antimicrobial activity of the tin compounds has been tested against the growth of bacteria in vitro to assess their bactericidal properties. While pentacoordinated compounds 1, 2, and 3 are described as moderate effective to noneffective drugs against both Gram-positive and Gram-negative bacteria, tetracoordinated tin(IV) compounds 4 and 5 are considered as moderate effective and most effective compounds, respectively, against the methicillin-resistant Staphylococcus aureus strains (Gram-positive).
PMCID: PMC3707209  PMID: 23864839
2.  Octa-n-butyl-1κ2 C,2κ2 C,3κ2,4κ2 C-bis­(μ-2,3-dibromo­propionato)-1:2κ2 O:O′,3:4κ2 O:O′-bis­(2,3-dibromo­propionato)-1κO,3κO-di-μ3-oxido-1:2:4κ3 O:O:O,2:3:4κ3 O:O:O-tetra­tin(IV) 
In the centrosymmetric tetra­nuclear title complex, [Sn4(C4H9)8(C3H3Br2O2)4O2], one of the two independent Sn atoms is five-coordinated by one O atom of the carboxyl­ate anion, two bridging O atoms and two n-butyl groups in a C2SnO3 distorted trigonal bipyramidal geometry. The other Sn atom also has a distorted trigonal bipyramidal geometry, being coordinated by two O atoms of two carboxyl­ate anions, one bridging O atom and two butyl groups. An inter­esting feature of the crystal structure is the short Sn⋯O [2.756 (4) Å] and O⋯O [2.608 (3) Å] inter­actions. The –BrCH2—CHBr– segments of the two carboxyl­ate anions are disordered over two positions [site occupancies of 0.60 (1)/0.40 (1) and 0.53 (2)/0.47 (2)]. Weak non-directional C—H⋯O inter­actions lead to the formation of infinte chains along the a axis; other weak inter­molecular C—H⋯π inter­actions are also present.
PMCID: PMC2959824  PMID: 21581176
3.  (Picolinato-κ2 N,O)[tris(2-isopropyl-1H-imidazol-4-yl-κN 3)phosphane]cobalt(II) nitrate 
Single crystals of the title compound, [Co(C6H4NO2)(C18H27N6P)]NO3, were obtained from the reaction of nitrato[tris­(2-isopropyl­imidazol-4-yl)phosphane]cobalt(II) nitrate with picolinic acid in the presence of potassium tert-butoxide as base. The coordination polyhedron around the central CoII ion is about halfway between square-pyramidal and trigonal-bipyramidal geometry. In the structure, the nitrate counter-anion is connected by N—H⋯O hydrogen bonding to the complex cation. Additionally, the complex cations form one-dimensional chains along [010] by hydrogen bonding of the NH group of an imidazole ring to the picolinate group of a neighbouring complex cation.
PMCID: PMC3297228  PMID: 22412418
4.  Bis(μ2-2-amino-5-nitro­benzoato)bis­(2-amino-5-nitro­benzoato)octa­butyldi-μ3-oxido-tetra­tin(IV) 
In the title complex, [Sn4(C4H9)8(C7H5N2O4)4O2], all four SnIV atoms are five-coordinated with distorted trigonal–bipyramidal SnC2O3 geometries. Two SnIV atoms are coordin­ated by two butyl groups, one benzoate O atom and two bridging O atoms, whereas the other two SnIV atoms are coordinated by two butyl groups, two benzoate O atoms and a bridging O atom. All the butyl groups are equatorial with respect to the SnO3 trigonal plane. In the crystal, mol­ecules are linked into a two-dimensional layer parallel to the ab plane by inter­molecular N—H⋯O and C—H⋯O hydrogen bonds and further stabilized by a π–π inter­action [centroid–centroid distance = 3.6489 (11) Å]. Intra­molecular N—H⋯O and C—H⋯O hydrogen bonds stabilize the mol­ecular structure. Two of the butyl groups are each disordered over two sets of sites with site-occupancy ratios of 0.510 (4):0.490 (4) and 0.860 (5):0.140 (5).
PMCID: PMC3212181  PMID: 22090883
5.  Nonadditive effects of PAHs on Early Vertebrate Development: mechanisms and implications for risk assessment 
Toxicological Sciences  2007;105(1):5-23.
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants. Traditionally, much of the research has focused on the carcinogenic potential of specific PAHs, such as benzo(a)pyrene, but recent studies using sensitive fish models have shown that exposure to PAHs alters normal fish development. Some PAHs can induce a teratogenic phenotype similar to that caused by planar halogenated aromatic hydrocarbons, such as dioxin. Consequently, mechanism of action is often equated between the two classes of compounds. Unlike dioxins, however, the developmental toxicity of PAH mixtures is not necessarily additive. This is likely related to their multiple mechanisms of toxicity and their rapid biotransformation by CYP1 enzymes to metabolites with a wide array of structures and potential toxicities. This has important implications for risk assessment and management as the current approach for complex mixtures of PAHs usually assumes concentration addition. In this review we discuss our current knowledge of teratogenicity caused by single PAH compounds and by mixtures and the importance of these latest findings for adequately assessing risk of PAHs to humans and wildlife. Throughout, we place particular emphasis on research on the early life stages of fish, which has proven to be a sensitive and rapid developmental model to elucidate effects of hydrocarbon mixtures.
PMCID: PMC2734299  PMID: 18156145
PAHs; DLCs; developmental toxicity; synergism; AHR; CYP1A; risk assessment
6.  Bis(μ2-4-amino-3-nitro­benzoato)bis­(4-amino-3-nitro­benzoato)octa­butyldi-μ3-oxido-tetra­tin(IV) 
The tetranuclear molecules of the title compound, [Sn4(C4H9)8(C7H5N2O4)4O2], reside on a crystallographic inversion center. Both the two independent Sn atoms are five-coordinate, with distorted trigonal–bipyramidal geometries. One Sn atom is coordinated by two O atoms of the carboxyl­ate anions, one bridging O atom and two butyl groups and the other Sn atom is coordinated by an O atom of the carboxyl­ate anion, two bridging O atoms and two butyl groups. All the butyl groups are equatorial with respect to the SnO3 trigonal plane. The mol­ecular structure is stabilized by intra­molecular N—H⋯O hydrogen bonds. In the crystal, pairs of inter­molecular bifurcated acceptor N—H⋯O and C—H⋯O hydrogen bonds link the mol­ecules into chains along [10]. Weak inter­molecular C—H⋯π and π–π inter­actions [centroid–centroid distance = 3.713 (2) Å] are also observed.
PMCID: PMC3009280  PMID: 21588838
7.  The catalytic pocket of the ring-hydroxylating dioxygenase from Sphingomonas CHY-1 
Ring-hydroxylating dioxygenases are multicomponent bacterial enzymes that catalyze the first step in the oxidative degradation of aromatic hydrocarbons. The dioxygenase from Sphingomonas CHY-1 is unique in that it can oxidize a wide range of polycyclic aromatic hydrocarbons (PAHs). With a crystal structure similar to that of the seven other known dioxygenases, its catalytic domain features the largest hydrophobic substrate binding cavity characterized so far. Molecular modeling studies indicated that the catalytic cavity is large enough to accommodate a five-ring benzo[a]pyrene molecule. The predicted positions of this and other PAHs in the substrate binding pocket are consistent with the product regio- and stereo-selectivity of the enzyme.
PMCID: PMC1820764  PMID: 17157819
dioxygenase; catalytic domain; mononuclear iron; bioremediation; high molecular weight polycyclic aromatic hydrocarbons
8.  Thermodynamic study of (anthracene + benzo[a]pyrene) solid mixtures 
The Journal of chemical thermodynamics  2010;42(11):1356-1360.
To characterize better the thermodynamic behavior of a binary polycyclic aromatic hydrocarbon mixture, thermochemical and vapor pressure experiments were used to examine the phase behavior of the {anthracene (1) + benzo[a]pyrene (2)} system. A solid-liquid phase diagram was mapped for the mixture. A eutectic point occurs at x1 = 0.26. The eutectic mixture is an amorphous solid that lacks organized crystal structure and melts between T = (414 and 420) K. For mixtures that contain 0.10 < x1 < 0.90, the enthalpy of fusion is dominated by that of the eutectic. Solid-vapor equilibrium studies show that mixtures of anthracene and benzo[a]pyrene at x1 < 0.10 sublime at the vapor pressure of pure benzo[a]pyrene. These results suggest that the solid-vapor equilibrium of benzo[a]pyrene is not significantly influenced by moderate levels of anthracene in the crystal structure.
PMCID: PMC2929985  PMID: 20814451
Polycyclic aromatic hydrocarbons; Anthracene; Benzo[a]pyrene; Binary mixtures; Phase equilibria; Vapor pressure
9.  Specificity of Human Aldo-Keto Reductases, NAD(P)H: Quinone Oxidoreductase and Carbonyl Reductases to Redox-Cycle Polycyclic Aromatic Hydrocarbon Diones and 4-Hydroxyequilenin-o-Quinone 
Chemical research in toxicology  2011;24(12):2153-2166.
Polycyclic aromatic hydrocarbons (PAH) are suspect human lung carcinogens and can be metabolically activated to remote quinones, e.g. benzo[a]pyrene-1,6-dione (B[a]P-1,6-dione) and B[a]P-3,6-dione by the action of either P450 monooxygenase or peroxidases and to non-K region o-quinones by aldo-keto reductases (AKRs). B[a]P-7,8-dione also structurally resembles 4-hydroxyequilenin o-quinone. These three classes of quinones can redox cycle, generate reactive oxygen species (ROS) and produce the mutagenic lesion 8-oxo-dGuo, and may contribute to PAH- and estrogen-induced carcinogenesis. We compared the ability of a complete panel of human recombinant AKRs to catalyze reduction of PAH o-quinones in the phenanthrene, chrysene, pyrene and anthracene series. The specific activities for NADPH-dependent quinone reduction were often 100-1,000 times greater than the ability of the same AKR isoform to oxidize the cognate PAH-trans-dihydrodiol. However, the AKR with the highest quinone reductase activity for a particular PAH o-quinone was not always identical to the AKR isoform with the highest dihydrodiol dehydrogenase activity for the respective PAH-trans-dihydrodiol. Discrete AKRs also catalyzed the reduction of B[a]P-1,6-dione, B[a]P-3,6-dione and 4-hydroxyequilenin o-quinone. Concurrent measurements of oxygen consumption, superoxide anion and hydrogen peroxide formation established that ROS were produced as a result of the redox-cycling. When compared with human recombinant NAD(P)H: quinone oxidoreductase (NQO1) and carbonyl reductases (CBR1 and CBR3), NQO1 was a superior catalyst of these reactions followed by AKRs and lastly CBR1 and CBR3. In A549 cells two-electron reduction of PAH o-quinones causes intracellular ROS formation. ROS formation was unaffected by the addition of dicumarol suggesting that NQO1 is not responsible for the two-electron reduction observed and does not offer protection against ROS formation from PAH o-quinones.
PMCID: PMC3251162  PMID: 21910479
o-quinones; redox-cycling; reactive oxygen species; chemical carcinogenesis; hormonal carcinogenesis
10.  Investigation of the genotoxicity of dibenzo[c,p]chrysene in human carcinoma MCF-7 cells in culture 
Chemico-biological interactions  2006;164(3):181-191.
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants that have been linked to certain human cancers. The fjord region PAH dibenzo[a,l]pyrene exhibits the highest levels of carcinogenic activity of all PAH as yet tested in rodent tumor models. Another hexacyclic aromatic hydrocarbon, dibenzo[c,p]chrysene (DBC), is a unique PAH that possesses one bay region and two fjord regions within the same molecule. Due to its structure, which is a merger of the fjord region PAHs benzo[c]phenanthrene, benzo[c]chrysene, and benzo[g]chrysene, DBC is of considerable research interest. In order to investigate the pathway of regioselective metabolism we have studied the cytotoxicity, metabolic activation and DNA adduct formation of DBC in human mammary carcinoma MCF-7 cells in culture. The cytotoxicity assay indicated undisturbed cell proliferation even at concentrations as high as 4.5 μM (1.5 μg/ml) DBC. Concurrently, DNA adducts were detected in MCF-7 cells treated with DBC only in low amounts (0.6 pmol adducts/mg DNA). On the contrary, exposure to anti-DBC-1,2-diol-3,4-epoxide and anti-DBC-11,12-diol-13,14-epoxide, two putatively genotoxic metabolites of DBC, resulted in high levels of DNA adducts (33 and 51 pmol adducts/mg DNA, respectively). Although DBC was not efficiently transformed into DNA-reactive metabolites in MCF-7 cells in culture, the results from our study indicate that the two fjord region diol-epoxide derivatives of DBC may serve as ultimate genotoxic metabolites once they are enzymatically generated under certain circumstances in vitro or in vivo.
PMCID: PMC1794669  PMID: 17094953
Abbreviations: PAH polycyclic aromatic hydrocarbon;  BP benzo [a] pyrene; DBP dibenzo [a l] pyrene; DBC dibenzo[c p] chrysene; BcC benzo[c]chrysene; BgC benzo[g]chrysene; BPh benzo[c]phenanthrene; DBA dibenz[a h]anthracene; MTT methylthiazolyldiphenyl-tetrazolium bromide; EROD ethoxyresorufin O-deethylase; DMSO dimethylsulfoxide; HPLC high performance liquid chromatography; CYP cytochrome P450
11.  Aqua­bis(3′-hydr­oxy-2,2′-bipyridine-3-olato-κ2 N,N′)zinc(II) 
In the title complex, [Zn(C10H7N2O2)2(H2O)], the ZnII ion and water O atom are located on a crystallographic twofold rotation axis and the metal atom assumes a distorted trigonal-bipyramidal ZnN4O coordination geometry. An intra­molecular O—H⋯O hydrogen bond occurs within the ligand and inter­molecular O—H⋯O hydrogen bonds involving the water mol­ecule result in a sheet structure in the crystal structure. In addition, a short C—O⋯π contact between the O atom of the deprotonated hydroxyl group and a nearby pyridine ring [O⋯Cg = 3.977 (2) Å, where Cg is the centroid of the pyridine ring] is observed.
PMCID: PMC2960646  PMID: 21201589
12.  Bacillus subtilis is a Potential Degrader of Pyrene and Benzo[a]pyrene 
Polycyclic Aromatic Hydrocarbons (PAHs) are a group of compounds that pose many health threats to human and animal life. They occur in nature as a result of incomplete combustion of organic matter, as well as from many anthropogenic sources including cigarette smoke and automobile exhaust. PAHs have been reported to cause liver damage, red blood cell damage and a variety of cancers. Because of this, methods to reduce the amount of PAHs in the environment are continuously being sought. The purpose of this study was to find soil bacteria capable of degrading high molecular weight PAHs, such as pyrene (Pyr) and benzo[a]pyrene (BaP), which contain more than three benzene rings and so persist in the environment. Bacillus subtilis, identified by fatty acid methyl ester (FAME) analysis, was isolated from PAH contaminated soil. Because it grew in the presence of 33μg/ml each of pyrene, 1-AP and 1-HP, its biodegradation capabilities were assessed. It was found that after a four-day incubation period at 30°C in 20μg/ml pyrene or benzo[a]pyrene, B. subtilis was able to transform approximately 40% and 50% pyrene and benzo[a]pyrene, respectively. This is the first report implicating B. subtilis in PAH degradation. Whether or not the intermediates resulting from the transformation are more toxic than their parent compounds, and whether B. subtilis is capable of mineralizing pyrene or benzo[a]pyrene to carbon dioxide and water, remains to be evaluated.
PMCID: PMC3810630  PMID: 16705827
Polycyclic Aromatic Hydrocarbons; bioremediation; Bacillus subtilis
13.  (Salicylato)[tris­(1-methyl-1H-benz­imidazol-2-ylmeth­yl)amine]copper(II) perchlorate dimethyl­formamide disolvate 
In the title complex, [Cu(C7H5O3)(C27H27N7)]ClO4·2C3H7NO, the CuII ion is five-coordinated by four N atoms from the tris­(1-methyl-1H-benzimidazol-2-ylmeth­yl)amine ligand and an O atom of the monodentate salicylate ligand. The N4O donor set defines a coordination geometry inter­mediate between square-pyramidal and trigonal–bipyramidal. The crystal structure is stabilized by O—H⋯O inter­actions. The atoms of the aromatic ring of the salicylate ligand are disordered over two sites of equal occupancy. In addition, one of the dimethyl­formamide solvent mol­ecules is partially disordered over two positions, of approximately equal occupancy.
PMCID: PMC2914911  PMID: 21200537
14.  Acrylato[tris­(1-methyl-1H-benzimidazol-2-ylmeth­yl)amine]cobalt(II) perchlorate–dimethyl­formamide–methanol (2/2/3) 
In the title complex, [Co(C3H3O2)(C27H27N7)]ClO4·C3H7NO·1.5CH4O, the CoII ion is five-coordinated by four N atoms from a tris­(1-methyl-1H-benzimidazol-2-ylmeth­yl)amine (mentb) ligand and one O atom from an acrylate ligand in a distorted trigonal–bipyramidal geometry with approximate mol­ecular C 3 symmetry. The atoms of the acrylate ligand are disordered over two sites, with approximate occupancies of 0.90 and 0.10. In addition, the solvent hemimethanol mol­ecule is disordered over two positions with equal occupancies. The crystal structure is stabilized by weak intermolecular O—H⋯O hydrogen bonds.
PMCID: PMC2959638  PMID: 21580847
15.  Acrylato[tris­(1-methyl­benzimidazol-2-ylmeth­yl)amine]zinc(II) perchlorate–dimethyl­formamide–methanol (1/1/1.5) at 153 (2) K 
In the title complex, [Zn(C3H3O2)(C27H27N7)](ClO4)·C3H7NO·1.5CH4O, the ZnII ion is five-coordinated by four N atoms from a tris­(1-methyl­benzimidazol-2-ylmeth­yl)amine (Mentb) ligand and one O atom from an acrylate ligand in a distorted trigonal–bipyramidal geometry with approximate mol­ecular C 3 symmetry. The atoms of the acrylate ligand are disordered over two sites, with approximate occupancies of 0.84 and 0.16. In addition, a methanol solvent mol­ecule is disordered over two sites with equal occupancies. In the crystal structure, the full-occupancy methanol is linked to a dimethyl­formamide mol­ecule by an inter­molecular O—H⋯O hydrogen bond.
PMCID: PMC2960207  PMID: 21201287
16.  Effects of cluster formation on spectra of benzo[a]pyrene and benzo[e]pyrene 
Chemical physics letters  2008;454(4-6):269-273.
Absorption and fluorescence emission spectra of the polycyclic aromatic hydrocarbons benzo[a]pyrene (BaP) and benzo[e]pyrene (BeP) in solution and adsorbed on silica have been obtained and compared to examine the spectroscopic effects of clustering. Molecular mechanics calculations with the UFF potential were done to optimize monomer, dimer and trimer geometries, and energy differences were determined by MP2/6-31G* calculations. Fluorescence emission spectra of adsorbed BeP and BaP display a red shift that progresses with increased loading, and the two differ in their photodegradation kinetics. The experimental and theoretical results are found to be consistent.
PMCID: PMC2390778  PMID: 18496588
17.  Cancer risk assessment, indicators, and guidelines for polycyclic aromatic hydrocarbons in the ambient air. 
Environmental Health Perspectives  2002;110(Suppl 3):451-488.
Polycyclic aromatic hydrocarbons (PAHs) are formed during incomplete combustion. Domestic wood burning and road traffic are the major sources of PAHs in Sweden. In Stockholm, the sum of 14 different PAHs is 100-200 ng/m(3) at the street-level site, the most abundant being phenanthrene. Benzo[a]pyrene (B[a]P) varies between 1 and 2 ng/m(3). Exposure to PAH-containing substances increases the risk of cancer in humans. The carcinogenicity of PAHs is associated with the complexity of the molecule, i.e., increasing number of benzenoid rings, and with metabolic activation to reactive diol epoxide intermediates and their subsequent covalent binding to critical targets in DNA. B[a]P is the main indicator of carcinogenic PAHs. Fluoranthene is an important volatile PAH because it occurs at high concentrations in ambient air and because it is an experimental carcinogen in certain test systems. Thus, fluoranthene is suggested as a complementary indicator to B[a]P. The most carcinogenic PAH identified, dibenzo[a,l]pyrene, is also suggested as an indicator, although it occurs at very low concentrations. Quantitative cancer risk estimates of PAHs as air pollutants are very uncertain because of the lack of useful, good-quality data. According to the World Health Organization Air Quality Guidelines for Europe, the unit risk is 9 X 10(-5) per ng/m(3) of B[a]P as indicator of the total PAH content, namely, lifetime exposure to 0.1 ng/m(3) would theoretically lead to one extra cancer case in 100,000 exposed individuals. This concentration of 0.1 ng/m(3) of B[a]P is suggested as a health-based guideline. Because the carcinogenic potency of fluoranthene has been estimated to be approximately 20 times less than that of B[a]P, a tentative guideline value of 2 ng/m(3) is suggested for fluoranthene. Other significant PAHs are phenanthrene, methylated phenanthrenes/anthracenes and pyrene (high air concentrations), and large-molecule PAHs such as dibenz[a,h]anthracene, benzo[b]fluoranthene, benzo[k]fluoranthene, and indeno[1,2,3-cd]pyrene (high carcinogenicity). Additional source-specific indicators are benzo[ghi]perylene for gasoline vehicles, retene for wood combustion, and dibenzothiophene and benzonaphthothiophene for sulfur-containing fuels.
PMCID: PMC1241197  PMID: 12060843
18.  Succession of Phenotypic, Genotypic, and Metabolic Community Characteristics during In Vitro Bioslurry Treatment of Polycyclic Aromatic Hydrocarbon-Contaminated Sediments 
Dredged harbor sediment contaminated with polycyclic aromatic hydrocarbons (PAHs) was removed from the Milwaukee Confined Disposal Facility and examined for in situ biodegradative capacity. Molecular techniques were used to determine the successional characteristics of the indigenous microbiota during a 4-month bioslurry evaluation. Ester-linked phospholipid fatty acids (PLFA), multiplex PCR of targeted genes, and radiorespirometry techniques were used to define in situ microbial phenotypic, genotypic, and metabolic responses, respectively. Soxhlet extractions revealed a loss in total PAH concentrations of 52%. Individual PAHs showed reductions as great as 75% (i.e., acenapthene and fluorene). Rates of 14C-PAH mineralization (percent/day) were greatest for phenanthrene, followed by pyrene and then chrysene. There was no mineralization capacity for benzo[a]pyrene. Ester-linked phospholipid fatty acid analysis revealed a threefold increase in total microbial biomass and a dynamic microbial community composition that showed a strong correlation with observed changes in the PAH chemistry (canonical r2 of 0.999). Nucleic acid analyses showed copies of genes encoding PAH-degrading enzymes (extradiol dioxygenases, hydroxylases, and meta-cleavage enzymes) to increase by as much as 4 orders of magnitude. Shifts in gene copy numbers showed strong correlations with shifts in specific subsets of the extant microbial community. Specifically, declines in the concentrations of three-ring PAH moieties (i.e., phenanthrene) correlated with PLFA indicative of certain gram-negative bacteria (i.e., Rhodococcus spp. and/or actinomycetes) and genes encoding for naphthalene-, biphenyl-, and catechol-2,3-dioxygenase degradative enzymes. The results of this study suggest that the intrinsic biodegradative potential of an environmental site can be derived from the polyphasic characterization of the in situ microbial community.
PMCID: PMC92767  PMID: 11282603
19.  The influence of diesel exhaust on polycyclic aromatic hydrocarbon-induced DNA damage, gene expression and tumor initiation in Sencar mice in vivo 
Cancer letters  2008;265(1):135-147.
The carcinogenic effects of individual polycyclic aromatic hydrocarbons (PAH) are well established. However, their potency within an environmental complex mixture is uncertain. We evaluated the influence of diesel exhaust particulate matter on PAH-induced cytochrome P450 (CYP) activity, PAH-DNA adduct formation, expression of certain candidate genes and the frequency of tumor initiation in the two-stage Sencar mouse model. To this end, we monitored the effects of treatment of mice with diesel exhaust, benzo[a]pyrene (BP), dibenzo[a,l]pyrene (DBP), or a combination of diesel exhaust with either carcinogenic PAH. The applied diesel particulate matter (SRM1975) altered the tumor initiating potency of DBP: a statistically significant decrease in overall tumor and carcinoma burden was observed following 25 weeks of promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA), compared with DBP exposure alone. From those mice that were treated at the beginning of the observation period with 2 nmol DBP all survivors developed tumors (9 out of 9 animals, 100%). Among all tumors counted at the end, 9 carcinomas were detected and an overall tumor incidence of 2.6 tumors per tumor-bearing animal (TBA) was determined. By contrast, co-treatment of DBP with 50 mg SRM1975 led to a tumor rate of only 66% (19 out of 29 animals), occurrence of only 3 carcinomas in 29 animals and an overall rate of 2.1 tumors per TBA (P = 0.04). In contrast to the results with DBP, the tumor incidence induced by 200 nmol BP was found slightly increased when co-treatment with SRM1975 occurred (71% vs. 85% after 25 weeks). Despite this difference in tumor incidence, the numbers of carcinomas and tumors per TBA did not differ statistically significant between both treatment groups possibly due to the small size of the BP treatment group. Since bioactivation of DBP, but not BP, predominantly depends on CYP1B1 enzyme activity, SRM1975 affected PAH-induced carcinogenesis in an antagonistic manner when CYP1B1-mediated bioactivation was required. The explanation most likely lies in the much stronger inhibitory effects of certain PAHs present in diesel exhaust on CYP1B1 compared to CYP1A1. In the present study we also found molecular markers such as highly elevated AKR1C21 and TNFRSF21 gene expression levels in tumor tissue derived from animals co-treated with SRM1975 plus DBP. Therefore we validate microarray data as a source to uncover transcriptional signatures that may provide insights into molecular pathways affected following exposure to environmental complex mixtures such as diesel exhaust particulates.
PMCID: PMC2519885  PMID: 18353537
DNA adducts; carcinogenesis; diesel exhaust; PAH; cytochrome P450
20.  Influence of Cadmium and Mercury on Activities of Ligninolytic Enzymes and Degradation of Polycyclic Aromatic Hydrocarbons by Pleurotus ostreatus in Soil 
The white-rot fungus Pleurotus ostreatus was able to degrade the polycyclic aromatic hydrocarbons (PAHs) benzo[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene, dibenzo[a,h]anthracene, and benzo[ghi]perylene in nonsterile soil both in the presence and in the absence of cadmium and mercury. During 15 weeks of incubation, recovery of individual compounds was 16 to 69% in soil without additional metal. While soil microflora contributed mostly to degradation of pyrene (82%) and benzo[a]anthracene (41%), the fungus enhanced the disappearance of less-soluble polycyclic aromatic compounds containing five or six aromatic rings. Although the heavy metals in the soil affected the activity of ligninolytic enzymes produced by the fungus (laccase and Mn-dependent peroxidase), no decrease in PAH degradation was found in soil containing Cd or Hg at 10 to 100 ppm. In the presence of cadmium at 500 ppm in soil, degradation of PAHs by soil microflora was not affected whereas the contribution of fungus was negligible, probably due to the absence of Mn-dependent peroxidase activity. In the presence of Hg at 50 to 100 ppm or Cd at 100 to 500 ppm, the extent of soil colonization by the fungus was limited.
PMCID: PMC110561  PMID: 10831426
21.  Estimating Individual-Level Exposure to Airborne Polycyclic Aromatic Hydrocarbons throughout the Gestational Period Based on Personal, Indoor, and Outdoor Monitoring 
Environmental Health Perspectives  2008;116(11):1509-1518.
Current understanding on health effects of long-term polycyclic aromatic hydrocarbon (PAH) exposure is limited by lack of data on time-varying nature of the pollutants at an individual level. In a cohort of pregnant women in Krakow, Poland, we examined the contribution of temporal, spatial, and behavioral factors to prenatal exposure to airborne PAHs within each trimester and developed a predictive model of PAH exposure over the entire gestational period.
We monitored nonsmoking pregnant women (n = 341) for their personal exposure to pyrene and eight carcinogenic PAHs—benz[a]anthracene, chrysene/isochrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene [B(a)P], indeno[1,2,3-c,d]pyrene, dibenz[a,h]anthracene, and benzo[g,h,i]perylene—during their second trimester for a consecutive 48-hr period. In a subset (n = 78), we monitored indoor and outdoor levels simultaneously with the personal monitoring during the second trimester with an identical monitor. The subset of women was also monitored for personal exposure for a 48-hr period during each trimester. We repeatedly administered a questionnaire on health history, lifestyle, and home environment.
The observed personal, indoor, and outdoor B(a)P levels we observed in Krakow far exceed the recommended Swedish guideline value for B(a)P of 0.1 ng/m3. Based on simultaneously monitored levels, the outdoor PAH level alone accounts for 93% of total variability in personal exposure during the heating season. Living near the Krakow bus depot, a crossroad, and the city center and time spent outdoors or commuting were not associated with higher personal exposure. During the nonheating season only, a 1-hr increase in environmental tobacco smoke (ETS) exposure was associated with a 10–16% increase in personal exposure to the nine measured PAHs. A 1°C decrease in ambient temperature was associated with a 3–5% increase in exposure to benz[a]anthracene, benzo[k]fluoranthene, and dibenz[a,h]anthracene, after accounting for the outdoor concentration. A random effects model demonstrated that mean personal exposure at a given gestational period depends on the season, residence location, and ETS.
Considering that most women reported spending < 3 hr/day outdoors, most women in the study were exposed to outdoor-originating PAHs within the indoor setting. Cross-sectional, longitudinal monitoring supplemented with questionnaire data allowed development of a gestation-length model of individual-level exposure with high precision and validity. These results are generalizable to other nonsmoking pregnant women in similar exposure settings and support reduction of exposure to protect the developing fetus.
PMCID: PMC2592271  PMID: 19057704
coal; long-term personal exposure; polycyclic aromatic hydrocarbons; spatial and temporal variability
22.  Poly[(μ5-5-carboxylatotetrahydrofuran-2,3,4-tricarboxylic acid)sodium] 
The search for the novel metal-organic frameworks (MOFs) materials using tetra­hydro­furan-2,3,4,5-tetra­carboxylic acid (THFTCA) as a versatile multi-carboxyl ligand, lead to the synthesis and the structure determination of the title compound, [Na(H3THFTCA)] or [Na(C8H7O9)]n, which was obtained by a solution reaction at room temperature. The ligand is mono-deprotonated, coordinating five sodium ions through one furan oxygen atom and six carboxyl oxygen atoms. The sodium ion exhibits a distorted penta­gonal-bipyramidal NaO7 geometry consisting of seven O atoms derived from five surrounding ligands. Two adjacent pentagonal bipyramids share an O—O edge, forming a dinuclear sodium cluster. Finally, these clusters are effectively linked by the carboxyl groups of THFTCA ligands, forming a firm metal organic framework and O—H⋯O hydrogen bonds contribute to the crystal packing.
PMCID: PMC2971171  PMID: 21578156
23.  Exposure of iron foundry workers to polycyclic aromatic hydrocarbons: benzo(a)pyrene-albumin adducts and 1-hydroxypyrene as biomarkers for exposure. 
Exposure to polycyclic aromatic hydrocarbons (PAHs) in foundry workers has been evaluated by determination of benzo(a)pyrene-serum albumin adducts and urinary 1-hydroxypyrene. Benzo(a)pyrene binding to albumin and 1-hydroxypyrene were quantitatively measured by enzyme linked immunosorbent assay (ELISA) and reverse phase high performance liquid chromatography (HPLC), respectively. 70 male foundry workers and 68 matched controls were investigated. High and low exposure groups were defined from breathing zone hygienic samples, consisting of 16 PAH compounds in particulate and gaseous phase. Mean total PAH was 10.40 micrograms/m3 in the breathing zone, and mean dust adsorbed PAH was 0.15 microgram/m. All carcinogenic PAH was adsorbed to dust. Median benzo(a)pyrene-albumin adduct concentrations (10-90% percentiles) were similar in foundry workers (smokers 0.55 (0.27-1.00) and non-smokers 0.58 (0.17-1.15)) pmol/mg albumin and age matched controls (smokers 0.57 (0.16-1.45) and non-smokers 0.70 (0.19-1.55) pmol/mg albumin). Median 1-hydroxypyrene concentrations were significantly higher (P < 0.0001) in smoking and non-smoking foundry workers (0.022 (0.006-0.075) and 0.027 (0.006-0.164)) mumol/mol creatinine than in smoking and non-smoking controls (0 (0-0.022) and 0 (0-0.010) mumol/mol creatinine). Dose-response relations between total PAH, pyrene, carcinogenic PAHs, and 1-hydroxypyrene for smokers, and polycyclic aromatic hydrocarbons adsorbed to dust for non-smokers are suggested. Exposure to PAHs adsorbed to dust showed an additive effect. There was no correlation between the concentrations of 1-hydroxypyrene and benzo(a)pyrene-albumin adducts. The change in 1-hydroxypyrene over a weekend was also studied. Friday morning median 1-hydroxypyrene concentrations were significantly higher in both smokers and non-smokers (0.021 (0-0.075) and 0.027 (0.06-0.164)) mumol/mol creatinine than Monday morning median concentrations (0.007 (0-0.021) and 0.008 (0-0.021) mumol/mol creatinine). Smoking did not affect the concentrations of 1-hydroxypyrene or benzo(a)pyrene-albumin adducts. These data suggest that 1-hydroxypyrene is a sensitive biomarker for low dose PAH exposure. Exposure to PAHs may be aetiologically related to increased risk of lung cancer in foundry workers.
PMCID: PMC1128029  PMID: 7951774
24.  Photomutagenicity of 16 polycyclic aromatic hydrocarbons from the US EPA priority pollutant list 
Mutation research  2004;557(1):99-108.
The photomutagenicity of 16 polycyclic aromatic hydrocarbons (PAHs), all on the United States Environmental Protection Agency (US EPA) priority pollutant list, was studied. Concomitant exposing the Salmonella typhimurium bacteria strain TA102 to one of the PAHs and light (1.1 J/cm2 UVA+2.1 J/cm2 visible) without the activation enzyme S9, strong photomutagenic response is observed for anthracene, benz[a]anthracene, benzo[ghi]perylene, benzo[a]pyrene, indeno[1,2,3-cd]pyrene, and pyrene. Under the same conditions, acenaphthene, acenaphthylene, benzo[k]fluoranthene, chrysene, and fluorene are weakly photomutagenic. Benzo[b]fluoranthene, fluoranthene, naphthalene, phenanthrene, and dibenz[a,h]anthracene are not photomutagenic. These results indicate that PAHs can be activated by light and become mutagenic in Salmonella TA102 bacteria. At the same time, the mutagenicity for all the 16 PAHs was examined with the standard mutagenicity test with 10% S9 as the activation system. Benzo[b]fluoranthene, benzo[k]fluoranthene, chrysene, acenaphthylene, and fluorene are weakly mutagenic, while the rest of the PAHs are not. In general, the photomutagenicity of PAHs in TA102 does not correlate with their S9-activated mutagenicity in either TA102 or TA98/TA100 since they involve different activation mechanisms.
PMCID: PMC2713671  PMID: 14706522
Polycyclic aromatic hydrocarbons; Photomutagenicity; Light irradiation; Salmonella typhimurium TA102 and TA98
25.  (N-Benzyl-N-ethyl­dithio­carbamato)di-tert-butyl­chloridotin(IV) 
The SnIV atom in the title diorganotin dithio­carbamate, [Sn(C4H9)2Cl(C10H12NS2)], is penta­coordinated by an asymmetrically coordinating dithio­carbamate ligand, a Cl and two C atoms of the Sn-bound tert-butyl groups. The resulting C2ClS2 donor set defines a coordination geometry inter­mediate between square pyramidal and trigonal bipyramidal with a slight tendency towards the former. In the crystal structure, C—H⋯π contacts link centrosymmetrically related mol­ecules into dimeric aggregates.
PMCID: PMC3051941  PMID: 21522295

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