Aromatic compounds are a class of organic compounds with benzene ring(s). Aromatic compounds are hardly decomposed due to its stable structure and can be accumulated in the food cycle, posing a great threat to the ecological environment and human health. Bacteria have a strong catabolic ability to degrade various refractory organic contaminants (e.g., polycyclic aromatic hydrocarbons, PAHs). The adsorption and transportation are prerequisites for the catabolism of aromatic compounds by bacteria. While remarkable progress has been made in understanding the metabolism of aromatic compounds in bacterial degraders, the systems responsible for the uptake and transport of aromatic compounds are poorly understood. Here we summarize the effect of cell-surface hydrophobicity, biofilm formation, and bacterial chemotaxis on the bacterial adsorption of aromatic compounds. Besides, the effects of outer membrane transport systems (such as FadL family, TonB-dependent receptors, and OmpW family), and inner membrane transport systems (such as major facilitator superfamily (MFS) transporter and ATP-binding cassette (ABC) transporter) involved in the membrane transport of these compounds are summarized. Moreover, the mechanism of transmembrane transport is also discussed. This review may serve as a reference for the prevention and remediation of aromatic pollutants.
Humans ; Adsorption ; Bacteria/metabolism* ; Organic Chemicals ; Biological Transport ; ATP-Binding Cassette Transporters ; Polycyclic Aromatic Hydrocarbons/metabolism*

Polycyclic aromatic hydrocarbons (PAHs) are a class of persistent organic pollutants, which have received widespread attentions due to their carcinogenic and mutagenic toxicity. The microbial degradation of PAHs are usually started from the hydroxylation, followed by dehydrogenation, ring cleavage and step-by-step removal of branched chains, and finally mineralized by the tricarboxylic acid cycle. Rieske type non-heme iron aromatic ring-hydroxylating dioxygenases (RHOs) or cytochrome P450 oxidases are responsible for the conversion of hydrophobic PAHs into hydrophilic derivatives by the ring hydroxylation. The ring hydroxylation is the first step of PAHs degradation and also one of the rate-limiting steps. Here, we review the distribution, substrate specificity, and substrate recognition mechanisms of RHOs, along with some techniques and methods used for the research of RHOs and PAHs.
Bacteria/metabolism* ; Biodegradation, Environmental ; Dioxygenases/metabolism* ; Iron ; Polycyclic Aromatic Hydrocarbons ; Substrate Specificity

Adult ; Aged ; Aged, 80 and over ; Air Pollutants ; adverse effects ; Blood Chemical Analysis ; Coke ; adverse effects ; Environmental Exposure ; Female ; Humans ; Immunoglobulins ; metabolism ; Male ; Middle Aged ; Polycyclic Aromatic Hydrocarbons ; adverse effects ; Young Adult

With the rapid development of socialization and industrialization, more and more pollutes were produced and discharged into natural environment. It is harmful to human health and life. These pollutes included refractory degradation organic compounds like PAHs, RDX, HMX, CL-20, PCBs and alkanes and their relative substances. Various compounds exist in nature with long life span. They are the most hazardous than other organics. The impact of pollutes can be treated by microorganisms. Results showed that it is an effective way for bioremediation of these pollutes with microbial metabolism or cometabolism. A few key enzymes, mainly oxidative and reductive enzymes, connected with the first step of initial degradation. Normally, enzymes grouped with other active fraction on the cell membrane are composed of one oxidative and reductive system for substrates oxidation. The metabolic intermediates can be used with TCA by microorganisms. The pathways of metabolism and the key enzymes were summarized. The further research topics should be focused on microorganism screen and its relative enzyme, pathway and mechanism of metabolism or cometabolism for such compounds degradation, and the result was hoped for the environmental protection.
Bacteria ; enzymology ; metabolism ; Biodegradation, Environmental ; Environmental Pollutants ; metabolism ; Nitroreductases ; metabolism ; Organic Chemicals ; isolation & purification ; metabolism ; Oxidation-Reduction ; Oxidoreductases ; metabolism ; Polychlorinated Biphenyls ; metabolism ; Polycyclic Aromatic Hydrocarbons ; metabolism

OBJECTIVETo explore the relationship between the expression of heat shock protein 90, 60 and 27 (HSP90, HSP60 and HSP27) and genetic damage in peripheral blood of workers exposed to coke oven emissions.

METHODS288 coke oven workers in a steel factory were divided into the high-dose group and the low-dose group on the basis of environment monitoring result and work place. There were 172 men in high-dose group (workers who worked at the oven top and oven side) and 116 men in low-dose group (workers who worked at the oven bottom and others who were engaged to aided work). 38 workers unexposed occupationally to carcinogenic substances were selected as the control group, who were employed in medical therapy unit nearby 2 kilometers from the steel factory. Their general information, history of personal and occupational exposure, and the work environment were investigated. Blood samples were collected immediately after a shift at the end of a working day from 288 coke oven workers and 38 control workers. Levels of HSP90, HSP60 and HSP27 in peripheral blood lymphocytes were measured by Western blot, and the degree of DNA damage was detected by the comet assay.

RESULTSLevels of HSP90 in peripheral blood lymphocytes in three groups were 0.24 +/- 0.32, 0.12 +/- 0.30 and 0.06 +/- 0.33 respectively. They increased significantly compared with that of the control. But levels of HSP60 and HSP27 were not significantly different among those groups. Compared with the control group, there was significant difference in tail length, olive tail moment et al of SCGE (G +/- s(G)) of occupational exposure workers. High-dose group > low-dose group > control group (P < 0.05). The degree of DNA damage increased with the rise of exposure BaP dose (Spearman r = -0.345, P < 0.01).

CONCLUSIONLevels of HSP90 in peripheral blood lymphocytes and the degree of DNA damage increase with the rise of exposure polycyclic aromatic hydrocarbons (PAHs) dose.

Adult ; Chaperonin 60 ; blood ; Coke ; adverse effects ; Comet Assay ; DNA Damage ; drug effects ; HSP27 Heat-Shock Proteins ; blood ; HSP90 Heat-Shock Proteins ; blood ; Humans ; Lymphocytes ; metabolism ; Male ; Occupational Exposure ; adverse effects ; Polycyclic Aromatic Hydrocarbons ; adverse effects

The aromatic-ring-hydroxylating dioxygenase is a key enzyme that initiates the biodegradation of polycyclic aromatic hydrocarbons in bacteria. In the present study, a novel dioxygenase sequence was cloned from Terrabacter sp. FLO using a genome walking method. The dioxygenase was cloned into pET17 and actively expressed in E.coli BL21 (DE3) in co-expression with electron transfer chain proteins. The recombinant dioxygenase was found to transform phenanthrene, fluorene, pyrene and fluoranthene into the cis-dihydrodiol metabolites.
Actinomycetales ; enzymology ; genetics ; Bacterial Proteins ; genetics ; metabolism ; Biodegradation, Environmental ; Cloning, Molecular ; Dioxygenases ; genetics ; metabolism ; Electrophoresis, Polyacrylamide Gel ; Escherichia coli ; genetics ; metabolism ; Fluorenes ; metabolism ; Hydroxylation ; Molecular Sequence Data ; Phenanthrenes ; metabolism ; Polycyclic Aromatic Hydrocarbons ; metabolism ; Pyrenes ; metabolism ; Recombinant Proteins ; metabolism

Epidemiologic studies have suggested the association between environmental exposure to volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbons (PAHs) and the increased risk of incurring asthma. Yet there is little data regarding the relationship between personal exposure to air pollution and the incidence of asthma in children. This study was designed to evaluate the effect of exposure to air pollution on children with asthma by using exposure biomarkers. We assessed the exposure level to VOCs by measuring urinary concentrations of hippuric acid and muconic acid, and PAHs by 1-OH pyrene and 2-naphthol in 30 children with asthma and 30 children without asthma (control). The mean level of hippuric acid was 0.158+/-0.169micromol/mol creatinine in the asthma group and 0.148+/-0.249micromol/mol creatinine in the control group, with no statistical significance noted (p=0.30). The mean concentration of muconic acid was higher in the asthma group than in the control group (7.630+/-8.915micromol/mol creatinine vs. 3.390+/-4.526micromol/mol creatinine p=0.01). The mean level of urinary 1-OHP was higher in the asthma group (0.430+/-0.343micromol/mol creatinine) than the control group (0.239+/-0.175micromol/mol creatinine), which was statistically significant (p=0.03). There was no difference in the mean concentration of 2-NAP between the two groups (9.864+/-10.037micromol/mol in the asthma group vs. 9.157+/-9.640micromol/mol in the control group, p=0.96). In conclusion, this study suggests that VOCs and PAHs have some role in asthma.
Air Pollutants/*pharmacology ; Asthma/*physiopathology/urine ; Case-Control Studies ; Child, Preschool ; Creatinine/urine ; Female ; Hippurates/urine ; Humans ; Male ; Naphthols/urine ; Organic Chemicals/chemistry/*pharmacology ; Polycyclic Hydrocarbons, Aromatic/*pharmacology ; Pyrenes/metabolism ; Sorbic Acid/*analogs & derivatives/metabolism ; Volatilization

OBJECTIVETo study whether the argyrophil nucleolar organizer regions (AgNOR) in T lymphocytes of peripheral blood in coke-oven workers can be used as a biomarker of effect for polycyclic aromatic hydrocarbon (PAH) exposure.

METHODSFifty-two male coke-oven workers were divided into three groups according to exposure levels of coke oven emissions: high-exposure, middle-exposure and low-exposure workers. Additionally 10 men without occupational PAH exposure were chosen as control group. Peripheral blood T lymphocytes were cultured, spread on slides and stained with silver nitrate. The ratio of AgNOR area vs. nuclear area (I/S) in T lymphocytes was analyzed. Urinary 1-hydroxypyrene (1-OHP) was measured as the internal dose of PAH exposure.

RESULTSMean urinary 1-OHP level in high-exposure group (16.56 +/- 2.77 micromol/mol Cr) was significantly higher than those in low-exposure group (3.30 +/- 2.77 micromol/mol Cr, P < 0.001) and control group (3.04 +/- 1.58 micromol/mol Cr, P < 0.01). The mean I/S of AgNOR in T lymphocytes in high-exposure group (0.056 +/- 0.010) was significantly lower than those in middle-exposure group (0.065 +/- 0.013, P < 0.05), low-exposure group (0.067 +/- 0.008, P < 0.01) and control group (0.076 +/- 0.007, P < 0.001). It was also found that I/S of AgNOR were significantly decreased in middle-exposure group and low-exposure group in comparison with control group (P < 0.01, P < 0.05).

CONCLUSIONSThe occupational exposure to PAH resulted in increase of 1-OHP in urine and decrease of AgNOR in T lymphocytes. PAH exposure might lead to damage T lymphocytes function and AgNOR may be considered as a biomarker of effect for PAH exposure.

Antigens, Nuclear ; blood ; Biomarkers ; blood ; urine ; Coke ; poisoning ; Humans ; Lymphocytes ; cytology ; drug effects ; metabolism ; Male ; Occupational Exposure ; analysis ; Polycyclic Aromatic Hydrocarbons ; poisoning ; Pyrenes ; analysis

OBJECTIVETo investigate the relationship between lymphocyte DNA damage and polycyclic aromatic hydrocarbons (PAHs) exposure in coke oven workers.

METHODSTwo hundred and thirty-five coke oven workers and 30 controls were selected in this study. Alkaline single-cell gel electrophoresis was used to evaluate the lymphocyte DNA damage, HPLC was employed to measure 1-hydroxypyrene levels in spot urine samples which were obtained at the end of a workweek (4 days of 8 hours/day) and personal information including occupational exposure, age, sex, smoking and drinking status was collected by the questionnaire.

RESULTSThe lymphocyte DNA damage level expressed as olive moment in coke oven workers was significantly higher than that of controls [2.47 (0.22 approximately 46.68) vs 0.94 (0.42 approximately 4.21), P < 0.01], and correlation between urinary 1-hydroxypyrene concentrations and olive moment was found (Spearman Partial correlation coefficient = 0.22, P < 0.01) in coke oven workers. The 1.9 of olive moment value was used as the limit to determine whether the subject DNA damage was positive. The coke oven workers had significantly higher risk in DNA damage (adjusted OR = 5.38, 95% CI = 2.07 approximately 14.08) than did controls, and dose-response relationships were also found between external exposure (exposure category) or internal doses (urinary 1-hydroxypyrene) and DNA damage.

CONCLUSIONThere are dose-effect and dose-response relationships between PAHs exposure and lymphocyte DNA damage in coke oven workers.

Adult ; Animals ; Coke ; adverse effects ; DNA Damage ; drug effects ; Dose-Response Relationship, Drug ; Female ; Humans ; Lymphocytes ; metabolism ; Male ; Occupational Exposure ; Polycyclic Aromatic Hydrocarbons ; poisoning ; Pyrenes ; analysis ; metabolism ; Surveys and Questionnaires

OBJECTIVETo investigate the associations of polymorphisms of metabolic enzyme genes with urinary 1-hydroxypyrene levels in coke oven workers.

METHODSOne hundred and forty-eight workers from a coke oven plant and 69 controls without occupational PAHs exposure were selected in this study. Urinary 1-hydroxypyrene was detected by high performance liquid chromatography with florescence detector. The genotypes at I462V site in exon 7 of CYP1A1 gene, GSTM1, GSTT1, I105V site in GSTP1gene, Pst1 and Dra1 sites in CYP2E1 gene, P187S site in NQO1 gene, Kpn1, BamH1 and Taq1 sites in NAT2 gene, and H113Y, R139H sites in mEH gene were determined by PCR-based methods. Personal information including occupational exposure history, age, sex, smoking and drinking status was collected by the questionnaire.

RESULTSThe level of urinary 1-hydroxypyrene in coke oven workers [(5.61 +/- 1.04) mol/mol Cr] was higher than that in control [(0.74 +/- 0.32) micro mol/mol Cr]. After adjusting external occupational exposure category and smoking, coke oven workers with variant homozygotes at H113Y site of mEH gene had significantly higher urinary 1-hydroxypyrene concentrations than those with heterozygotes, and wild homozygotes (6.41 +/- 1.09 vs. 6.24 +/- 1.08, and 4.62 +/- 0.95 micro mol/mol Cr, P < 0.05), and gene-gene interaction was found between CYP1A1 and mEH.

CONCLUSIONGenetic polymorphism of mEH gene could be a susceptible biomarker in coke oven workers which was involved in the individual susceptibility on metabolism of PAHs.

Coke ; adverse effects ; Cytochrome P-450 CYP1A1 ; genetics ; DNA Damage ; genetics ; Epoxide Hydrolases ; genetics ; Genetic Predisposition to Disease ; genetics ; Glutathione Transferase ; genetics ; Humans ; Male ; Occupational Exposure ; Polycyclic Aromatic Hydrocarbons ; poisoning ; Polymorphism, Genetic ; Pyrenes ; analysis ; metabolism