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PubMed1993

Aldose reductase the major protein associated with naphthalene dihydrodiol dehydrogenase activity in rat lens.

PURPOSE: Recent studies have indicated that certain aldose reductase inhibitors prevent the formation of cataracts in naphthalene-fed rats. The study was designed to investigate whether aldose reductase itself is involved in the metabolism of naphthalene in the lens and the mechanism of this cataract formation. METHODS: Aldose reductase was purified from whole rat lens using a series of chromatographic steps that include gel filtration, affinity chromatography, and chromatofocusing. The dehydrogenase activity of the purified enzyme was evaluated with 1,2-dihydro-1,2-dihydroxynaphthalene (naphthalene dihydrodiol) as substrate. The same dehydrogenase activity was also examined with the recombinant protein obtained from rat lens aldose reductase clone. RESULTS: Throughout the purification steps, dehydrogenase activity with naphthalene dihydrodiol as substrate coeluted with aldose reductase activity assayed with DL-glyceraldehyde as substrate. The purified aldose reductase, which appeared as a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, displayed dehydrogenase activity with naphthalene dihydrodiol as a substrate similar to that observed with the crude extract from whole rat lens. Recombinant protein from rat lens aldose reductase clone also displayed dehydrogenase activity similar to that observed with purified rat lens aldose reductase. Both the reductase and dehydrogenase activities of purified aldose reductase were inhibited by aldose reductase inhibitors. However, inhibition of dehydrogenase activity was less than reductase activity. Aldehyde reductase, an another nicotinamide adenine dinucleotide phosphate-dependent reductase, also displayed dihydrodiol dehydrogenase activity with naphthalene dihydrodiol and this activity was also inhibited by aldose reductase inhibitors. CONCLUSIONS: Aldose reductase displays dehydrogenase activity in addition to reductase activity. In rat lens aldose reductase is a major protein associated with naphthalene dihydrodiol dehydrogenase activity. This suggests that aldose reductase is linked to 1,2-dihydroxynaphthalene formation in rat lens and the subsequent formation of cataracts in naphthalene-fed rats.

Alcohol Oxidoreductases↗
PubMed2002

Quantitative analysis of experiments on bacterial chemotaxis to naphthalene.

A mathematical model was developed to quantify chemotaxis to naphthalene by Pseudomonas putida G7 (PpG7) and its influence on naphthalene degradation. The model was first used to estimate the three transport parameters (coefficients for naphthalene diffusion, random motility, and chemotactic sensitivity) by fitting it to experimental data on naphthalene removal from a discrete source in an aqueous system. The best-fit value of naphthalene diffusivity was close to the value estimated from molecular properties with the Wilke-Chang equation. Simulations applied to a non-chemotactic mutant strain only fit the experimental data well if random motility was negligible, suggesting that motility may be lost rapidly in the absence of substrate or that gravity may influence net random motion in a vertically oriented experimental system. For the chemotactic wild-type strain, random motility and gravity were predicted to have a negligible impact on naphthalene removal relative to the impact of chemotaxis. Based on simulations using the best-fit value of the chemotactic sensitivity coefficient, initial cell concentrations for a non-chemotactic strain would have to be several orders of magnitude higher than for a chemotactic strain to achieve similar rates of naphthalene removal under the experimental conditions we evaluated. The model was also applied to an experimental system representing an adaptation of the conventional capillary assay to evaluate chemotaxis in porous media. Our analysis suggests that it may be possible to quantify chemotaxis in porous media systems by simply adjusting the model's transport parameters to account for tortuosity, as has been suggested by others.

Biodegradation, Environmental↗
PubMed2001

A physiologically based pharmacokinetic model for inhalation and intravenous administration of naphthalene in rats and mice.

A diffusion limited physiologically based pharmacokinetic model for rats and mice was developed to characterize the absorption, distribution, metabolism, and elimination of naphthalene after inhalation exposure. This model includes compartments for arterial and venous blood, lung, liver, kidney, fat, and other organs. Primary sites for naphthalene metabolism to naphthalene oxide are the lung and the liver. The data used to create this model were generated from National Toxicology Program inhalation and iv studies on naphthalene and consisted of blood time-course data of the parent compound in both rats and mice. To examine the basis for possible interspecies differences in response to naphthalene, the model was extended to describe the distribution and metabolism of naphthalene oxide and the depletion and resynthesis of glutathione. After testing several alternative models, the one presented in this paper shows the best fit to the data with the fewest assumptions possible. The model indicates that tissue dosimetry of the parent compound alone does not explain why this chemical was carcinogenic to the female mouse lung but not to the rat lung. The species difference may be due to a combination of higher levels of naphthalene oxide in the mouse lung and a greater susceptibility of the mouse lung to epoxide-induced carcinogenesis. However, conclusions regarding which metabolite(s) may be responsible for the lung toxicity could not be reached.

Administration, Inhalation↗
PubMed1988

Organ-specific effects of naphthalene on tissue peroxidation, glutathione peroxidases and superoxide dismutase in the rat.

Male, weanling Blue-Spruce rats were treated with naphthalene (p.o.) in defined dose increments up to 750 mg/kg body weight over 9 weeks. At necropsy, treated rats showed a 20% decrease in body weight compared to controls. Naphthalene treatment resulted in enhanced peroxidation (p less than 0.001) only in the liver. This increased peroxidation was associated with reductions (p less than 0.05) in the activity of the selenoenzyme glutathione peroxidase in hepatic cytosolic fractions and an associated increase (p less than 0.05) in the selenium-independent glutathione peroxidase. No increase in peroxidation was observed in the lung, eye or heart of these rats and the activities of the selenoenzyme and the selenium-independent glutathione peroxidases were also unaffected by naphthalene in these organs. Naphthalene also did not affect superoxide dismutase activity in any of the organs examined. Thus, in addition to the known effects of naphthalene on tissue glutathione, naphthalene-induced reductions in the selenoenzyme glutathione peroxidase can also contribute to peroxidation in the liver and must be considered as a contributing factor in naphthalene toxicity in vivo.

Animals↗
PubMed1991

Role of biotransformation in the in vitro preimplantation embryotoxicity of naphthalene.

The in vitro developmental toxicity of the bicyclic aromatic hydrocarbon naphthalene was characterized with a preimplantation mouse embryo culture system. Day 3 ICR mouse blastocysts were co-cultured with naphthalene for 1 h either alone or in media supplemented with an Aroclor-induced rat S-9 preparation and cofactors. Toxin-treated blastocysts were subsequently cultured in NCTC 109 media with 10% fetal bovine serum for 72 h to observe the developmental effects of exposure. Developmental parameters observed included viability, hatching, culture dish attachment and trophoblastic outgrowth with the presence of a distinct inner cell mass. At media concentrations up to 0.78 mM, naphthalene alone exhibited negligible toxic effects in culture; however naphthalene co-cultured with Aroclor-induced rat hepatic S-9 fractions exhibited concentration-dependent embryolethality with an approximate LC50 of 0.18 mM in media. Naphthalene also induced concentration-dependent embryotoxicity at all observed parameters in S-9-supplemented media at concentrations ranging from 0.20 to 0.78 mM. These findings document the role of biotransformation in naphthalene's embryotoxicity to early mouse blastocysts and implicate naphthalene as a potentially embryotoxic and abortifacient component of polycyclic aromatic hydrocarbon mixtures.

Animals↗
PubMed2006

Disparity in the induction of glutathione depletion, ROS formation, poly(ADP-ribose) polymerase-1 activation, and apoptosis by quinonoid derivatives of naphthalene in human cultured cells.

The purpose of this study is to examine the differences in the induction of cytotoxic effects and poly(ADP-ribose) polymerase-1 activation in human MCF-7 breast cancer cells by quinonoid derivatives of naphthalene, including 1,2-naphthalenediol (NCAT), 1,4-naphthalenediol (NHQ), 1,2-naphthoquinone (1,2-NQ), and 1,4-naphthoquinone (1,4-NQ). Results from the cytotoxic response analyses in cells indicated that all naphthalene quinonoids induced cell death in MCF-7 cells at concentrations ranging from 0.1 to 100microM where NHQ and 1,4-NQ were more efficient than NCAT and 1,2-NQ in the induction of cell death. Results from Western blot analyses confirmed that treatment of cells with NCAT and NHQ resulted in up-regulation of p53 protein expression and a significant shift in bax/bcl2 ratio, suggesting the induction of p53-dependent apoptosis in MCF-7 cells. Additionally, we observed that all naphthalene quinonoids induced increases in reactive oxygen species (ROS) formation and glutathione (GSH) depletion in MCF-7 cells. The induction of ROS formation and GSH depletion in cells by naphthalene quinonoids decreases in the rank order 1,4-NQ>NHQ>1,2-NQ approximately equal to NCAT. Further investigation indicated that least-squares estimates of the overall rates of elimination (k(e)) of naphthalene quinonoids in MCF-7 cells decreased in the rank order 1,4-NQ>1,2-NQ>NHQ>NCAT. Values of k(e) were estimated to be between 0.280h(-1)(T(1/2)=151min) and 13.8h(-1)(T(1/2)=3.05min). These results provide evidence that the para-isomeric form of naphthalene quinonoids tend to induce acute production of ROS and alterations in intracellular redox status in cells, leading to the subsequent cell death. Further, all naphthalene quinonoids induced decreases in intracellular NAD(P)H and NAD(+) in MCF-7 cells at non-cytotoxic concentrations. The reduction of intracellular NAD(P)H in cells exposed to NCAT and 1,2-NQ was blocked by two types of poly(ADP-ribose) polymerase (PARP) inhibitors whereas PARP inhibitors did not prevent the reduction of NAD(P)H in cells exposed to NHQ and 1,4-NQ. Further investigation confirmed that increases in the number of DNA single-strand breaks were detected in MCF-7 cells exposed to NCAT and 1,2-NQ as measured by the single-cell gel electrophoresis (Comet) assay whereas NHQ and 1,4-NQ did not induce increases in the number of single-strand breaks in MCF-7 cells. Overall, results from our investigation suggest that while NHQ and 1,4-NQ are more efficient in the induction of cell death, NCAT and 1,2-NQ are prone to induce depletion of NAD(P)H and NAD(+) mediated by PARP-1 activation through formation of DNA single-strand breaks in human cultured cells.

Antineoplastic Agents↗
PubMed2006

Formation of depurinating N3adenine and N7guanine adducts after reaction of 1,2-naphthoquinone or enzyme-activated 1,2-dihydroxynaphthalene with DNA. Implications for the mechanism of tumor initiation by naphthalene.

Naphthalene is considered by the US Environmental Protection Agency to be a carcinogenic compound based on inhalation studies in rats. The primary metabolite of naphthalene is naphthalene 1,2-arene oxide. This unstable intermediate can lead to formation of 1-naphthol and naphthalene-1,2-dihydrodiol. Secondary metabolites include 1,2-dihydroxynaphthalene (1,2-DHN), which can be further oxidized to 1,2-naphthoquinone (1,2-NQ). Based on the metabolism of naphthalene and its similarity to the metabolic activation of carcinogenic natural estrogens, synthetic estrogens and benzene, we hypothesize that naphthalene is activated to initiate cancer by reaction of 1,2-NQ with DNA to form the depurinating adducts 1,2-DHN-4-N3Ade and 1,2-DHN-4-N7Gua. These adducts were synthesized by reaction of 1,2-NQ with Ade or dG in acetic acid/water/DMF (1:1:1). 1,2-NQ was reacted with DNA, and the depurinating 1,2-DHN-4-N3Ade and 1,2-DHN-4-N7Gua adducts were analyzed by ultraperformance liquid chromatography/tandem mass spectrometry and HPLC with electrochemical detection. After the reaction of 1,2-NQ with DNA, the N3Ade and N7Gua adducts were found. Similarly, when 1,2-DHN was activated by tyrosinase in the presence of DNA, higher amounts of the N3Ade and N7Gua adducts were detected. These same adducts were also formed when 1,2-DHN was activated by prostaglandin H synthase or 3-methylcholanthrene-induced rat liver microsomes in the presence of DNA. These depurinating adducts are analogous to those obtained from the ortho-quinones of natural estrogens, synthetic estrogens and benzene. These results suggest that reaction of ortho-quinones with DNA by 1,4-Michael addition is a general mechanism of weak carcinogenesis that occurs with naphthalene and a number of other aromatic compounds.

Adenine↗
PubMed2004

PAH Growth from the pyrolysis of CPD, indene and naphthalene mixture.

In this study, the addition of cyclopentadienyl (CPDyl) moieties to aromatic rings has been investigated experimenNaphthalene was selected as the representative aromatic compound and its pyrolytic reactivity was studied first to obtain background information for the pyrolysis of cyclopentadiene-indene-naphthalene mixture. The experiments were conducted in a 5 s laminar flow reactor over the temperature range of 700-850 degrees C with 50 degrees C increments. PAH growth from naphthalene pyrolysis is mainly attributed to aryl-aryl addition of naphthyl radicals and naphthalene fragmentation, with lower product formation rates comparing with hydrocarbons with CPDyl moieties. The results indicate that naphthalene is less reactive than the CPDyl containing hydrocarbon radical-molecule addition of CPDyl radicals to naphthalene results in phenanthrene, which can also be formed substantially from other growth pathways. This addition occurs mainly at low temperatures and is less favored due to the competition from more reactive indenyl and CPDyl radicals. CPDyl radical addition to naphthalene exhibits limited aromatic growth due to the aromaticity restrictions of naphthalene. The studies of hydrocarbons with and without CPDyl moieties suggest that the reaction pathways of CPDyl bearing hydrocarbons are different from those without these moieties and cannot be adequately accounted for by the existing acetylene addition and aryl-aryl addition mechanisms.

Cyclopentanes↗
PubMed2004

Complete nucleotide sequence and organization of the naphthalene catabolic plasmid pND6-1 from Pseudomonas sp. strain ND6.

Pseudomonas sp. strain ND6, which was isolated from industrial wastewater in Tianjin, China, was capable of dissimilating naphthalene as sole carbon and energy sources. We identified one plasmid, pND6-1, which was associated with the metabolism of naphthalene and determined the complete nucleotide sequence of pND6-1 (101,858 bp) using a whole-genome-shotgun approach. Computational analyses indicated that the naphthalene metabolism of the strain ND6 is associated with this plasmid. This is the first report of a complete sequence of naphthalene catabolic plasmid. pND6-1 encodes 102 putative coding sequences (CDSs). Among them, 23 CDSs were predicted to be involved in naphthalene catabolism, 14 were predicted to be involved in transposition and integration, 2 encoded putative transporters, 3 were putative transcriptional regulators, and 9 were proteins necessary for plasmid replication and partitioning. Most of the naphthalene catabolic genes of pND6-1 have 99-100% identity in amino acid sequences homologous to their nearest counterparts found in plasmid pDTG1, NAH7 and in a chromosome region in Pseudomonas stutzeri AN10 except for two duplicated genes (ND013 and ND016). Results of this study indicated that globally distributed naphthalene catabolic genes are highly conserved among different bacterial species.

Bacterial Proteins↗
PubMed2003

Mechanisms for naphthalene removal during electrolytic aeration.

Batch tests were performed to investigate chemical and physical processes that may result during electrolytic aeration of a contaminated aquifer using naphthalene as a model contaminant. Naphthalene degradation of 58-66% took place electrolytically and occurred at the same rates at a pH of 4 and 7. 1,4-naphthoquinone was identified as a product of the electrolysis. Stripping due to gases produced at the electrodes did not result in any naphthalene loss. Hydrogen peroxide (which may be produced at the cathode) did not have any effect on naphthalene, but the addition of ferrous iron (which may be present in aquifers) resulted in 67-99% disappearance of naphthalene. Chlorine (which may be produced from the anodic oxidation of chloride) can effectively degrade naphthalene at pH of 4, but not at a pH of 7. Mono-, di- and poly chloronaphthalenes were identified as oxidation products. Ferric iron coagulation (due to the oxidation of ferrous iron) did not significantly contribute to naphthalene loss. Overall, electrolytic oxidation and chemical oxidation due to the electrolytic by-products formed are significant abiotic processes that could occur and should be accounted for if bioremediation of PAH-contaminated sites via electrolytic aeration is considered. Possible undesirable products such as chlorinated compounds may be formed when significant amounts of chlorides are present.

Chlorine↗
PubMed2003

Predictive value of comparative molecular field analysis modelling of naphthalene inhibition of human CYP2A6 and mouse CYP2A5 enzymes.

The objects of this study were first to compare how well the recently constructed structure-inhibition activity relationship models of mouse CYP2A5 and human CYP2A6 predict the interaction of naphthalene in liver microsomes and secondly to study if these CYP enzymes actually oxidize naphthalene. The CoMFA model of CYP2A5 predicted the IC(50) value of naphthalene to be 42 microM (18-115 microM 95% CL) whereas in the in vitro experiment the result was 74 microM (65-83 microM) with the corresponding values for CYP2A6 being 41 microM (18-112 microM) and 25 microM (21-30 microM), respectively. Naphthalene appeared to be a competitive inhibitor both for mouse and human liver microsomal coumarin 7-hydroxylase, which is the specific probe activity for CYP2A5 and CYP2A6. The K(i)-value for the mouse enzyme was between 12-26 microM and for the human enzyme 1.2-5.6 microM. A 1-h in vitro incubation of naphthalene with human and pyrazole treated mouse liver microsomes produced more 1-naphthol than 2-naphthol. Antibody against the purified CYP2A5 inhibited 50-60% of the formation of 1-naphthol and 30-40% of the formation of 2-naphthol. These results indicate that in silico CoMFA models predict relatively well the interaction of naphthalene with CYP2A5 and CYP2A6 and that these CYPs actually oxidize naphthalene in vitro. CoMFA CYP2A5 and CYP2A6 models are thus useful as a technique for elucidating the interaction and potency of untested chemicals with these CYPs.

Animals↗
PubMed2006

Utility of urinary 1-naphthol and 2-naphthol levels to assess environmental carbaryl and naphthalene exposure in an epidemiology study.

We recently reported associations between urinary 1-naphthol (1N) levels and several intermediate measures of male reproductive health, namely sperm motility, serum testosterone levels, and sperm DNA damage. However, because 1N is a major urinary metabolite of both naphthalene and the insecticide carbaryl, exposure misclassification stemming from differences in exposure source was probable and interpretation of the results was limited. As naphthalene, but not carbaryl, is also metabolized to 2-naphthol (2N), the relationship of urinary 1N to 2N within an individual may give information about source of 1N. Utilizing data from two previous studies that measured both 1N and 2N in urine of men exposed to either carbaryl or naphthalene, the present study employed several methods to differentiate urinary 1N arising from exposures to carbaryl and naphthalene among men in the reproductive health study. When re-evaluating the reproductive health data, techniques for identifying 1N source involved exploring interaction terms, stratifying the data set based on 1N/2N ratios, and performing an exposure calibration using a linear 1N to 2N relationship from a study of workers exposed to naphthalene in jet fuel. Despite some inconsistencies between the methods used to distinguish 1N source, we found that 1N from carbaryl exposure is likely responsible for the previously observed association between 1N and sperm motility, whereas 1N from naphthalene exposure is likely accountable for the association between 1N and sperm DNA damage. We demonstrate that studies of health effects associated with carbaryl should utilize a 1N/2N ratio to identify subgroups in which carbaryl is the primary source of 1N. Conversely, studies of naphthalene-related outcomes may utilize 2N levels to estimate exposure.

Adult↗
PubMed2006

Uptake and elimination of naphthalene from liver, lung, and muscle tissue in the leopard frog (Rana pipiens).

The effects of a 0-12-hour naphthalene exposure on pulmonary CO(2) excretion and bioaccumulation in the leopard frog, Rana pipiens, were investigated. The data showed that naphthalene transport occurred from the aqueous phase into the frog tissue. The first-order rate constant (k in day-1) for the entry of naphthalene from the water into the frog was 0.079 +/- 0.007 (k +/- 95% C.I.). Bioaccumulation of naphthalene was measured in liver, lung, and thigh muscle tissue. Exposure to naphthalene caused a significant reduction in pulmonary CO(2) excretion, particularly following the first 30 minutes of exposure. Pulmonary CO(2) excretion returned to baseline levels after 8 hours of exposure, indicating that some degree of acclimation had occurred. Depuration experiments were used to monitor recovery from naphthalene exposure. Recovery of CO(2) excretion was evident following 2 hours of depuration and complete elimination of naphthalene from tissues occurred after 3 hours. The data indicate that accumulated polycyclic aromatic hydrocarbons (PAHs) may alter normal physiologic functions such as gas exchange. Since amphibians, such as frogs, are one of the first organisms to come into contact with contaminated water and sediments, the information in this study suggests that this species may be used to assess bioaccumulation and toxicity of PAHs in ecosystems.

Animals↗
PubMed2002

Stability of hemoglobin and albumin adducts of naphthalene oxide, 1,2-naphthoquinone, and 1,4-naphthoquinone.

Naphthalene is an important industrial chemical, which has recently been shown to cause tumors of the respiratory tract in rodents. It is thought that one or more reactive metabolites of naphthalene, namely, naphthalene-1,2-oxide (NPO), 1,2-naphthoquinone (1,2-NPQ), and 1,4-naphthoquinone (1,4-NPQ) contribute to the tumorigenicity of this chemical. These electrophiles are all capable of covalent binding to macromolecules including DNA and proteins. The stability of cysteinyl adducts of NPO, 1,2-NPQ, and 1,4-NPQ were investigated in both hemoglobin (Hb) and albumin (Alb) of male F344 rats following a single administration of 2 different doses (400 or 800 mg naphthalene per kg body weight). To assess the stability of Alb adducts, we compared the rates of NPO-Alb turnover (half-life of approximately 2 days) and 1,2-NPQ-Alb (half-life of approximately 1 day) to the normal turnover rate of Alb in the rat (half-life = 2.5-3 days). Based on the rapid turnover of these adducts relative to Alb itself, we concluded that they were unstable. However, the stability of Alb adducts was not affected by the dose of naphthalene administered (400 or 800 mg/kg). In contrast, NPO-Hb adducts were relatively stable (rate constant of adduct instability <or= 0.01) following a 400 mg/kg dose of naphthalene, but their stability could not be estimated following an 800 mg/kg dose due to high variability among animals. The rate constants of adduct instability obtained in this study allow application of NPO and NPQ adducts to estimate the exposure to reactive electrophilic metabolites of naphthalene in the rat. In addition, some limitations of current methods for estimating adduct instability were identified.

Albumins↗
PubMed2006

Methylation is the initial reaction in anaerobic naphthalene degradation by a sulfate-reducing enrichment culture.

The sulfate-reducing culture N47 can utilize naphthalene or 2-methylnaphthalene as the sole carbon source and electron donor. Here we show that the initial reaction in the naphthalene degradation pathway is a methylation to 2-methylnaphthalene which then undergoes the subsequent oxidation to the central metabolite 2-naphthoic acid, ring reduction and cleavage. Specific metabolites occurring exclusively during anaerobic degradation of 2-methylnaphthalene were detected during growth on naphthalene, i.e. naphthyl-2-methyl-succinate and naphthyl-2-methylene-succinate. Additionally, all three enzymes involved in anaerobic degradation of 2-methylnaphthalene to 2-naphthoic acid that could be measured in vitro so far, i.e. naphthyl-2-methyl-succinate synthase, succinyl-CoA:naphthyl-2-methyl-succinate CoA-transferase and naphthyl-2-methyl-succinyl-CoA dehydrogenase were also detected in naphthalene-grown cells with similar activities. Induction experiments were performed to study the growth behaviour of the cell when transferred from naphthalene to 2-methylnaphthalene or vice versa. When the cells were transferred from naphthalene to 2-methylnaphthalene they grew immediately, indicating that no new enzymes had to be induced. On the contrary, the transfer of cells from 2-methylnaphthalene to naphthalene caused a lag-phase of almost 100 days demonstrating that an additional catabolic enzyme has to be activated in this case. We propose the methylation as a novel general mechanism of activation reactions in anaerobic degradation of unsubstituted aromatic hydrocarbons.

Anaerobiosis↗
PubMed2006

Effects of naphthalene on microbial community composition in the Delaware estuary.

The effects of naphthalene on microbial communities in the bottom boundary layer of the Delaware Bay estuary were investigated in microcosms using denaturing gradient gel electrophoresis (DGGE) and fluorescent in situ hybridization (FISH) with oligonucleotide probes. Three days after the addition of naphthalene, rates of bacterial production and naphthalene mineralization were higher than in no-addition controls and than in cases where glucose was added. Analyses using both DGGE and FISH indicated that the bacterial community changed in response to the addition of naphthalene. FISH data indicated that a few major phylogenetic groups increased in response to the glucose addition and especially to the naphthalene addition. DGGE also demonstrated differences in community composition among treatments, with four phylotypes being unique to naphthalene-amended treatments and three of these having 16S rRNA genes similar to known hydrocarbon degraders. The bacterial community in the naphthalene-amended treatment was distinct from the communities in the glucose-amended treatment and in the no-addition control. These data suggest that polycyclic aromatic hydrocarbons may have large effects on microbial community structure in estuaries and probably on microbially mediated biogeochemical processes.

Acinetobacter↗
PubMed2005

In vitro metabolism of naphthalene by human liver microsomal cytochrome P450 enzymes.

The polycyclic aromatic hydrocarbon naphthalene is an environmental pollutant, a component of jet fuel, and, since 2000, has been reclassified as a potential human carcinogen. Few studies of the in vitro human metabolism of naphthalene are available, and these focus primarily on lung metabolism. The current studies were performed to characterize naphthalene metabolism by human cytochromes P450. Naphthalene metabolites from pooled human liver microsomes (pHLMs) were trans-1,2-dihydro-1,2-naphthalenediol (dihydrodiol), 1-naphthol, and 2-naphthol. Metabolite production generated Km values of 23, 40, and 116 microM And Vmax values of 2860, 268, and 22 pmol/mg protein/min, respectively. P450 isoform screening of naphthalene metabolism identified CYP1A2 as the most efficient isoform for producing dihydrodiol and 1-naphthol, and CYP3A4 as the most effective for 2-naphthol production. Metabolism of the primary metabolites of naphthalene was also studied to identify secondary metabolites. Whereas 2-naphthol was readily metabolized by pHLMs to produce 2,6- and 1,7-dihydroxynaphthalene, dihydrodiol and 1-naphthol were inefficient substrates for pHLMs. A series of human p450 isoforms was used to further explore the metabolism of dihydrodiol and 1-naphthol. 1,4-Naphthoquinone and four minor unknown metabolites from 1-naphthol were observed, and CYP1A2 and 2D6*1 were identified as the most active isoforms for the production of 1,4-naphthoquinone. Dihydrodiol was metabolized by P450 isoforms to three minor unidentified metabolites with CYP3A4 and CYP2A6 having the greatest activity toward this substrate. The metabolism of dihydrodiol by P450 isoforms was lower than that of 1-naphthol. These studies identify primary and secondary metabolites of naphthalene produced by pHLMs and P450 isoforms.

Cytochrome P-450 Enzyme System↗
PubMed1995

Biodegradation of naphthalene in aqueous nonionic surfactant systems.

The principal objective of this study was to quantify the bioavailability of micelle-solubilized naphthalene to naphthalene-degrading microorganisms comprising a mixed population isolated from contaminated waste and soils. Two nonionic surfactants were used, an alkylethoxylate, Brij 30 (C12E4), and an alkylphenol ethoxylate, Triton X-100 (C8PE9.5). Batch experiments were used to evaluate the effects of aqueous, micellized nonionic surfactants on the microbial mineralization of naphthalene and salicylic acid, an intermediate compound formed in the pathway of microbial degradation of naphthalene. The extent of solubilization and biodegradation under aerobic conditions was monitored by radiotracer and spectrophotometric techniques. Experimental results showed that surfactant concentrations above the critical micelle concentration were not toxic to the naphthalene-degrading bacteria and that the presence of surfactant micelles did not inhibit mineralization of naphthalene. Naphthalene solubilized by micelles of Brij 30 or Triton X-100 in liquid media was bioavailable and degradable by the mixed culture of bacteria.

Bacteria↗