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PubMed1978

Distribution and elimination of naphthalene and 2-methylnaphthalene in rainbow trout during short- and long-term exposures.

The accumulation and elimination of 14C in rainbow trout tissues following short- and long-term exposures to aqueous 14C-naphthalene or 14C-2-methylnaphthalene were studied. After exposure for eight hr to 0.005 mg/L or 0.023 mg/L of 14C-naphthalene most tissues of fingerling rainbow trout studied contained 14C at 20 to 100 times the water levels while fat and bile contained 14C at several hundred times water levels. The half-lives for elimination of 14C from all tissues except fat were less than 24 hr. Exposure of fingerling rainbow trout to 14C-naphthalene or 14C-2-methylnaphthalene for four weeks in a continuous-flow delivery system resulted in maximum tissue levels of these chemicals of from 40 to 300 times the water concentration. Maximum bile 14C levels were 13,000 and 23,500 times the water concentration for 14C-naphthalene and 14C-2-methylnaphthalene exposure, respectively. Elimination of 14C accumulated from 14C-naphthalene in this long-term exposure was much slower than after short-term exposures, while elimination of 14C accumulated from 14C-2-methylnaphthalene was biphasic. The presence of parent compounds and metabolites in acetone extracts of muscles was determined by TLC. The data suggest that the biphasic release of 14C from muscle of trout exposed to 14C-2-methylnaphthalene may be due to differential elimination of parent compound and metabolites.

Animals↗
PubMed2006

Isolation and characterization of naphthalene-catabolic genes and plasmids from oil-contaminated soil by using two cultivation-independent approaches.

Two different cultivation-independent approaches were applied to isolate genes for naphthalene dioxygenase (NDO) from oil-contaminated soil in Japan. One approach was the construction of a broad-host-range cosmid-based metagenomic DNA library, and the other was the so-called exogenous plasmid isolation technique. Our screening of NDO genes in both approaches was based on the functional complementation of Pseudomonas putida strains which contained Tn4655K, a transposon carrying the entire set of naphthalene-catabolic (nah) genes but lacking the NDO-encoding gene. We obtained in the former approach a cosmid clone (pSLX928-6) that carried an nah upper pathway operon for conversion of naphthalene to salicylate, and this operon showed a significantly high level of similarity to the corresponding operon on an IncP-9 naphthalene-catabolic plasmid, pDTG1. In the latter approach, the microbial fraction from the soil was mated with a plasmid-free P. putida strain containing a chromosomal copy of Tn4655K, and transconjugants were obtained that received either a 200- or 80-kb plasmid containing all the nah genes for the complete degradation of naphthalene. Subsequent analysis revealed that (1) both plasmids belong to the IncP-9 incompatibility group; (2) their nah upper pathway operons are significantly similar, but not completely identical, to those of pDTG1 and pSLX928-6; and (3) these plasmids carried genes for the salicylate metabolism by the meta-cleavage pathway.

Biotechnology↗
PubMed2005

Current external and internal exposure to naphthalene of workers occupationally exposed to polycyclic aromatic hydrocarbons in different industries.

OBJECTIVES: External and internal exposure to naphthalene was examined in the most important industries that are typically concerned with polycyclic aromatic hydrocarbon (PAH)-induced diseases (cancer). Furthermore, a control collective from the general population was investigated. METHODS: External naphthalene was determined by personal air sampling (n = 205). The internal exposure was examined by urinary metabolites 1-naphthol and 2-naphthol (n = 277). RESULTS: Highest median concentrations of naphthalene in air were found in converter infeed (93.2 microg/m3) and coal-tar distillation (35.8 microg/m3). Moderate and low levels were determined in coking plants (14.5 microg/m3) and in the production of refractories (6.1 microg/m3) and graphite electrodes (0.7 microg/m3). Biological monitoring revealed concentrations of the sum of both metabolites [(1+2)-NOL] in smokers to be increased by 1.6-6.4 times compared with that in non-smokers at the same workplaces. Among non-smokers we found high median (1+2)-NOL levels in converter bricklayers (120.1 microg/l), in coal-tar distillation workers (56.0 microg/l) and in coking plant workers (29.5 microg/l). (1+2)-NOL concentrations around 10 microg/l were found in the production of refractories and graphite electrodes. There was a rough coherency between external and internal naphthalene exposure. In the controls, median (1+2)-NOL concentrations were 10.9 microg/l in non-smokers' urine and 40.3 microg/l in smokers' urine samples. CONCLUSIONS: Actual conditions of occupational hygiene at the workplaces investigated in this comprehensive study are better than those that current limit values of 50,000 microg/m3 (TLV, TRK) seem to induce. It has become obvious that tobacco smoking is a crucial confounding factor in biological monitoring of naphthalene-exposed humans, making interpretation of occupationally increased naphthol excretions very difficult at low exposure levels.

Adult↗
PubMed1992

Reduction properties of nitrated naphthalenes: relationship between electrochemical reduction potential and the enzymatic reduction by microsomes or cytosol from rat liver.

The nitroreductase activities of rat liver microsomes and cytosol towards various nitrated naphthalenes (1-, 2-mononitro-, 1,3-, 1,5-, 1,7-, 1,8-dinitro-1,3,5- and 1,3,8-trinitronaphthalenes) were characterized as follows. (1) The rates of reduction of nitrated naphthalenes in either microsomal or cytosolic incubation were found to increase in the order of trinitro- > dinitro- > mono-nitronaphthalene, although, in the case of microsomal nitroreduction, trinitronaphthalenes were reduced more rapidly than in cytosol. (2) The effective cofactors, electron donors, in the nitroreduction of nitrated naphthalenes in cytosol were NADH and hypoxanthine, but not NADPH. (3) The nitrated naphthalenes with a nitro group at a beta-position appear to be more easily reduced among the various isomers. The cytosolic nitroreductase activities towards the nitrated naphthalenes were closely related to the single-electron reduction potentials measured by cyclic voltammetry and hence, there was a good relationship between the logarithm of nitroreductase activities and the electrochemical reduction potentials. In microsomes, nitroreductase activities were rather less well related to electrochemical reduction potentials.

Animals↗
PubMed1984

Naphthalene toxicity in CD-1 mice: general toxicology and immunotoxicology.

Random bred CD-1 mice were used to evaluate the acute oral toxicity and subchronic toxicity of naphthalene administered in corn oil. The acute oral LD50 of naphthalene was 533 and 710 mg/kg in male and female mice, respectively. Subchronic toxicity was evaluated with 14- and 90-day daily oral gavage studies. Doses utilized in the 14-day study were 27, 53, and 267 mg/kg, with the latter representing one-half of the male LD50. Both males and females demonstrated a 5-10% mortality and depressed body weight at the high dose only. Males had decreased thymus weights, and females had decreased spleen and increased lung weights at the high dose only. Other organ weights were unaffected at any dosage level. Serum enzyme and electrolyte levels were not altered in a dose-related manner. To assess the potential immunotoxicity of naphthalene the following screen was utilized: humoral immune response, response to mitogens, delayed hypersensitivity response, popliteal lymph node response, bone marrow stem cell number, and DNA synthesis. No evidence of immunotoxicity was demonstrated. The 90-day study employed daily oral doses of 5.3, 53, and 133 mg/kg. There was no treatment-related mortality in either sex, nor was body weight affected. Organ weights were not affected in males, and females showed reduced spleen weights only at the high dose. Serum enzyme and electrolyte levels, as well as the immunotoxicity screen, indicated that naphthalene doses up to one-fourth the LD50 for 90 days failed to elicit consistent statistically significant and biologically relevant compound-related effects. A screen of the effects of the 90-day naphthalene treatment on various aspects of the hepatic drug metabolizing system indicated no alterations, with the exception of a specific dose-related inhibition of aryl hydrocarbon hydroxylase activity in both male and female mice.

Animals↗
PubMed1984

Effect of naphthalene on color changes of the sand fiddler crab, Uca pugilator.

The polycyclic aromatic hydrocarbon, naphthalene, inhibited the melanin dispersion, which normally occurs in the fiddler crab, Uca pugilator, during the dark phase of its circadian rhythm of color change. Naphthalene produced this inhibition no matter whether the melanin was fully aggregated or more or less dispersed at the time of initial exposure. Inhibition of the circadian melanin dispersion does not appear to be due to a direct action of naphthalene on the melanophores. This inhibition was concentration-dependent with acute daily exposure. Naphthalene does not, however, inhibit melanin dispersion in response to a black background, indicating thereby that naphthalene-exposed crabs continue to synthesize melanin-dispersing hormone and norepinephrine.

Animals↗
PubMed1991

Effects of naphthalene metabolites on cultured cells from eye lens.

Naphthalene is toxic to the eye and results in opacification of the lens. To investigate the metabolic events that may be occurring in the lens epithelial cells, a cell line of lens from a transgenic mouse was incubated with various metabolites of naphthalene. Naphthoquinone at 50 microM was toxic to most cells with a depletion of glutathione levels noted within 6 h of incubation. At 10 microM, naphthoquinone caused an increase in specific activity of the enzyme DT-diaphorase. This enzyme is thought to be a defense against quinones since semiquinone formation is thought to be lessened. Naphthalene-1,2-dihydrodiol at 50 microM also caused an increase in the specific activity of the DT-diaphorase, while at 10 microM no apparent change occurred in the cells. Although there was evidence of metabolic alterations in the cells with the metabolites of naphthalene, the protein profile by two-dimensional gel electrophoresis did not change and there was no indication of an increase in carbonyl formation in the soluble proteins of the cells. These experiments indicate that the metabolites of naphthalene can cause alteration in the metabolism of the lens cells but may not cause apparent changes in the major proteins within the lens epithelium.

Animals↗
PubMed1996

Naphthalene-induced oxidative stress in rats and the protective effects of vitamin E succinate.

Quinone metabolites of naphthalene (NAP) are known to produce lipid peroxidation. However, the ability of naphthalene to induce oxidative stress in experimental animals has not been extensively investigated. Furthermore, the effects of vitamin E succinate [(+)-alpha-tocopherol acid succinate; VES] on naphthalene-induced oxidative stress and tissue damage were assessed. Female Sprague-Dawley rats were treated with a single oral dose of 1100 mg naphthalene/kg (0.50 LD50) in corn oil. Vitamin E succinate-treated rats received 100 mg VES/kg/day orally for 3 d before naphthalene treatment, and 40 mg VES/kg/d after NAP administration. Hepatic and brain tissues and urine samples were collected 0, 12, 24, 48, and 72 h after NAP treatment. Naphthalene treatment resulted in a 2.1-fold increase in lipid peroxidation in liver and brain mitochondria at the 24-h time point. Increases in hepatic and brain mitochondrial lipid peroxidation in VES plus NAP-treated rats were 39-46% less than NAP treated rats at 24 h. DNA-single strand breaks increased 3.0-fold in hepatic tissues in NAP treated rats, and increased only 1.6-fold in VES protected rats at the 24-h time point. Glutathione (GSH) decreased by 83 and 49% in hepatic and brain tissues, respectively, in NAP-treated rats at the 24-h time point, while GSH content in VES plus NAP-treated rats decreased 47 and 21% in hepatic and brain tissues, respectively, at this same time point. Microsomal membrane fluidity, a measurement of membrane damage, increased 1.9- and 1.7-fold in liver and brain tissues, respectively, in NAP-treated rats, and only 1.3- and 1.2-fold in NAP plus VES-treated rats at the 24-h time point. The urinary excretion of malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT), and acetone (ACON) was determined at 0-96 h after NAP administration. Between 12-24 h after NAP administration maximal excretion of the four urinary lipid metabolites was observed, with increases of 4.5-, 2.7-, 2.3-, and 2.8-fold for MDA, FA, ACT, and ACON, respectively, at the 24-h time point. VES reduced the NAP-induced excretion of these urinary metabolites by 28-49% 24 h after NAP administration. These results support the hypothesis that NAP induces oxidative stress and tissue damage, and that vitamin E succinate provides significant protection.

Animals↗
PubMed1994

Oxidation of 2-methoxynaphthalene by toluene, naphthalene and biphenyl dioxygenases:structure and absolute stereochemistry of metabolites.

2-Methoxynaphthalene was subjected to biooxidation by whole cells of six organisms: Pseudomonas putida F39/D containing toluene dioxygenase, Escherichia coli JM109(pDTG601), containing recombinant toluene dioxygenase from Pp F39/D, Pseudomonas sp. NCIB 9816/11, containing naphthalene dioxygenase. E. coli JM109(pDTG141), containing recombinant naphthalene dioxygenase from NCIB 98161/11, E. coli C534(ProR/Sac) containing recombinant naphthalene dioxygenase from Pp G7, and Beijerinckia sp. B8/36, containing biphenyl dioxygenase. The major product of oxidation by the naphthalene and biphenyl dioxygenases has been isolated and identified as (1R,2S)-dihydroxy-7-methoxy-1,2-dihydronaphthalene, 2c. A minor product, (1R,2S)-dihydroxy-6-methoxy-1,2-dihydronaphthalene, 3c, has also been detected. Oxidation by the toluene dioxygenase-containing organisms led to the isolation of 3c as the major product. Minor products detected in these reactions were 2c, and a third compound, (1S,2S)-dihydroxy-3-methoxy-1,2-dihydronaphthalene, 4c. Structural studies and dehydration of the diols to a mixture of naphthols are described. The absolute stereochemistry of these new diols has been established by correlation with known compounds. The organisms' potential in the production of new metabolites as useful chiral synthons by biooxidation of 2-substituted naphthalenes is indicated.

Bacteria↗
PubMed2005

Fungal biodegradation of naphthalene: microcosms studies.

The present work is aimed to ascertain naphthalene biodegradation capability of P. chrysosporium and T. harzianum in soil microcosms. Considering the high naphthalene volatility, a suitable soil microcosm was set-up and used. Several degradation tests were conducted with different C/N ratio media for the two fungi in order to enquire the best range of working conditions. The kinetic studies were conducted at a maximal naphthalene concentration of 600 mg kg(-1). During experimental time course naphthalene concentration, CO2 evolution as well as phytotoxicity tests were performed as monitoring parameters. The results shown in the current paper, put in evidence that T. harzianum, differently than in liquid culture, is not able to biodegrade naphthalene directly in soil microcosm, while P. chrysosporium in the same conditions biodegrades the PAH till about 600 mg kg(-1). As concern the founded kinetics for P. chrysosporium, a saturation shape in presence of N-limited medium (high C/N ratio) was evaluated while a growing form more than linear in no-N limited medium (normal C/N ratio) was determined.

Basidiomycota↗
PubMed2005

Naphthalene biodegradation kinetics in an aerobic slurry-phase bioreactor.

The research was focused on the slurry-phase biodegradation of naphthalene in soil. Among ex situ techniques, the slurry phase offers the advantage of increased availability of contaminants to bacteria. From naphthalene contaminated soil, a Pseudomonas putida M8 strain capable to degrade naphthalene was selected. Experiments were performed in a stirred and oxygenated reactor. In this study, the influence of air flow rate and agitation rate on volatilisation and biodegradation of naphthalene was investigated. The hydrocarbon disappearance, the carbon dioxide production, and the ratio of total heterotrophic and naphthalene-degrading bacteria was monitored. The results obtained confirm that the selected bioremediation technology is successful in the treatment of contaminated soils.

Bacteria, Aerobic↗
PubMed2006

Effects of mixed surfactants on the volatilization of naphthalene from aqueous solutions.

The effects of mixed anionic-nonionic surfactants, Tween40-SDS (sodium dodecyl sulfate), Tween40-SDBS (sodium dodecylbenzene sulfonate), Tween20-SDS and Tween20-SDBS, on the solubility and volatilization of naphthalene from static aqueous solutions were investigated. The experiment results indicated that mixed anionic-nonionic surfactants can solubilize naphthalene synergistically, which was resulted from the reduction in critical micelle concentration (CMC) of the mixed surfactant and the increase in micellar partition coefficient (K(mc)) of naphthalene between micelles and aqueous phase. The synergistic effects of mixed surfactants resulted in further reduction in volatilization of naphthalene than that induced by single surfactant. A positive linear correlation was found between the synergistic solubilization ratio (DeltaS) and the synergistic inhibitory capacity on naphthalene volatilization (DeltaC) in the presence of mixed surfactants. Results from this study imply that mixed surfactants can be employed in environmental remediation to formulate the needed solubility and volatilization of volatile and semivolatile compounds in aqueous solutions.

Environmental Pollution↗
PubMed2005

Changes in fatty acid composition in Pseudomonas putida and Pseudomonas stutzeri during naphthalene degradation.

The effects of naphthalene on the whole cell-derived fatty acid composition of Pseudomonas putida and Pseudomonas stutzeri during naphthalene degradation were investigated. These strains differed in their abilities to degrade naphthalene and in 1,2-catechol dioxygenase activities. The cells of both strains reacted to the addition of naphthalene with an increase in the saturated/unsaturated ratio. The dynamic changes comprised also alterations in the percentage of hydroxy, cyclopropane and branched fatty acids. Upon the exposure of naphthalene, new fatty acids were detected.

Biodegradation, Environmental↗
PubMed2006

Molecular classification of IncP-9 naphthalene degradation plasmids.

A large collection of naphthalene-degrading fluorescent Pseudomonas strains isolated from sites contaminated with coal tar and crude oil was screened for the presence of IncP-9 plasmids. Seventeen strains were found to carry naphthalene catabolic plasmids ranging in size from 83 to 120 kb and were selected for further study. Results of molecular genotyping revealed that 15 strains were closely related to P. putida, one to P. fluorescens, and one to P. aeruginosa. All catabolic plasmids found in these strains, with the exception of pBS216, pSN11, and p8909N-1, turned out to belong to IncP-9 beta-subgroup. Plasmids pBS216, pSN11, and p8909N-1 were identified as members of IncP-9 delta-subgroup. One plasmid, pBS2, contains fused replicons of IncP-9beta and IncP-7 groups. RFLP analyses of the naphthalene catabolic plasmids revealed that organisation of the replicon correlates well with the overall plasmid structure. Comparative PCR studies with conserved oligonucleotide primers indicated that genes for key enzymes of naphthalene catabolism are highly conserved among all studied plasmids. Three bacterial strains, P. putida BS202, P. putida BS3701, and P. putida BS3790, were found to have two different salicylate hydroxylase genes one of which has no similarity to the "classic" enzyme encoded by nahG gene. Discovery of a large group of plasmid with unique nahR suggested that the regulatory loop may also represent a variable part of the pathway for catabolism of naphthalene in fluorescent Pseudomonas spp.

Biochemistry↗
PubMed2001

Anaerobic biodegradation of naphthalene, phenanthrene, and biphenyl by a denitrifying enrichment culture.

In previous results [Rockne and Strand (1998) Environ. Sci. Technol. 32, 2962-3967], anaerobic biodegradation of the polycyclic aromatic hydrocarbons, naphthalene, phenanthrene, and biphenyl in a fluidized bed reactor (FBR) enrichment was demonstrated. In this paper, re-feeding and mineralization experiments with sub-cultures of the nitrate-reducing enrichment are described. The subcultures continued to remove the PAHs after three feedings. PAH biodegradation ceased when nitrate was depleted and resumed when the enrichment was fed nitrate, demonstrating that PAH biodegradation was dependent upon nitrate reduction. Tests with radiolabeled PAH confirmed that PAH was mineralized, although the extent of mineralization differed greatly with different PAHs. Only partial mineralization (17% of initial carbon) was observed when the culture was fed naphthalene, whereas nearly complete mineralization (96%) was observed with phenanthrene. PAH carbon was incorporated into cell mass and mineralized after complete biodegradation of the PAHs, with 78-102% recoveries of radiolabel for naphthalene and phenanthrene, respectively. PAH carbon incorporation into biomass also varied considerably. Minor assimilation of biphenyl or phenanthrene was observed in the culture, whereas extensive assimilation of naphthalene carbon (57%) was observed when the culture was challenged with naphthalene. PAH degradation was approximately stoichiometric with the amount of nitrate consumed. Headspace analysis showed production of N2O, suggesting the enrichment coupled the biodegradation of PAH to denitrification.

Anaerobiosis↗
PubMed2001

The use of a solid adsorber resin for enrichment of bacteria with toxic substrates and to identify metabolites: degradation of naphthalene, O-, and m-xylene by sulfate-reducing bacteria.

Anaerobic sulfate-reducing bacteria were enriched from contaminated aquifer samples with naphthalene, o-, and m-xylene as sole carbon and energy source in the presence of Amberlite-XAD7, a solid adsorber resin. XAD7 served as a substrate reservoir maintaining a constantly low substrate concentration in the culture medium. In equilibration experiments with XAD7, the aromatic hydrocarbons needed up to 5 days to achieve equilibrium between the water and the XAD7 phase. The equilibrium concentration was directly correlated with the amount of added substrate and XAD7. In the enrichments presented here, XAD7 and aromatic hydrocarbons were adjusted to maintain substrate concentrations of 100 microM m-, or o-xylene, or 50 microM naphthalene. After five subsequent transfers, the three cultures were able to grow with higher substrate concentrations in the absence of XAD7 although they grew best with lower hydrocarbon concentrations. Two new xylene-degrading cultures were obtained that could not utilise toluene as carbon source. O-xylene was degraded anaerobically by a culture, which could also oxidise m-xylene but not p-xylene. Eighty-three percent of the electrons from o-xylene oxidation were recovered in the produced sulfide, indicating a complete oxidation to CO2. Another sulfate-reducing enrichment culture oxidised m-xylene completely to CO2 but not o-, or p-xylene. A naphthalene-degrading sulfate-reducing enrichment culture oxidised naphthalene completely to CO2. Metabolites of naphthalene degradation were recovered from the XAD7 phase and subjected to GC/MS analysis. Besides the metabolites 2-naphthoic acid and decahydro-2-naphthoic acid which were identified by the mass spectrum and coelution with chemically synthesised reference compounds, the reduced 2-naphthoic acid derivatives 5,6,7,8-tetrahydro-2-naphthoic acid and octahydro-2-naphthoic acid were tentatively identified by their mass spectra. Cultivation of bacterial cultures in the presence of XAD7 and subsequent derivatisation and extraction of metabolites directly from the solid XAD7 resin provides a new method for the isolation of sensitive bacteria and identification of metabolites.

Acrylic Resins↗
PubMed2002

Comparative effects of TCDD, endrin, naphthalene and chromium (VI) on oxidative stress and tissue damage in the liver and brain tissues of mice.

The mechanism of toxicity of structurally diverse environmental toxicants including heavy metals and polyhalogenated and polycyclic hydrocarbons may involve a common cascade of events which entails an oxidative stress and production of reactive oxygen species. We have determined the comparative effects of single 0.01, 0.10 and 0.50 LD(50) doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), endrin, naphthalene and sodium dichromate (chromium VI) on lipid peroxidation, DNA fragmentation and enhanced production of superoxide anion (cytochrome c reduction) in liver and brain tissues of C57BL/6NTac mice. The effects of a single acute oral 0.50 LD(50) dose of these xenobiotics on hepatic and brain lipid peroxidation were investigated at 0, 12, 24, 48, and 96 h after treatment, while the effects of 0.10 LD(50) and 0.01 LD(50) doses of these xenobiotics were at 0, 24, 48, 72, and 96 h after treatment. Dose- and time-dependent effects were observed with all four xenobiotics. At a 0.50 LD(50) dose of TCDD, endrin, naphthalene and chromium VI, maximum increases in cytochrome c reduction (superoxide anion production) of approximately 5.7-, 5.4-, 5.3- and 4.1-fold, respectively, were observed in hepatic tissues. TCDD showed an increasing effect through 96 h. Endrin and naphthalene demonstrated a maximum effect at 12-24 h, while chromium VI exhibited a maximum effect at 48 h. With respect to lipid peroxidation, at a 0.50 LD(50) dose both endrin and chromium VI induced the maximum effect at 48 h of treatment, while naphthalene demonstrated the maximum effect after 24 h of treatment. TCDD demonstrated a continued effect through 96 h of treatment. At a 0.50 LD(50) dose TCDD, endrin, naphthalene and chromium VI produced maximum increases in hepatic lipid peroxidation of approximately 3.5-, 3.1-, 3.7- and 3.3-fold in hepatic tissues, respectively. Similar results were obtained in hepatic and brain DNA fragmentation at 0.50 LD(50) doses. Lesser effects were observed with 0.10 and 0.01 LD(50) doses of these xenobiotics as compared to the 0.50 LD(50) dose. The results clearly demonstrate that these diverse xenobiotics induce dose- and time-dependent oxidative stress and tissue damage in the liver and brain tissues of mice.

Air Pollutants↗
PubMed2002

Naphthalene toxicity and antioxidant nutrients.

Naphthalene is a bicyclic aromatic compound that has wide industrial and commercial applications. It is used as the starting material for the synthesis of other compounds, as a moth repellent, soil fumigant and lavatory deodorant. Most exposure occurs through low dose chronic inhalation, dermal contact or ingestion through the food chain. The lungs and eyes appear to be most susceptible to toxicity, although biochemical markers of toxicity can be demonstrated in other tissues, such as the kidney, brain and liver. In addition to lens opacification (cataracts) and histological changes associated with pneumotoxicity, other biomarkers of toxic effects include glutathione depletion, lipid peroxidation, DNA fragmentation and the production of the active oxygen species as superoxide anion and hydroxyl radical. In addition, the urinary excretion of lipid metabolites occurs. A role for the tumor suppressor gene p53 has been demonstrated. Toxic manifestations of naphthalene are associated with its oxidative metabolism to various products including quinones. The ability to protect against the toxic effects of naphthalene by using various antioxidants and free radical scavengers has been demonstrated. Studies have been conducted with vitamin E, vitamin E succinate, melatonin, curcumin, various L-cysteine prodrugs, several aldose reductase inhibitors and spin-trapping agents. The ability to prevent the toxic manifestations of naphthalene is dependent on the pharmacokinetic properties of the agents, which have been studied. The appropriate selection of chemoprotectants can be useful in preventing naphthalene toxicity.

Animals↗