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At least 19 recordsLinked to original sources

PubMed2003

Survival of naphthalene-degrading Pseudomonas putida NCIB 9816-4 in naphthalene-amended soils: toxicity of naphthalene and its metabolites.

Survival of naphthalene-degrading Pseudomonas putida NCIB 9816-4 was measured in nonsterile soil samples (coal tar-contaminated and pristine) with and without added crystalline naphthalene over a period of 21 days. A 2-3 log decrease in cfu occurred in the presence, but not absence, of added naphthalene. We used aqueous suspensions of crystalline naphthalene to explore potential mechanisms of its toxicity on the test bacterium under aerobic conditions. Measurements of dissolved naphthalene in medium indicated that uptake by P. putida NCIB 9816-4 maintained naphthalene at concentrations well below saturation. Accumulation of catechol was documented by high-performance liquid chromatography and gas chromatography/mass spectrometry in the presence of 0.5% (w/v) naphthalene crystals. Transient catechol accumulation was highest when cells entered stationary phase. A decrease in catechol concentration correlated with the development of brown color in the medium. Brown pigment accumulation correlated with a decrease in viable cell counts. These results suggested that catechol, related compounds, and their condensation products can accumulate to toxic levels in stationary phase P. putida NCIB 9816-4 cells. We hypothesize that the same mechanism of toxicity may occur under the nutrient-limited conditions expected in soil.

Biodegradation, Environmental↗

PubMed1990

Effects of naphthalene and naphthalene metabolites on the in vitro humoral immune response.

Naphthalene-induced pulmonary and renal toxicity and polycyclic aromatic hydrocarbon-induced carcinogenesis are known to be mediated by their reactive metabolites. Subchronic exposure (90 d) of mice to naphthalene does not alter humoral and cellular-mediated immune responses, whereas polycyclic aromatic hydrocarbons, such as benzo[a]pyrene and 7,12-dimethylbenzanthracene, are known to be immunosuppressive. To understand these differences, the antibody-forming cell (AFC) responses of splenocyte cultures exposed to naphthalene (2, 20, and 200 microM) were evaluated. At these concentrations, the antibody-forming cell response to sheep red blood cells (RBC) was not affected. To determine if reactive metabolites of naphthalene were immunosuppressive, splenocytes were exposed to naphthalene metabolites by direct addition or through the use of a metabolic activation system. The addition of 1-naphthol (70 and 200 microM) and 1,4-naphthoquinone (2, 7, and 20 microM) resulted in a decreased antibody-forming cell response. Suppression of AFC responses was also obtained by culturing splenocytes with liver S9 and naphthalene. Since splenic metabolism of naphthalene to nonimmunosuppressive metabolites may account for the absence of immunotoxicity, the types of naphthalene metabolites generated by splenic microsomes were determined. It was observed that splenic microsomes were unable to generate any detectable naphthalene metabolites, whereas liver microsomes were able to generate both 1,2-naphthalene diol and 1-naphthol. Thus, the absence of an immunosuppressive effect by naphthalene exposure may be related to the inability of splenocytes to metabolize naphthalene. Moreover, the concentration of naphthalene metabolites generated within the liver that may diffuse to the spleen may be inadequate to produce immunotoxicity.

Animals↗

PubMed1995

Relationship of cytochrome P450 activity to Clara cell cytotoxicity. IV. Metabolism of naphthalene and naphthalene oxide in microdissected airways from mice, rats, and hamsters.

Parenteral administration of naphthalene produces a dose-dependent and tissue-, species-, and cell-selective lesion of murine Clara cells. The rate and stereoselectivity of naphthalene metabolism by microsomal preparations correlate with tissue and species differences in cytotoxicity. Because earlier studies used microsomes obtained from whole tissue, differences in susceptibility of proximal and distal airways could not be related to differences in the metabolic activation or detoxication of naphthalene. Specific subcompartments of the respiratory system, obtained by microdissection, have been used to study the cytochrome P450-dependent metabolism of naphthalene and the epoxide hydrolase/glutathione transferase-dependent metabolism of naphthalene oxide. The rates of naphthalene metabolism were substantially higher in mouse airways than in comparable airways of hamsters or rats. Rates of metabolism were higher in distal airways than in the trachea of all species studied. Metabolism in mouse airways was highly stereoselective, whereas that in hamster and rat tissues was not. Nonciliated cells at all airway levels in mice were heavily labeled with an antibody to cytochrome P450 2F2; little labeling was observed in any portion of rat and hamster lungs. Postmitochondrial supernatants prepared from mouse and hamster airways metabolized racemic naphthalene oxide to diol and glutathione adducts at substantially higher rates than did comparable preparations from rats. Although glutathione levels varied 2-4-fold at different airway levels in the three species studied, levels at the most susceptible site (mouse distal bronchioles) were as high as or higher than those at other, less susceptible, sites. These studies support the view that the rate and stereoselectivity of naphthalene metabolism to naphthalene 1R,2S-oxide catalyzed by cytochrome P450 2F2 are critical determinants in the species-specific and region-selective cytotoxicity of naphthalene in mice. The lack of major differences in the catalytic activity or enantioselectivity of putative detoxication enzymes (epoxide hydrolase or glutathione transferases) between mouse and hamster tissue, combined with data showing that the differences in the metabolic fate of naphthalene oxide in proximal versus distal airways are not dramatic, suggests that the initial epoxidation of naphthalene is an important factor in site-selective toxicity. These studies support the need to use tissue from defined airway levels for studies on the relationship of biochemical and metabolic factors important in cellular injury by lung toxicants, such as naphthalene, where there are dramatic regional differences in susceptibility to injury within the respiratory system.

Animals↗

PubMed1988

Glutathione depletion by naphthalene in isolated hepatocytes and by naphthalene oxide in vivo.

Previous studies have shown that naphthalene oxide and reactive naphthalene metabolites diffuse from intact, isolated hepatocytes. The amount of naphthalene oxide diffusing from the cells as a percentage of the total formed remained constant over a wide range of substrate concentrations, thus suggesting that depletion of glutathione might not be required prior to significant naphthalene oxide efflux. However, the relative intracellular versus extracellular covalent binding of reactive metabolites increased with increasing naphthalene concentrations, thereby suggesting that glutathione might be involved in modulating the extent of intracellular covalent binding. To examine this question in detail, intracellular glutathione levels were monitored in mouse hepatocytes incubated in the presence of various concentrations of naphthalene. Naphthalene produced a concentration- and time-dependent decrease in intracellular glutathione levels and, at higher concentrations, a marked decrease in the rate of glutathione efflux from hepatocytes. This decrease in hepatocellular glutathione levels correlated well with the shift in binding from predominantly extracellular to intracellular. Inclusion of glutathione and glutathione transferases in the cell incubation medium partially blocked the depletion of intracellular glutathione by naphthalene, thus suggesting that naphthalene oxide diffusing into the cell medium was partially responsible for intracellular glutathione depletion. Finally, in vivo administration of naphthalene oxide to mice produced a dose-dependent depletion of pulmonary but not hepatic or renal glutathione but only at doses that were greater than 75 mg/kg. These studies support the view that there is not a glutathione threshold for the efflux of naphthalene oxide from intact hepatocytes and suggest that naphthalene oxide is capable of diffusing into as well as out of isolated hepatocytes.

Animals↗

PubMed1998

Growth kinetics of Pseudomonas putida G7 on naphthalene and occurrence of naphthalene toxicity during nutrient deprivation.

The objectives of this work were (1) to demonstrate how the chemostat approach could be modified to allow determination of kinetic parameters for a sparingly soluble, volatile substrate such as naphthalene and (2) to examine the influence of the interactions of various nutrients on possible growth-inhibitory effects of naphthalene. Pseudomonas putida G7 was used as a model naphthalene-degrading microorganism. Naphthalene was found to be toxic to P. putida G7 in the absence of a nitrogen source or oxygen. The death rate of cells grown on minimal medium plus naphthalene and then exposed to naphthalene under anoxic conditions was higher than that observed under oxic conditions in the absence of a nitrogen source. The presence of necessary nutrients for the biodegradation of PAH compounds is indicated to be important for the survival of microorganisms that are capable of PAH degradation. The amounts of ammonia and oxygen necessary for naphthalene biodegradation and for suppression of naphthalene toxicity were calculated from growth yield coefficients. A chemostat culture of P. putida G7 using naphthalene as a carbon and energy source was accomplished by using a feed augmented with a methanol solution of naphthalene so as to provide sufficient growth to allow accurate evaluation of kinetic parameters. When naphthalene was the growth-limiting substrate, the degradation of naphthalene followed Monod kinetics. Maximum specific growth rate (micrometer) and Monod constant (Ks) were 0.627 +/- 0.007 h-1 and 0.234 +/- 0.0185 mg/L, respectively. The evaluation of biodegradation parameters will allow a mathematical model to be applied to predict the long-term behavior of PAH compounds in soil when combined with PAH transport parameters.

Ammonia↗

PubMed1987

Efflux of naphthalene oxide and reactive naphthalene metabolites from isolated hepatocytes.

Naphthalene, a selective pulmonary bronchiolar cytotoxicant in the mouse, is metabolized in the liver to reactive metabolites that are capable of circulating and becoming bound irreversibly in extrahepatic tissues in vivo. Circulating reactive metabolites generated in the liver could interact with extrahepatic tissues either directly to produce toxicity or indirectly by depleting cellular defense capabilities. The studies reported here were to determine whether naphthalene oxide, an obligate and unstable intermediate in the metabolism of naphthalene, is capable of diffusing from intact hepatocytes. Efflux was measured by trapping the epoxide with [3H]glutathione followed by subsequent quantitation of the labeled glutathione adducts. Seventeen to 35% of the total amount of naphthalene oxide formed intracellularly was trapped extracellularly in 15- and 30-min incubations. The quantity of naphthalene oxide effluxing from isolated hepatocytes increased with increasing substrate concentrations. However, the relative amount of epoxide leaving the cell as a percentage of the total formed did not change over naphthalene concentrations ranging from 0.015 to 1.5 mM. Reactive naphthalene metabolites capable of binding covalently to extracellular proteins diffused from isolated hepatocytes in a time- and concentration-dependent manner. The ratio of extracellular to intracellular covalent binding was dependent upon the concentration of naphthalene in the incubation; at low naphthalene concentrations, covalent binding was higher extracellularly than intracellularly, whereas, at high concentrations, metabolites were predominantly bound intracellularly. These studies suggest that there is no threshold for the efflux of naphthalene oxide but that the relative amounts of reactive metabolite bound intra- vs. extra-cellularly may depend upon saturation of intracellular detoxication capabilities.

Animals↗

PubMed1997

Evidence of quinone metabolites of naphthalene covalently bound to sulfur nucleophiles of proteins of murine Clara cells after exposure to naphthalene.

Naphthalene-induced Clara cell toxicity in the mouse is associated with the covalent binding of electrophilic metabolites to cellular proteins. Epoxide and quinone metabolites of naphthalene are proposed to be the reactive metabolites responsible for covalent binding to proteins. To identify the nature of reactive metabolites bound to proteins (cysteine residues), we alkaline-permethylated proteins obtained from mouse Clara cells incubated with 0.5 mM naphthalene in vitro. Alkaline permethylation of protein adducts produced (methylthio)naphthalene derivatives detected by GC-MS. 3,4-Dimethoxy(methylthio)naphthalene was observed to be a predominant (methylthio)naphthalene derivative formed in the alkaline-permethylated protein sample obtained from Clara cells after exposure to naphthalene. This indicates that 1,2-naphthoquinone is a major metabolite covalently bound to cysteine residues of the cellular proteins. We have developed an immunoblotting approach to detect 1,2-naphthoquinone covalently bound to cysteine residues of proteins [Zheng, J., and Hammock, B. D. (1996) Chem. Res. Toxicol. 9, 904-909]. To identify 1,2-naphthoquinone covalently bound to sulfur nucleophiles of proteins, homogenates obtained from naphthalene-exposed Clara cells were separated by SDS-PAGE followed by Western blotting and immunostaining with the antibodies. Two protein bands with 24 and 25 kDa were detected by the antibodies, further supporting the view that 1,2-naphthoquinone is a reactive metabolite of naphthalene which binds to Clara cell proteins in vitro.

Animals↗

PubMed1995

Naphthalene contamination of sterilized milk drinks contained in low-density polyethylene bottles. Part 2. Effect of naphthalene vapour in air.

A survey on naphthalene vapour in air was conducted, revealing that the ambient atmosphere contained concentrations of naphthalene in the range of 0.005-0.100 mg m-3. The level of naphthalene vapour in air increased to 0.35 and 4.00 mg m-3 in places exposed to lacquer paint and naphthalene-based moth-repellent, respectively. The effect of naphthalene vapour in air on milk drinks contained in low-density polyethylene (LDPE) bottles was assessed. A mathematical model was suggested to describe the migration of naphthalene from the atmosphere into milk. The model was proved to be valid for milk drinks exposed to naphthalene-based moth-repellent during storage. Moreover, the extent of migration was found to increase with the fat content of foods, which might be ascribed to an increase in diffusion, in addition to the kinetic factor, that affects naphthalene migration.

Air↗

PubMedDate not supplied

A preliminary physiologically based pharmacokinetic model for naphthalene and naphthalene oxide in mice and rats.

Naphthalene is a toxicant with unusual species and tissue specificity that has been the subject of in vitro studies. We describe a preliminary physiologically based pharmacokinetic (PBPK) model for naphthalene constructed solely from in vitro data for comparison to animal data without the use of adjustable parameters. The prototypical PBPK model containing five lumped tissue compartments was developed to describe the uptake and metabolism of naphthalene by mice and rats dosed intraperitoneally (i.p.) and orally (po). The model incorporates circulation and biotransformation of the semistable reactive intermediate, naphthalene oxide, as well as the parent compound naphthalene. Circulation is included because the toxic action of naphthalene has been proposed to be caused by the formation of a reactive metabolite in one organ (liver) and its circulation to another organ (lung) being adversely affected by the metabolite. The model allows conversion of naphthalene oxide into dihydrodiol, glutathione (GSH) conjugates, 1-naphthol (non-enzymatically) and covalently bound adducts with proteins. Model simulations are compared with previously reported in vivo measurements of glutathione depletion, mercapturic acid formation, and covalently bound protein formation. The mouse model predicts accurately the amount of mercapturates excreted, the effect of various pretreatments, and the extent of covalent binding in the lung and liver resulting from ip administration, including the sharp increase in binding between 200 and 400 mg/kg.

Absorption↗

PubMed2000

Naphthalene degradation and incorporation of naphthalene-derived carbon into biomass by the thermophile Bacillus thermoleovorans.

The thermophilic aerobic bacterium Bacillus thermoleovorans Hamburg 2 grows at 60 degrees C on naphthalene as the sole source of carbon and energy. In batch cultures, an effective substrate degradation was observed. The carbon balance, including naphthalene, metabolites, biomass, and CO(2), was determined by the application of [1-(13)C]naphthalene. The incorporation of naphthalene-derived carbon into the bulk biomass as well as into specified biomass fractions such as fatty acids and amino acids was confirmed by coupled gas chromatography-mass spectrometry (GC-MS) and isotope analyses. Metabolites were characterized by GC-MS; the established structures allow tracing the degradation pathway under thermophilic conditions. Apart from typical metabolites of naphthalene degradation known from mesophiles, intermediates such as 2, 3-dihydroxynaphthalene, 2-carboxycinnamic acid, and phthalic and benzoic acid were identified for the pathway of this bacterium. These compounds indicate that naphthalene degradation by the thermophilic B. thermoleovorans differs from the known pathways found for mesophilic bacteria.

Amino Acids↗

PubMed1993

Metabolism of dibenzothiophene and naphthalene in Pseudomonas strains: complete DNA sequence of an upper naphthalene catabolic pathway.

From a soil isolate, Pseudomonas strain C18, we cloned and sequenced a 9.8-kb DNA fragment that encodes dibenzothiophene-degrading enzymes. Nine open reading frames were identified and designated doxABDEFGHIJ. Collectively, we refer to these genes as the DOX pathway. At the nucleotide level, doxABD are identical to the ndoABC genes that encode naphthalene dioxygenase of Pseudomonas putida. The DoxG protein is 97% identical to NahC (1,2-dihydroxynaphthalene dioxygenase) of P. putida. DoxE has 37% identity with cis-toluene dihydrodiol dehydrogenase. DoxF is similar to the aldehyde dehydrogenases of many organisms. The predicted DoxHIJ proteins have no obvious sequence similarities to known proteins. Gas chromatography with a flame ionization detector and mass spectroscopy confirmed that the DOX proteins convert naphthalene to salicylate and converting phenanthrene to 1-hydroxy-2-naphthoic acid. doxI mutants convert naphthalene to trans-o-hydroxybenzylidenepyruvate, indicating that the DoxI protein is similar to NahE (trans-o-hydroxybenzylidenepyruvate hydratase-aldolase). Comparison of the DOX sequence with restriction maps of cloned naphthalene catabolic pathway (NAH) genes revealed many conserved restriction sites. The DOX gene arrangement is identical to that proposed for NAH, except that the NAH equivalent of doxH has not been recognized. DoxH may be involved in the conversion of 2-hydroxy-4-(2'-oxo-3,5-cyclohexadienyl)-buta-2,4-dienoat e to cis-o-hydroxybenzylidenepyruvate. doxJ encodes an enzyme similar to NahD (isomerase). Our findings indicate that a single genetic pathway controls the metabolism of dibenzothiophene, naphthalene, and phenanthrene in strain C18 and that the DOX sequence encodes a complete upper naphthalene catabolic pathway similar to NAH.

Amino Acid Sequence↗

PubMed2002

Gender differences in naphthalene metabolism and naphthalene-induced acute lung injury.

Humans are widely exposed to polycyclic aromatic hydrocarbons, commonly found in cigarette smoke and diesel exhaust. These can undergo site- and cell-specific metabolism to cytotoxic intermediates. Metabolism of naphthalene and Clara cell cytotoxicity have been extensively studied in male animals. To address whether male and female mice are equally susceptible to naphthalene, mice were injected with naphthalene, and lungs were examined 1, 2, 3, 6, and 24 h after treatment. By analysis of acute injury using differential permeability to fluorescent nuclear dyes and high-resolution histopathology, injury in female mice was found to be more extensive, occur earlier, and include permeable cells in proximal airways, including airway bifurcations. HPLC analysis of the products of cytochrome P-450 (CYP)-mediated metabolism in microdissected airways indicated that although both genders produced a predominance of products from CYP2F2, female mice produced more naphthalene dihydrodiol in distal airways, the primary sites of injury. We conclude that there are clear gender differences in susceptibility to naphthalene-induced injury and that differences in metabolism of naphthalene may play a role in elevated susceptibility in female mice.

Animals↗

PubMed2002

Measurement of hemoglobin and albumin adducts of naphthalene-1,2-oxide, 1,2-naphthoquinone and 1,4-naphthoquinone after administration of naphthalene to F344 rats.

Naphthalene-1,2-oxide (NPO), 1,2-naphthoquinone (1,2-NPQ) and 1,4-naphthoquinone (1,4-NPQ) are the major metabolites of naphthalene that are thought to be responsible for the cytotoxicity and genotoxicity of this chemical. We measured cysteinyl adducts of these metabolites in hemoglobin (Hb) and albumin (Alb) from F344 rats dosed with 100-800 mg naphthalene per kg body weight. The method employs cleavage and derivatization of these adducts by trifluoroacetic anhydride and methanesulfonic acid followed by gas chromatography-mass spectrometry in negative ion chemical ionization mode. Cysteinyl adducts of both proteins with NPO, and 1,2- and 1,4-NPQ (designated NPO-Hb and -Alb, 1,2-NPQ-Hb and -Alb, and 1,4-NPQ-Hb and -Alb, respectively) were produced in a dose-dependent manner. Of the two structural isomers resulting from NPO, levels of NPO1 adducts were greater than those of NPO2 adducts in both Hb and Alb, indicating that aromatic substitution is favored in vivo at positions 1 over 2. Of the quinone adducts, 1,2-NPQ-Hb and -Alb were produced in greater quantities than 1,4-NPQ-Hb and -Alb, indicating either that the formation of 1,2-NPQ from NPO is favored or that more than one pathway leads to the formation of 1,2-NPQ. The shapes of the dose-response curves were generally nonlinear at doses above 200 mg naphthalene per kg body weight. However, the nature of nonlinearity differed, showing evidence of supralinearity for NPO-Hb, NPQ-Hb and NPQ-Alb and of sublinearity for NPO-Alb. Low background levels of 1,2-NPQ-Hb and -Alb and 1,4-NPQ-Hb and -Alb were detected in control animals without known exposure to naphthalene. However, the corresponding NPO-Hb and -Alb adducts were not detected in control animals.

Acetylcysteine↗

PubMed1997

Production of substituted naphthalene dihydrodiols by engineered Escherichia coli containing the cloned naphthalene 1,2-dioxygenase gene from Pseudomonas fluorescens N3.

Naphthalene dioxygenase, a key enzyme in the dihydroxylation of naphthalene, is encoded by the plasmid pN3, responsible for naphthalene metabolism in Pseudomonas fluorescens N3. The naphthalene dioxygenase, including all the sequences for its expression and the regulatory region, has been localized on the 4.3-kb HindIII-ClaI fragment and on the 3.5-kb HindIII fragment of the plasmid pN3, by Southern analysis using as probes nahA and nahR genes, the homologous genes of the plasmid NAH7 from Pseudomonas putida G7. We cloned in Escherichia coli JM109 the dioxygenase gene and its regulatory region and developed an efficient bacterial system inducible by salicylic acid, able to produce dihydrodiols. E. coli containing recombinant plasmids carrying the dioxygenase gene were analysed for their potential as a biocatalytic tool to produce dihydrodiols from different naphthalenes with the substituent on the aromatic ring at the alpha or beta position. The dihydrodiols, identified by HPLC (high-performance liquid chromatography) and 1H-NMR (nuclear magnetic resonance) were produced with yields ranging from 50 to 94%. The degree of bioconversion efficiency depends on the nature and the position of the substituent and indicates the broad substrate specificity of this dioxygenase and its potential for the production of a wide variety of fine chemicals.

Bacterial Proteins↗

PubMed2000

Further studies of the thermal and photochemical diels-alder reactions of N-methyl-1,2,4-triazoline-3,5-dione (MeTAD) with naphthalene and some substituted naphthalenes

MeTAD thermally reacted with naphthalene (2) and methylated naphthalenes to give equilibrium mixtures of starting materials and [4 + 2] cycloadducts. Methyl substitution on the naphthalene ring generally increased both the amount of cycloadduct formed and the rate of cycloaddition relative to 2. The isolated cycloadducts were all thermally labile and quantitatively reverted to the parent naphthalene in the presence of 2,3-dimethyl-2-butene as a trap for liberated MeTAD. The rates of the cycloreversion reactions were affected by substitution patterns but not appreciably by solvent. A mechanism for the cycloaddition reaction is presented that proposes the involvement of a charge-transfer complex. Photochemically, MeTAD demonstrated lower regioselectivity in its reactions with substituted naphthalenes relative to the corresponding thermal reactions.

Journal Article↗

PubMed1998

Metabolism and toxicity of diisopropylnaphthalene as compared to naphthalene and monoalkyl naphthalenes: a minireview.

Detailed knowledge does exist on the toxicological safety of diisopropylnaphthalene (DIPN). Its metabolism is the key to understanding its very low toxicity. The metabolic pathway of 2,6-DIPN in rats was found to proceed almost exclusively through oxidation of the isopropyl side-chain. This has decisive toxicological implications, which could be demonstrated by comparing the lung-specific toxic effects of naphthalenes in mouse: the lack of ring oxidation correlates well with lack of lung toxicity while, vice versa, the extent of enzymatic oxidative attack at the aromatic ring structure results in a toxic pattern that is observed with naphthalene and its monomethyl derivatives. It is concluded that DIPN and other highly alkylated naphthalenes are supposed to offer favourable safety properties because of their 'alkyl character' and therefore must not be compared with the toxic properties of naphthalene and closely related aromatic compounds.

Anemia, Hemolytic↗

PubMed2000

Naphthalene and donor cell density influence field conjugation of naphthalene catabolism plasmids.

We examined transfer of naphthalene-catabolic genes from donor microorganisms native to a contaminated site to site-derived, rifampin-resistant recipient bacteria unable to grow on naphthalene. Horizontal gene transfer (HGT) was demonstrated in filter matings using groundwater microorganisms as donors. Two distinct but similar plasmid types, closely related to pDTG1, were retrieved. In laboratory-incubated sediment matings, the addition of naphthalene stimulated HGT. However, recipient bacteria deployed in recoverable vessels in the field site (in situ) did not retrieve plasmids from native donors. Only when plasmid-containing donor cells and naphthalene were added to the in situ mating experiments did HGT occur.

Bacteria↗

PubMed1999

Naphthalene-induced cataract model in rats: A comparative study between slit and retroillumination images, biochemical changes and naphthalene dose and duration.

PURPOSE: The purpose of the study was to compare different methods of photographic evaluation of cataract formation in rats in response to different regimes of naphthalene treatment. Furthermore, we intended to study the relationship between cataract extension and biochemical parameters. METHODS: Brown Norway rats were treated with 0.10-1.5 g naphthalene/kg body weight, twice a week for ten weeks to induce cataract or placebo. Slit illumination and retroillumination (SI and RI) photographs were produced by an EAS-1000 instrument to document cataract formation as light-scattering intensity. The degree of the cataractous changes was quantified in SI photographs by the peak height and the integrated peak area, and in RI photographs by threshold setting. Finally, the lens concentration of Na(+) and K( +) and the protein composition were analyzed and correlated to the photographic analysis. RESULTS: The degree of the cataractous changes was most linearly related to dose and duration when the integrated peak area was estimated. However, protein fractions were non-linearly related to the cataractous changes estimated. Alterations in concentration of Na(+) and K(+) were small or insignificant, which indicate that naphthalene-induced cataract is not caused by osmotic changes. The lowest possible naphthalene dose to induce cataractous changes was between 0.10 and 0.50 g/kg twice a week for ten weeks. CONCLUSIONS: 0.50 and 1.0 g naphthalene/kg twice a week appeared to be optimal, because the rats in these groups were healthy and the cataractous changes were consistent between animals. Thus, the combination of the animal model with the cataract quantification system has the potential to be useful and reliable in studies of cataract-preventive compounds.

Animals↗