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PubMed1976

The direct spectrophotometric observation of benzo(a)pyrene phenol formation by liver microsomes.

Optical spectral repetitive scan analysis during the oxidative metabolism of benzo(a)pyrene by liver microsomal suspensions reveals the time-dependent formation of an intermediate(s) of which the visible spectra resemble those of several benzo(a)pyrene phenols. Liver microsomes from 3-methylcholanthrene-treated rats showed a greater rate of formation of the phenols than did microsomes from control animals; the rate of formation catalyzed by liver microsomes from phenobarbital-pretreated rats was intermediate. When 3-hydroxybenzo(a)pyrene was used as a standard for comparison of activity, the rates of formation of phenols were compared when measured by fluorometric, spectrophotometric, or high-pressure liquid chromatographic analytical techniques. An epoxide hydrase inhibitor, 1,1,1-trichloropropene-2,3-oxide, enhanced phenol formation regardless of the source of liver microsomes, and 7,8-benzoflavone inhibited control and 3-methylcholanthrene-induced microsomal metabolism of benzo(a)pyrene, 7,8-Benzoflavone did not effect benzo(a)pyrene metabolism by liver microsomes from phenobarbital-pretreated rats. The effect of inhibitors on the spectrophotometric assay correlates well with the results obtained from benzo(a)pyrene metabolite analysis using high-pressure liquid chromatography.

Adenosine Monophosphate↗
PubMed1975

Investigations on the carcinogenic burden by air pollution in man. XI. About the effect of aluminiumhydroxid upon the benzo(a)pyrene carcinogenesis.

Recent publications point towards a probable influence of trace elements on the cancerogenicity of chemical substances. On the basis of these reports we chose Al(OH)3 as trace element in our experiments, trying to clarify the influence of some adjuvants of vaccines on oncogenesis as described by several authors. To female NMRI-mice we applied subcutaneously 10 mug, 50 mug, 100 mug benzo(a)pyrene respectively in 0,5 ml tricaprylin-Al(OH)3-gel mixture and compared it with similar doses of benzo(a)pyrene in 0,5 ml tricaprylin-NaCl solutions. Results of experiments: 1. Al(OH)3 considerably reduced the tumor formation in the groups, treated with 10 and 50 mug benzo(a)pyrene; even tumor rates in the 100 mug benzo(a)pyrene group were diminished but much less than by the lower doses. 2. After ninety weeks the amount of tumors in the groups treated with 10 or 50 mug benzo(a)pyrene + Al(OH)3 was significantly lower than that of their control groups. At the highest doses (100 mug) a significant difference could not be noted. 3. Mean periods of tumor induction within all groups treated with benzo(a)pyrene-Al(OH)3 were significantly prolonged in comparison to controls. 4. In experiments with subcutaneously treated mice the doses-effect-relationship is changed when Al(OH)3 corresponds to the results of experiment with atmospheric dusts or exhaustion condensates. It is still pending whether adsorbtive or other processes make this effect.

Aluminum Hydroxide↗
PubMed1986

Binding of 2-hydroxybenzo(a)pyrene to estrogen receptors in rat cytosol.

The potent carcinogen 2-hydroxybenzo(a)pyrene (2-OH-BP) competes for binding to the estrogen receptor in the cytosol of rat uterus and liver. The dissociation constant (K1) for this interaction is congruent to 2 X 10(-5) M. In contrast, 4-hydroxybenzo(a)pyrene does not bind to the estrogen receptor; 1-hydroxybenzo(a)pyrene, 5-hydroxybenzo(a)pyrene, 6-hydroxybenzo(a)pyrene, and 12-hydroxybenzo(a)pyrene bind less tightly than does 2-OH-BP. These five chemicals are not carcinogenic. We suggest that the estrogen receptor may mediate the carcinogenic effect of 2-OH-BP or of related chemicals. One possibility is that the receptor might convey 2-OH-BP to specific sites in DNA.

Animals↗
PubMed1977

[Phenols as toxic metabolites of benz(a)pyrene].

The effect of benzo(a)pyrene and two its phenolic metabolites 3-hydroxybenzo(a)-pyrene and 6-hydroxybenzo(a)pyrene--on the cultures of normal and transformed fibroblasts has been studied. In was shown that unlike the parent carcinogen its phenolic metabolites exerted only toxic (but not transforming) effect on cultured cells, and this effect has been developed at a faster rate than that produced by benzo(a)pyrene. 6-hydroxybenzo(a)pyrene was more toxic than 3-hydroxybenzo(a) pyrene. It was concluded that both metabolites produced their effects without preliminary activation by microsomal enzymes.

Animals↗
PubMed1981

Species-specific enhancement by 7,8-benzoflavone of hepatic microsomal metabolism of benzo[e]pyrene 9,10-dihydrodiol to bay-region diol epoxides.

Metabolism of benzo[e]pyrene 9,10-dihydrodiol to the bay-region 9,10-diol-11,12-epoxides by hepatic microsomes from human, rat, mouse, guinea pig, hamster, and rabbit has been examined in the presence and absence of 7,8-benzoflavone. In the absence of 7,8-benzoflavone, the formation of bay-region diol epoxides from benzo[e]pyrene 9,10-dihydrodiol was low in all species except the hamster. With hamster liver microsomes, greater than 60% of total metabolites formed were bay-region diol epoxides, whereas human and mouse liver formed less than 5% of total metabolites as bay-region diol epoxides. Addition of 7,8-benzoflavone to the microsomal incubations stimulated the formation of diol epoxides, but this stimulation was species dependent. The most dramatic stimulation was observed with human and rabbit liver microsomes. In a parallel study, metabolic activation of benzo[e]pyrene 9,10-dihydrodiol to mutagens toward Salmonella typhimurium strain TA 100 by hepatic microsomes from the above species was examined in the presence and absence of 7,8-benzoflavone. In the absence of 7,8-benzoflavone, hepatic microsomes from all the species only weakly activated benzo[e]pyrene 9,10-dihydrodiol to mutagens. 7,8-Benzoflavone enhanced the metabolic activation catalyzed by microsomes from all species except rats and hamsters. Particularly high stimulation was observed with human and rabbit liver microsomes. 9,10-Dihydroxy-9,10,11,12-tetrahydrobenzo[e]pyrene, a compound which cannot be metabolized to a bay-region diol epoxide, was not metabolically activated to mutagenic metabolites in the presence or absence of 7,8-benzoflavone by any of the species examined. These results indicated that the effect of 7,8-benzoflavone on the enhanced mutagenic activity of benzo[e]pyrene 9,10-dihydrodiol is mediated by bay-region diol epoxides, which is consistent with the metabolism studies.

Animals↗
PubMedDate not supplied

Formation of dihydrodiol metabolites of benzo(alpha)pyrene in cultured human and murine skin cells.

The formation of the 7, 8-a and 9, 10-dihydrodiol metabolites of benzo(a)pyrene, which are believed to play a role in the chemical induction of tumors, was investigated in cultures of human and murine origin. It was found that cultures of mouse (strain C3Hz) epidermal and skin fibroblastic cells showed inducible benzo(a)pyrene metabolism towards dihydrodiol metabolites, after pre-incubation with benz(a)anthracene. This was consistent with the increased in vivo formation of dihydrodiol metabolites of benzo(a)pyrene after injection with 3-methylcholanthrene. In contrast, in human cell cultures the metabolism of benzo(a)pyrene to the dihydrodiol metabolites was not enhanced after pre-exposure to benz(a)anthracene. This was the case in low-passage skin fibroblasts, primary epidermal skin cells, and primary keratinocytes from hair follicles. Moreover, other inducers of microsomal oxygenases, such as phenobarbital and 3-methylcholanthrene, were also unable to increase benzo(a)pyrene metabolism towards the dihydrodiol compounds. In view of these results, obtained using in vitro human and murine model systems, we may conclude that human and murine skin cell culture systems respond differently to pre-treatment with inducers of microsomal monooxygenases with respect to the metabolism of benzo(a)pyrene to reactive dihydrodiol metabolites. The possible implications for the human in vivo situation are discussed.

Animals↗
PubMed1980

Comparative tumor-initiating activity of methylated benzo(a)pyrene derivatives in mouse skin.

The abilities of various mono and dimethyl derivatives of benzo(a)pyrene (BP) to initiate skin tumors in mice were determined by using a two-stage system of tumorigenesis. 11-Methylbenzo(a)pyrene was found to be approximately 3 times more active as a tumor initiator than was the parent hydrocarbon; 1-methyl benzo(a)pyrene was about twice as active as was BP. Substitution of a methyl group in positions 7, 8, 9, or 10 of BP, which would be involved in a bay-region diol-epoxide, completely counteracts the tumor-initiating ability of BP. 3-, 4-, and 12-methyl-benzo(a)pyrenes and activity equivalent to that of BP, whereas 2-, 5-, and 6-methylbenzo(a)pyrenes, as well as 1,2-, 4,5-, 1,6-, and 3,6-dimethylbenzo(a)pyrenes, were all less active than BP. The concepts of steric inhibition of metabolic activation and stereospecific activation are suggested to explain the tumor-initiating activities of various methylated derivatives.

Animals↗
PubMed1980

Benzo(a)pyrene metabolism in bovine aortic endothelial and bovine lung fibroblast-like cell cultures.

The metabolism of [3H]benzo(a)pyrene ([3H]BP) in bovine aortic endothelial and bovine lung fibroblast-like cells in vitro was investigated. Both cell types metabolized BP to organic solvent-extractable and water-soluble metabolites. The major organic solvent-extractable metabolites were 9-hydroxy-benzo(a)pyrene and 3-hydroxybenzo(a)pyrene; 7,8-dihydro-7,8-dihydroxybenzo(a)pyrene, 9,10-dihydro-9,10-dihydroxy-benzo(a)pyrene, and BP quinones were also formed. No glucuronide or sulfate conjugates of BP metabolites were detected. When exposed to [3H]-3-hydroxybenzo(a)pyrene, both cell types metabolized this phenol to water-soluble derivatives, probably through oxidation rather than conjugation of the molecule. These results demonstrate that endothelial cells metabolze BP to a proximate carcinogenic derivative, the 7,8-dihydrodiaol. Thus, efforts to predict the biological effects of hydrocarbons of an organism must take into account possible metabolic activation by endothelial cells as well as by other target tissues. The formation of unconjugated, phenolic hydrocarbon derivatives by bovine cells suggests their use as a model system for studying the contribution of phenols to the induction of biological effects by hydrocarbons.

Animals↗
PubMed1977

Metabolic activation of benzo(a)pyrene and binding to DNA in cultured human bronchus.

Human bronchus is one target site for the carcinogenic action of tobacco smoke, which contains chemical carcinogens, including benzo(a)pyrene. Human bronchi were obtained from surgery or "immediate" autopsy and then cultured in a chemically defined medium. The cultured bronchi were exposed to either benzo(a)pyrene or its metabolites, and their levels of binding to DNA were measured. One of the benzo(a)pyrene metabolites. (-)-trans-7,8-diol, is more active in binding to DNA than benzo(a)pyrene and several of its metabolites, including (-)-trans-4,5-diol, (-)-trans-9,10-diol, and phenols. The predominant metabolite formed by human bronchus from the (-)-trans-7,8-diol is found by high-pressure liquid chromatographic analysis to be the diol-epoxide r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo(a)pyrene. The results suggest that this diol-epoxide is the major benzo(a)pyrene metabolite bound to DNA in human bronchus.

Benzopyrenes↗
PubMed1985

Adduct formation in hemoglobin of the newborn mouse exposed in utero to benzo[a]pyrene.

The administration of benzo[a]pyrene topically to pregnant mice during days 13-17 of gestation results in adduct formation in the hemoglobin of the mother and progeny. Thus, exposure to a total maternal body burden of 500 micrograms of benzo[a]pyrene during the last 5 days before delivery resulted in an average level of 6.35 (+/- 0.70 S.E.M.) pg of anti-diolepoxide metabolite covalently attached per mg of hemoglobin analyzed in the mother and 1.40 (+/- 0.23 S.E.M.) in the newborn animals. These data indicate that benzo[a]pyrene administered to the skin of the mother passed across the placental membrane, either as benzo[a]pyrene or some metabolite(s), and was present in the fetal tissue as the "ultimate" carcinogenic form (anti-diolepoxide metabolite) before binding to the hemoglobin. Concomitant adduct formation in the DNA of the skin with benzo[a]pyrene in the progeny was not observed and was probably due to the small amount of carcinogen applied to the mother. The data obtained, along with previously published results [Toxicology, 34 (1985) 211], suggest the suitability of hemoglobin as a molecular dosimeter for estimating carcinogenic risk to polycyclic aromatic hydrocarbons.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1991

Mutagenicity of benzo[a]pyrene bay-region sulfonates.

The interaction between the sulfite anion and specific benzo[a]pyrene (B[a]P) derivatives produces a novel class of benzo[a]pyrene sulfonates. (+/-)-7,8,9-Trihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene-10-sulfonate (B[a]PT-10-sulfonate) is formed in high yields in incubations containing (+/-)-7r,8t-dihydroxy-9t,10t-epoxy-7,8,9,10-tetrahydrobenzo[a]pyre ne (anti-BPDE) and sulfite, and sulfite strongly enhances the mutagenicity of the diolepoxide toward Salmonella typhimurium under those conditions. Although B[a]PT-10-sulfonate itself shows little direct mutagenicity over a 1-20 microM concentration range, this reactive bay-region intermediate does enhance the mutagenicity of anti-BPDE in strains TA98 and TA100 by up to 280%. No significant enhancement was seen when up to 20 microM B[a]PT-10-sulfonate was used in concert with another direct-acting mutagen, N-acetoxy-acetylaminofluorene (N-AcO-AAF). The isomeric product derived from sulfite and (+/-)-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (B[a]P-7,8-diol) is (+/-)-7,8,10-trihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene-9-sulfonate (B[a]PT-9-sulfonate). Like B[a]PT-10-sulfonate, B[a]PT-9-sulfonate is not mutagenic to strains TA97, TA98 and TA100. This sulfonate exhibited little enhancing activity with anti-BPDE over a 1-20 microM concentration range, but did enhance the mutagenic response of strain TA98 to 0.2 microM N-Aco-AAF by up to 128%. Sulfite, anti-BPDE and B[a]PT-sulfonates were also examined for the ability to induce a forward mutation at the hgprt locus (8-azaguanine resistance) in strains of S.typhimurium. Sulfite caused a marked enhancement of forward mutation due to anti-BPDE in both TA98 and TA100. Surprisingly, concurrent administration of B[a]PT-10-sulfonate with anti-BPDE did not increase the number of mutant colonies. The extensive conversion of anti-BPDE to B[a]PT-10-sulfonate under conditions where sulfite enhances diolepoxide mutagenicity, when coupled with this enhancement of diolepoxide mutagenicity by B[a]PT-10-sulfonate in the reverse mutation assay, supports this novel B[a]P derivative as a mediator of the sulfite-dependent enhancement of B[a]P genotoxicity. Determining why this enhancing effect was not seen when selecting for mutation at the hgprt locus of S.typhimurium will require further study.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1990

Determination of benzo[a]pyrene diol epoxide-DNA adducts in white blood cell DNA from coke-oven workers: the impact of smoking.

We have undertaken a study among coke-oven workers to test the feasibility of an enzyme-linked immunosorbent assay with anti-trans-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene- DNA antibodies for monitoring occupational exposure to polycyclic aromatic hydrocarbons (PAH). Coke-oven workers are occupationally exposed to relatively high levels of PAH and are at increased risk for lung cancer. Three blood samples were collected from each of the 56 coke-oven workers exposed to PAH and 44 unexposed workers employed in a steel-rolling factory of the same plant. In addition, PAH levels were measured in ambient air by personal sampling, and the excretion of 1-hydroxypyrene in urine was also measured on 3 consecutive working days. All participants were interviewed regarding working conditions, personal hygiene, and smoking habits. The results showed that the coke-oven workers were exposed to substantial concentrations of atmospheric PAH (1-186 micrograms/m3), including benzo[a]pyrene (0.1-7.8 micrograms/m3) and pyrene (0.6-23.6 micrograms/m3). Both benzo[a]pyrene and pyrene were shown to be representative for the whole group of PAH. Forty-seven percent of the coke-oven workers had detectable levels of PAH-DNA adducts in their white blood cells, compared with 30% of the controls. In both groups, smokers had significantly higher levels of PAH-DNA adducts than did nonsmokers. At one site, we found the correlation positive between DNA adducts and the duration of exposure (r = .47, P = .005). Generally, the correlation was not significant between PAH-DNA adducts in blood and the concentration of PAH in the air and 1-hydroxypyrene in urine.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed2005

Intramolecular energy transfer in pyrene-bodipy molecular dyads and triads.

Molecules bearing a 4,4-difluoro-8-(aryl)-1,3,5,7-tetramethyl-2,6-diethyl-4-bora-3a,4a-diaza-s-indacene (bodipy) core and 1-pyrenyl-1-phenyl-4-(1-ethynylpyrene), or 1-phenyl-4-[1-ethynyl-(6-ethynylpyrene)pyrene] units were constructed in a step-by-step procedure based on palladium(0)-promoted cross-coupling reactions with the required preconstructed modules. X-ray structures of single crystals reveal a twisted arrangement of the two chromophores. In one case, an almost perfect orthogonal arrangement is found. These dyes are strongly luminescent in solution and display rich electrochemistry in which all redox processes of the bodipy and pyrene fragments are clearly resolved. The absorption spectra indicate that the bodipy and pyrene chromophores are spectrally isolated, thereby inducing a large "virtual" Stokes shift. The latter is realised by efficient transfer of intramolecular excitation energy by the Förster dipole-dipole mechanism. The rate of energy transfer depends on the structure of the dual-dye system and decreases as the centre-to-centre separation increases. The energy transfer efficiency, however, exceeds 90 % in all cases. The linkage of two pyrene residues by an ethyne group leads to a decrease in the energy-transfer efficiency, with the two polycycles acting as a single chromophore. The directly linked bodipy-pyrene dual dye binds to DNA and operates as an efficient solar concentrator when dispersed in plastic.

Boron Compounds↗
PubMed2000

Purification and characterization of hepatic and intestinal phenol sulfotransferase with high affinity for benzo[a]pyrene phenols from channel catfish, Ictalurus punctatus.

Cytosol from channel catfish liver and intestinal mucosa has high sulfotransferase activity with low concentrations of 3-, 7-, or 9-hydroxybenzo[a]pyrene. To further investigate this conjugation pathway, sulfotransferase activity toward 9-hydroxybenzo[a]pyrene was isolated from catfish intestinal and hepatic cytosol by chromatography on anion exchange and PAP-agarose affinity columns. SDS-PAGE of the active fractions showed that one major band with molecular size of about 41,000 Da was isolated from intestine, while two bands of about 41,000 and 31,000 Da were obtained from liver. Antibodies against human phenol-sulfating sulfotransferase cross-reacted strongly with the 41,000-Da bands from liver and intestine, but weakly with the hepatic 31,000-Da protein. N-Terminal sequence information could not be obtained from the pure proteins. Following digestion, an internal sequence of 20 amino acid residues was obtained from the hepatic 41,000-Da protein, which matched a sequence found in several mammalian sulfotransferases. No fish sulfotransferase sequences were available for comparison. The identity of the hepatic 31,000-Da protein was not established. The purified 41,000-Da proteins had very high activities with 3-, 7-, or 9-hydroxybenzo[a]pyrene, with K(m) values in the 40-100 nM range and V(max) 125-300 nmol/min/mg of protein. Substrate inhibition was observed when the concentrations of hydroxylated benzo[a]pyrenes were above 0.5 microM. As well as benzo[a]pyrene phenols, the purified 41,000-Da sulfotransferases catalyzed sulfation of 2-naphthol, 4-nitrophenol, 4-methylumbelliferone, 7-(hydroxymethyl)-12-methylbenz[a]anthracene, dehydroepiandrosterone, estrone, and 17beta-estradiol. Phenolic compounds were the preferred substrates for the purified enzymes.

Amino Acid Sequence↗
PubMed1996

Pyrene-labeled DNA probes for homogeneous detection of complementary DNA sequences: poly(C) model system.

DNA and RNA probes are important analytical reagents in molecular biology and in the detection of infectious and genetic diseases. However, the present polynucleotide probe technology is complex and labor-intensive. We have been investigating the possibility of using fluorescent-labeled DNA probes to develop assays which do not require the separation of free from hybridized probe (homogeneous assays). Such assays are possible if the fluorescence efficiency or fluorescence anisotropy of the fluorescent label changes upon hybridization of probe with target DNA. In this article we examine pyrene as a fluorescent label for DNA or RNA probes. Experiments were performed using a model system in which poly(C) and poly(I) are respectively the probe and target sequences. A small fraction of the nucleotide bases of poly(C) was randomly labeled with pyrene using the bisulfite-catalyzed diamine reaction. The results show that the uncorrected emission spectrum of pyrene-poly(C) decreases by a factor of 4 and shifts toward longer wavelengths upon hybridization with poly(I) at saturating concentrations. The average lifetime changes from 10.78 to 4 ns. These fluorescence changes occur in a wide range of chemical environments, including the high salt concentrations normally used to increase the velocity of the hybridization reaction in clinical assays. The pyrene label can thus be used to readily detect the amount of poly(I) in an unknown sample without having to separate free and bound labeled probe. To unravel the mechanism responsible for the observed changes in fluorescence intensity upon hybridization, we have performed polarized fluorescence intensity measurements and analyzed the results by approximate steady-state expressions that allow evaluation of the relative contributions of changes in lifetimes (fluorescence efficiency) and rotational motions to the changes in fluorescence intensity. The results indicate that the latter changes are due chiefly to changes in lifetime or fluorescence efficiency and that these changes seem to be due to the movement of the pyrene label to a more hydrophilic environment upon hybridization.

DNA Probes↗
PubMed2002

Development of peptide substrates for trypsin based on monomer/excimer fluorescence of pyrene.

An assay using fluorogenic peptides based on the monomer/excimer fluorescence features of pyrene was developed to measure the proteolytic activity of trypsin, a serine protease. Two pyrene moieties were incorporated into the respective N- and C-terminus of the peptides as (pyrene)-C-Xaa-C-(pyrene), where Xaa represents amino acid residues of 5-, 6-, 7-, or 8-mer containing the cleavage site of trypsin. The proteolytic cleavage of the substrates led to an increase in monomer fluorescence and a decrease in excimer fluorescence of pyrene. Kinetic parameters (k(cat) and K(m)) for the enzymatic hydrolysis of the substrates were successfully determined. The parameters are dependent on the chain length of the substrate and optimal catalytic activity was obtained with substrates that consisted of 9 or 10 amino acid residues. The present assay system is sensitive and the preparation of the substrate is very simple. We suggest that this method may be suitable for high-throughput screening and also applicable to the characterization of other proteases.

Animals↗
PubMed1997

Dependence of genotoxicity of benzo[a]pyrene suspensions in Mutatox test on dissolved concentration and S9 addition.

The Mutatox test is a novel genotoxicity test measuring the ability of a test chemical to restore the luminescent state in dark mutants of Vibrio fischeri. Chemicals can be tested with or without rat hepatic S9 enzymes for metabolic activity, so that promutagenic agents can be detected as well. In the Microbics Mutatox Manual (1993, Microbics Corp., Carlsbad, CA), benzo[a]pyrene is recommended as positive control for S9 medium at a nominal concentration of 10 mg/liter with 2% DMSO as carrier solvent. The concentration of benzo[a]pyrene dissolved in this test suspension without addition of S9 was determined by GC-MS. It was significantly lower than the nominal concentration and did not reveal a genotoxic effect in the Mutatox test with S9. The analytical concentration of benzo[a]pyrene in the supernatant of the test suspension in S9 medium was significantly higher and induced the luminescence of bacteria. Therefore, S9 microsomes seem, apart from metabolizing benzo[a]pyrene to its genotoxic epoxide, to increase transfer of benzo[a]pyrene into V. fischeri in such a way that the genotoxic effect is produced. This suggests that sparingly soluble compounds might have different ecotoxicological effects as suspensions than as solutions. Therefore, the possible uptake of suspended particles by organisms without being completely dissolved before should be considered in ecotoxicological tests.

Animals↗
PubMed1985

Fluorescence decay of pyrene in small and large unilamellar L, alpha-dipalmitoylphosphatidylcholine vesicles above and below the phase transition temperature.

The fluorescence decays of pyrene in small and large unilamellar L, alpha-dipalmitoylphosphatidylcholine vesicles have been investigated as a function of probe concentration and temperature. When the molar ratio of pyrene to phospholipid equals 1:3000, no excimer emission is observed and the fluorescence decays are mono-exponential. When this ratio is equal to or higher than 1:120, excimer formation is observed. Above the phase transition temperature the observed fluorescence decays of monomer and excimer can be adequately described by a bi-exponential function. The monomer decays can be equally well fitted to a decay law which takes into account a time-dependence in the probe diffusion rate constant. The fluorescence decay kinetics are compatible with the excimer formation scheme which is valid in an isotropic medium. The excimer lifetime and the (apparent) rate constant of excimer formation have been determined as a function of probe concentration at different temperatures above the phase transition temperature. The activation energy of excimer formation is found to be 29.4 +/- 1.3 kJ/mol. In small unilamellar vesicles the diffusion constant associated with the pyrene excimer formation process varies from 8.0 X 10(-7) cm2/s at 40 degrees C to 2.2 X 10(-6) cm2/s at 70 degrees C. Below the phase transition temperature the monomer decays can be described by a decay law which takes into account a time dependence of the rate constant of excimer formation. The lateral diffusion coefficient of pyrene calculated from the decay fitting parameters of the monomer region varies from 4.0 X 10(-9) cm2/s at 20 degrees C to 7.9 X 10(-8) cm2/s at 35 degrees C. No significant difference could be observed between the pyrene fluorescence decay kinetics in small and large unilamellar vesicles.

Diffusion↗