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PubMed2006

Humic substance adsorptive fractionation by minerals and its subsequent effects on pyrene sorption isotherms.

Changes in the nonlinearity of pyrene sorption isotherms on humic substance (HS)-coated minerals (kaolinite and hematite) due to HS adsorptive fractionation processes were examined in model environmental systems at low mass fraction organic carbon (f(oc)) levels (0.0001-0.0011) using purified Aldrich humic acid (PAHA) and Suwannee River fulvic acid (SRFA). At a constant pH of 7, higher molecular weight (MW) fractions of PAHA were preferentially adsorbed on kaolinite whereas no adsorptive fractionation of PAHA occurred on hematite. At a constant f(oc) level of 0.0005, preferential adsorption of higher MW PAHA fractions on kaolinite was enhanced with increasing pH. Nonlinear pyrene sorption isotherms were observed with the bulk PAHA-coated mineral systems, whereas more linear pyrene sorption isotherms were observed for the PAHA-mineral systems undergoing adsorptive fractionation. Although the degree of isotherm linearity may be affected by pH and/or structural rearrangement of the adsorbed HS fractions on minerals, this study suggests that HS adsorptive fractionation is more important than are changes in pH and f(oc) levels with regard to the resulting pyrene sorption isotherms. Similar effects were not observed with SRFA, suggesting that the impacts of HS adsorptive fractionation on pyrene sorption isotherm nonlinearity are also influenced by the source and other biogeochemical characteristics of HS.

Adsorption↗
PubMed1991

Pharmacokinetics and bioavailability of pyrene in the rat.

Groups of 6 male Wistar rats, of about 400 g body weight, were dosed with 14C-labeled pyrene, dissolved in an Emulphor/water solvent vehicle, at 5 different dose levels by the intravenous or oral routes. Appropriate mathematical models were fitted to blood concentration-time data for [14C]pyrene and pyrene per se and dose-trend analyses were carried out. Areas under these curves were used to assess the bioavailability of the orally administered doses. Tissue concentrations, measured at the termination of the blood sampling period, gave a quantitative measure of the distribution of the administered dose. Attempts to repeat these studies with similar doses of tritium-labeled benzo[a]pyrene were frustrated by the lack of meaningful blood-level data. Dose trends for the derived pharmacokinetic parameters for pyrene revealed that the kinetics were nonlinear and strongly suggestive of enterohepatic recycling. Biliary excretion, measured in a separate experiment, gave support to this hypothesis. The bioavailability of the orally administered doses was between 50 and 60%. Over a 6-d period postdosing, some 45 and 40% of the administered dose was excreted via the urine and feces, respectively, irrespective of the route of administration. Distribution to the tissues of the 14C-label was highest in the perirenal fat, intermediate in the liver, kidneys, and lungs, and lowest in the heart, testes, spleen, and brain.

Administration, Oral↗
PubMed1993

Percutaneous uptake, distribution, and excretion of pyrene in rats.

Groups of 12 male Wistar rats, of about 400 g body weight, were dosed with 2, 6, or 15 mg/kg of 14C-labeled pyrene, dissolved in acetone, applied to 4 cm2 of a shaved area of the mid back. Three animals in each dose group were killed at 1, 2, 4, and 6 d post-dosing, and their principal organs were removed and analyzed for pyrene and [14C]pyrene equivalents. Urine and feces, as well as the area of skin to which the dose was applied, were also analyzed for [14C]pyrene equivalents. The rate of uptake from the skin was rapid (t1/2 0.5-0.8 d) relative to rate processes for the other organs, and about 50% of the applied dose was excreted over the 6 d of the study. The significant decrease in the fraction of the dose excreted and in the normalized amounts distributed to the various organs and tissues, as the dose increased for all chemical species measured, was strongly suggestive of nonlinear kinetics, as has been observed in previous studies. Levels of pyrene were highest in the liver, kidneys, and fat. Levels of metabolites were also high in the lung. It was evident that the dermal route of uptake was not insignificant for this model polycyclic aromatic hydrocarbon and may represent a significant exposure route for exposed humans.

Adipose Tissue↗
PubMed1994

Pharmacokinetics of inhaled pyrene in rats.

Male Wistar rats were exposed to micronized aerosol concentrations of a 14C-labeled model polycyclic aromatic hydrocarbon (pyrene) at 200, 500, and 800 mg/m3 for a period of 95 min. Both the 14C label and free pyrene were monitored in the blood, urine, and feces. At the termination of the blood sampling, three of the six rats per dose group were killed and the distribution of [14C]pyrene to eight major tissues was analyzed. The analysis of blood concentration data using a one-compartment pharmacokinetic model revealed that the uptake and elimination kinetic parameters were dose dependent, for both total radioactivity (pyrene plus metabolites) and for pyrene per se, over the range of exposures used in this study. The ratio of the percent excreted via the urinary and fecal routes, collected over a 5-d period postexposure was about 1.0 at each exposure level.

Absorption↗
PubMed2004

Bacterial community evaluation during establishment of tall fescue (Festuca arundinacea) in soil contaminated with pyrene.

A greenhouse study was conducted to monitor microbial community dynamics related to contaminant concentration and plant growth during the phytoremediation of pyrene. Soil microbial communities in both bulk and rhizosphere soils were assessed using a polymerase chain reaction--denaturing gradient gel electrophoresis (PCR-DGGE). However, no correlation between pyrene concentration and bacterial community shifts was observed. Even though plants significantly enhanced pyrene degradation (undetectable after 91 d for planted treatments compared with 82 mg/kg for unplanted treatments after 147 d with initial concentration of 758 mg/kg), biodegradation may have been accomplished by the pre-existing microbial community. It is also possible that the method was unable to pick up subtle community shifts, considering that the carbon source from pyrene was only 3.7% of the existing soil organic matter. This research suggests that plants significantly enhance degradation and mineralization of pyrene in soil, although there was no conclusive evidence supporting any specific bacterial activity responsible for this enhancement.

Bacteria↗
PubMed1990

Covalent binding of dibenzpyrenes and benzo[a]pyrene to DNA: evidence for synergistic and inhibitory interactions when applied in combination to mouse skin.

Several well-documented examples of human exposure to carcinogens involve complex mixtures of polycyclic aromatic hydrocarbons (PAHs). Although the biological properties of many pure PAHs have been investigated, less is known about their effects when present as components of mixtures. As the ability to form DNA adducts in vivo is generally indicative of carcinogenic activity of PAHs, we have compared the DNA binding potencies of dibenzo[a,e]pyrene (DB[a,e]P), dibenzo[a,e]pyrene (DB[a,h]P), dibenzo[a,i]pyrene (DB[a,i]P), dibenzo[a,l]pyrene (DB[a,l]P) and benzo[a]pyrene (B[a]P), when applied topically, either singly or in combination, to the skin of male Parkes mice. DNA isolated from the skin and lungs was analysed by 32P-postlabelling. The adducts formed by each PAH exhibited markedly different chromatographic mobilities on polyethyleneimine-cellulose TLC plates. The relative binding potencies of the compounds in both skin and lungs were: DB[a,l]P much greater than B[a]P greater than DB[a,h]P greater than DB[a,i]P greater than DB[a,e]P, in good agreement with their reported carcinogenicities in mouse skin. The majority of adducts were removed from DNA within 21 days of treatment, but low levels of adducts were found to persist for at least 3 months in both tissues. When DB[a,l]P, DB[a,e]P and B[a]P were applied together to mouse skin, a total binding 31% lower than expected was detected, while with a mixture of DB[a,e]P and B[a]P the binding to DNA in skin was 65% higher than expected from the binding levels of the carcinogens when applied singly. Other binary combinations of these three PAHs gave adduct levels similar to the sum of the binding levels of the individual components when applied singly. The results demonstrate the usefulness of 32P-post-labelling for the assessment of the DNA binding potencies of PAHs in mouse tissues, and for the detection of interactions between components of mixtures of carcinogens.

Animals↗
PubMed1992

Identification and quantitative detection of isomeric benzo[a]pyrene diolepoxide--DNA adducts by low-temperature conventional fluorescence methods.

The pyrene-like fluorescence of adducts derived from the covalent binding of (+/-)-trans-7,8-dihydroxy-anti-9,10-epoxy-7,8,9, 10-tetrahydrobenzo[a]pyrene [+/-]-anti-BPDE] to DNA increases in intensity by factors of 20 or more as the temperature is lowered from ambient to approximately 100 K. This effect is primarily associated with the strong quenching of the pyrene-like fluorescence of BPDE-deoxyguanosyl adducts at room temperature, and the suppression of the electron-transfer quenching mechanism at 100 K. In contrast, the fluorescence of BPDE-deoxyadenosyl adducts is not quenched at ambient temperatures, and the fluorescence yields of (+/-)-anti-BPDE-poly(dA-dT).(dA-dT) adducts increases by only a factor of 2 in this same temperature range. Utilizing an internal fluorescein fluorescence standard to correct for differences in light scattering and variations in instrumental factors, a fluorescence method is described for quantitatively determining the levels of benzo[a]pyrene diolepoxide derivatives covalently bound to cellular DNA at 100 K. The method is illustrated with (+/-)-reverse-BPDE [(+/-)-trans-9,10-dihydroxy-anti-7, 8-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene]. Adduct levels as low as 10 pmol in a 400 microliters sample volume can be detected and identified from their excitation and fluorescence emission spectra using a conventional and commercially available fluorometer. In the case of modified DNA extracted from BPDE-treated Chinese hamster ovary cells or from mouse skin (approximately 1 BPDE residue/20,000 bases), such an analysis requires only 100 micrograms of DNA. Conformationally different adducts derived from the binding of the isomeric (+/-)-anti-BPDE, (+/-)-reverse-BPDE or (+/-)-syn-BPDE to cellular DNA can be distinguished by their low-temperature fluorescence excitation spectra. Specifically, the quasi-intercalated site I BPDE adducts (believed to be associated with cis-addition stereochemistry) can be distinguished from site II adducts situated at external BPDE binding sites (trans-addition stereochemistry). These results suggest that the fates of these conformationally different BPDE-DNA adducts, e.g. due to enzymatic repair, can be monitored as a function of time in DNA extracted from intact, functioning cells.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1998

A comparison of the tumors induced by coal tar and benzo[a]pyrene in a 2-year bioassay.

The tumorigenicity of two coal tar mixtures was compared to that of benzo[a]pyrene after 2 years of feeding. Mixture 1, a composite of coal tar from seven coal gasification plant waste sites, was fed to female B6C3F1 mice (48 mice per group) for 2 years at doses of 0.0, 0.01, 0.03, 0.1, 0.3, 0.6 and 1.0%. Mixture 2, which was composed of coal tar from two of the seven waste sites and another site having a high benzo[a]pyrene content, was fed at doses of 0.0, 0.03, 0.1 and 0.3%. Additional groups of mice were fed 0, 5, 25 and 100 ppm benzo[a]pyrene. The coal tar diets induced a dose-related increase in hepatocellular adenomas and carcinomas, alveolar/bronchiolar adenomas and carcinomas, forestomach squamous epithelial papillomas and carcinomas, small intestine adenocarcinomas, histiocytic sarcomas, hemangiosarcomas in multiple organs and sarcomas. Benzo[a]pyrene treatment resulted in an increased incidence of papillomas and/or carcinomas of the forestomach, esophagus and tongue. A comparison of the results indicated that the benzo[a]pyrene in the coal tar diets could be responsible for the forestomach tumors. In contrast, the lung and liver tumors appeared to be due to other genotoxic components contained within the coal tar mixture, while the small intestine tumors resulted from chemically-induced cell proliferation that occurred at high doses of coal tar.

Adenoma↗
PubMed1982

Indirect immunofluorescent localization of benzo[a]pyrene adducted to nucleic acids in cultured mouse keratinocyte nuclei.

The localization of benzo[a]pyrene-deoxyguanosine adducts was studied by indirect immunofluorescence in cultured BALB/c epidermal cells exposed to (+/-) 7 alpha, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (the anti-isomer) utilizing an antiserum specific for the major benzo[a]pyrene-deoxyguanosine adduct in DNA. This antiserum does not cross-react with benzo[a]pyrene or DNA alone. When cultured keratinocytes were incubated with the carcinogen for 1 h, the immunofluorescence was localized in the nucleus as intense spots on a background of diffuse fluorescence. Fluorescence was absent from cells not exposed to carcinogen and from carcinogen-exposed cells incubated with normal rabbit serum in place of the antiserum. Fluorescence was abolished when the specific antiserum was absorbed with the immunogen DNA prior to incubation with cells, and substantially diminished when exposed cells were preincubated with deoxyribonuclease before the application of the specific antiserum. Incubation of exposed cells with ribonuclease prior to incubation with the specific antiserum removed the bright fluorescent spots and resulted in fluorescent nuclei containing dark sports in similar frequency. Dose-response studies in which benzo[a]pyrene-deoxyguanosine adducts were quantified by enzyme-linked immunosorbent assay and compared with intensity of immunofluorescence demonstrated that decreasing doses of the carcinogen resulted in fewer numbers of adducts as well as proportionally less fluorescence. When cells were exposed to non-toxic doses of the activated carcinogen for 1 h, nuclear fluorescence was detectable in immediately-fixed cells but faded to non-detectable levels when cells were washed and cultured for an additional 24-48 h before fixation.

Animals↗
PubMed1984

Ellagic acid: a potent naturally occurring inhibitor of benzo[a]pyrene metabolism and its subsequent glucuronidation, sulfation and covalent binding to DNA in cultured BALB/C mouse keratinocytes.

The metabolism of [3H]benzo[a]pyrene (BP) by cultured primary keratinocytes prepared from BALB/C mouse epidermis was found to be largely inhibited by the dietary plant phenol, ellagic acid. Varying concentrations of ellagic acid added to the keratinocyte cultures resulted in a dose-dependent inhibition of the cytochrome P-450-dependent monooxygenases aryl hydrocarbon hydroxylase (AHH) and 7-ethoxycoumarin-O-deethylase (ECD). The major organic solvent-extractable metabolites found intracellularly in the cultured cells were trans-7,8-dihydro-7,8-dihydroxybenzo[a]-pyrene (BP-7,8-diol) and 3-hydroxybenzo[a]pyrene (3-OH-BP), although small amounts of 9-hydroxybenzo[a]pyrene, quinones and trans-9,10-dihydro-9,10-dihydroxybenzo[a]-pyrene (BP-9,10-diol) were also present. The major organic solvent-extractable metabolites found in the extracellular culture medium were BP-7,8-diol and BP-9,10-diol, with smaller quantities of unconjugated phenols and quinones. The major intracellular and extracellular water-soluble metabolites of BP were conjugated with glucuronide (primarily 3-OH-BP and several BP-quinones), and to a lesser extent with sulfate (primarily BP-7,8-diol). Both intracellular and extracellular metabolism of organic solvent-extractable and water-soluble conjugates was significantly inhibited by ellagic acid in a dose-dependent manner. The intracellular enzyme-mediated binding of BP to mouse keratinocyte DNA was also largely inhibited in a dose-dependent fashion by ellagic acid. Our results indicate that cultured primary mouse keratinocytes offer a useful model system for studying factors affecting the metabolic activation and detoxification of polycyclic aromatic hydrocarbon carcinogens in the epidermis, and that polyphenolic compounds such as ellagic acid may prove useful in modulating the risk of cutaneous cancer that results from exposure to these environmental chemicals.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1984

Arachidonic acid-dependent activation of benzo[a]pyrene to bind to proteins with cytosolic and microsomal fractions from rat liver and lung.

Activation of benzo[a]pyrene to bind to proteins by co-oxidation with prostaglandin synthesis was studied in rat liver and lung microsomes and cytosols. The kinetics of this activation showed a two-phase reaction; a rapid initial reaction for 2-4 min after addition of arachidonic acid and then a slow reaction or a plateau state. The reaction was linear only with low contents of the enzyme proteins, and was slower with more than 1 mg of enzyme per ml of incubation mixture. Other unsaturated fatty acids were also effective in activating benzo[a]pyrene with both microsomes and cytosols. With microsomal proteins linoleic acid was more effective than arachidonic acid, whereas with cytosolic proteins arachidonic acid was the best cofactor. Linolenic acid could also activate benzo[a]pyrene, though less efficiently, but oleic acid had no influence on the binding. Indomethacin did not inhibit the activation, but nordihydroguaiaretic acid and quercetin significantly reduced the binding. Addition of hematin significantly increased the binding. The NADPH-dependent bindings of benzo[a]pyrene to proteins with liver and lung microsomes were one-third and one-twelfth the values after incubation with arachidonic acid. Addition of glutathione or Ca2+ ion reduced the binding significantly. The present results suggest the importance of co-oxidation with lipoxygenase for activation of benzo[a]pyrene and the possible role of both the arachidonic acid cascade system and the NADPH-dependent cytochrome P-450 system in metabolic activation of chemical carcinogens.

Animals↗
PubMed1996

The identification and repair of DNA adducts induced by waterborne benzo[a]pyrene in developing Xenopus laevis larvae.

We report on the formation and subsequent repair of benzo[a]pyrene-induced DNA adducts in Xenopus laevis larvae in vivo, as monitored by 32P-post labelling. In vivo benzo[a]pyrene is metabolized by the cytochrome P450 family of enzymes to metabolites, of which the 7,8-diol-9,10-epoxides have been implicated as causing potentially tumourigenic lesions. Larvae were exposed to waterborne benzo[a]pyrene (0.01, 0.05 and 0.1 mg/l) for 24 h at stages 38, 45 and 50 of development (24 h, 5 days and 2 weeks post-hatching, respectively) and allowed to recover for up to 6 days. A wide range of adduct lesions were observed at stage 50, three of which were observed at all stages investigated. Adduct repair was biphasic, with an initial rapid repair over the first 24 h post exposure, followed by a much slower decline, resulting in persistence of adducts for at least 6 days post exposure. The individual lesions were repaired at different rates, with some being almost completely repaired after 6 days recovery, whereas one of the main adducts showed restricted repair at stage 50 and another no repair at all. Identification of some adducts has been achieved, by the inclusion of isomeric standards of (+)- or (-)-anti-benzo[a]pyrene diol epoxide reacted with deoxyguanosine and adenosine 3'-monophosphates prepared in vitro. The non-repairable lesion at stage 50 has been shown to be the (+)-trans-anti-benzo[a]pyrene diol epoxide-N2-guanine adduct. This adduct was observed at all stages, but was only maximally repaired at stages 38 and 45.

Amphibians↗
PubMed2000

Fluorescence resonance energy transfer from pyrene to perylene labels for nucleic acid hybridization assays under homogeneous solution conditions.

We characterized the fluorescence resonance energy transfer (FRET) from pyrene (donor) to perylene (acceptor) for nucleic acid assays under homogeneous solution conditions. We used the hybridization between a target 32 mer and its complementary two sequential 16 mer deoxyribonucleotides whose neighboring terminals were each respectively labeled with a pyrene and a perylene residue. A transfer efficiency of approximately 100% was attained upon the hybridization when observing perylene fluorescence at 459 nm with 347-nm excitation of a pyrene absorption peak. The Förster distance between two dye residues was 22.3 A (the orientation factor of 2/3). We could change the distance between the residues by inserting various numbers of nucleotides into the center of the target, thus creating a gap between the dye residues on a hybrid. Assuming that the number of inserted nucleo-tides is proportional to the distance between the dye residues, the energy transfer efficiency versus number of inserted nucleotides strictly obeyed the Förster theory. The mean inter-nucleotide distance of the single-stranded portion was estimated to be 2.1 A. Comparison between the fluorescent properties of a pyrene-perylene pair with those of a widely used fluorescein-rhodamine pair showed that the pyrene-perylene FRET is suitable for hybridization assays.

DNA, Bacterial↗
PubMed2002

Integrity of duplex structures without hydrogen bonding: DNA with pyrene paired at abasic sites.

DNA polymerases specifically insert the hydrophobic pyrene deoxynucleotide (P) opposite tetrahydrofuran (F), an stable abasic site analog, and DNA duplexes containing this non-hydrogen-bonded pair possess a high degree of thermodynamic stability. These observations support the hypothesis that steric complementarity and stacking interactions may be sufficient for maintaining stability of DNA structure and specificity of DNA replication, even in the absence of hydrogen bonds across the base pair. Here we report the NMR characterization and structure determination of two DNA molecules containing pyrene residues. The first is a 13mer duplex with a pyrene.tetrahydrofuran pair (P.F pair) at the ninth position and the second mimics a replication intermediate right after incorporation of a pyrene nucleoside opposite an abasic site. Our data indicate that both molecules adopt right-handed helical conformations with Watson- Crick alignments for all canonical base pairs. The pyrene ring stays inside the helix close to its baseless partner in both molecules. The single-stranded region of the replication intermediate folds back over the opposing strand, sheltering the hydrophobic pyrene moiety from water exposure. The results support the idea that the stability and replication of a P.F pair is due to its ability to mimic Watson-Crick structure.

Base Pairing↗
PubMed2006

Fluorescence of covalently attached pyrene as a general RNA folding probe.

Fluorescence techniques are commonly and powerfully applied to monitor biomolecular folding. In a limited fashion, the fluorescence emission intensity of covalently attached pyrene has been used as a reporter of RNA conformational changes. Here, we pursue two goals: we examine the relationship between tether identity and fluorescence response, and we determine the general utility of pyrene fluorescence to monitor RNA folding. The P4-P6 domain of the Tetrahymena group I intron RNA was systematically modified at multiple nucleotide positions with pyrene derivatives that provide a range of tether lengths and compositions between the RNA and chromophore. Certain tethers typically lead to a superior fluorescence signal upon RNA folding, as demonstrated by equilibrium titrations with Mg2+. In addition, useful fluorescence responses were obtained with pyrene placed at several nucleotide positions dispersed throughout P4-P6. This suggests that monitoring of tertiary folding by fluorescence of covalently attached pyrene will be generally applicable to structured RNA molecules.

Base Sequence↗
PubMed2005

Alignment of pyrene aromatics along RNA double helix.

Multiple pyrene modified RNA duplex exhibits pyrene excimer fluorescence. The pyrene excimer fluorescence is significantly enhanced with an increase in the number of incorporated pyrenes. The pyrenes in the RNA helically aggregate with partial pi-stacking along outside of double stranded helical backbone.

Fluorescent Dyes↗
PubMed1994

X-ray diffraction study of the crystal structure of the pi-molecular compound pyrene ... pyromellitic dianhydride at 19 K.

The crystal structure of the pyrene ... pyromellitic dianhydride (PMDA) pi-molecular compound [(C16H10:C10H2O6); PYRPMA] has been refined from intensities measured at 19 K using the low-temperature accessory designed by Samson, Goldish & Dick [J. Appl. Cryst. (1980), 13, 425-432] for a four-circle diffractometer. Earlier results for the ordered structure [Herbstein & Snyman (1969). Philos. Trans. R. Soc. London Ser. A, 264, 635-666] are confirmed and extended; at 19 K, a = 13.664 (3), b = 9.281 (2), c = 14.420 (3) A, beta = 91.80 (2) degrees, space group P2(1)/n, Z = 4, with two sets of pyrenes at independent centres of symmetry and the four PMDAs at general positions. The geometrical structures of the two components are in good agreement with quantum mechanical calculations. Analyses of thermal motion and packing show that one set of pyrenes is more tightly packed than the other; the principal interactions in the crystal are pi-pi* plane-to-plane interactions between pyrene and PMDA and > CH ... O = C <, between pyrene and PMDA, and between PMDAs.

Benzoates↗
PubMed1976

Reaction of N-(3-pyrene)maleimide with thiol groups of reticulocyte ribosomes.

The reaction of N-(3-pyrene)maleimide with thiol groups of rabbit reticulocyte ribosomes offers a possible fluorescent probe for studying ribosomal structure and conformation. At relatively low concentrations of N-(3-pyrene)maleimide a group of 30-40 readily reactive sulfhydryl residues is derivatized. The major ribosomal proteins containing these thiol groups are identified as S2 + S3, S5, S7, S8, S29, S31, S32, L1, L5, L6, L10 + L14, L15, L18 + L19, and L36. Ribosomal activity, as measured by the nonenzymic binding of phenylalanyl-tRNA and polyphenylalanine synthesis, is inhibited by this degree of reaction with N-(3-pyrene)maleimide. The inhibition is relieved by the prior binding of polyuridylic acid to the ribosomes while the extent of derivatization by N-(3-pyrene)-maleimide is diminished only slightly. The average relative polarization of the fluorescence of the ribosomal bound N-(3-pyrene)maleimide changes significantly with the degree of derivatization of ribosomal thiol groups or with the binding of polyuridylic acid, indicating the value of such a fluorescent thiol-derivatizing agent as a probe of ribosomal structure.

Animals↗