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PubMed2006

Bioactive constituents of brazilian red propolis.

In a new propolis type, red Brazilian propolis, 14 compounds were identified (six of them new for propolis), among them simple phenolics, triterepenoids, isoflavonoids, prenylated benzophenones and a naphthoquinone epoxide (isolated for the first time from a natural source). Three of the major components demonstrated significant antimicrobial activity, and two (obtained as inseparable mixture) possessed radical scavenging activity against 1,1-diphenyl-2-picrylhydrazyl (DPPH).

Journal Article↗

PubMedDate not supplied

Analysis of urinary benzodiazepines using solid-phase extraction and gas chromatography-mass spectrometry.

A solid-phase extraction and GC-MS confirmation method was developed for certain urinary diazolo- and triazolobenzodiazepines, including the metabolites of lorazepam, clonazepam, alprazolam, and triazolam. The latter two do not form benzophenones, and the others are not readily confirmed by conventional thin-layer chromatography or GC-MS techniques. Samples were hydrolyzed with glucuronidase at 37 degrees C, adjusted to pH 4.5, extracted with Bond Elut Certify columns, dried, and derivatized using BSTFA with 1% TMCS. Sample preparation time averaged 4 hours. A GC-MS selected-ion-monitoring acquisition method targeting retention time, molecular ion abundances, and qualifier ion ratios was used to determine positive results. The recovery of 7-NH2-clonazepam was 95%, and recoveries of alpha-hydroxyalprazolam, alpha-hydroxytriazolam, and lorazepam were greater than 66%. Linearity was demonstrated from 0.1 to 1.0 microgram/mL for each drug. Within-run CVs were less than 11%, and between-run CVs were less than 16%. Using this technique, we have been able to confirm suspected cases of abuse that had not been confirmed by previous techniques.

Anti-Anxiety Agents↗

PubMedDate not supplied

Serum and urine concentrations of flunitrazepam and metabolites, after a single oral dose, by immunoassay and GC-MS.

A clinical study was conducted to assess the ability of commercially available immunoassays to detect flunitrazepam (FNP) in plasma and urine samples and to compare the results with those obtained by gas chromatography-mass spectrometry (GC-MS). The clinical study consisted of four individuals (two male and two female) who had taken a single 2-mg dose of FNP. Serum was collected over a 48-h period and urine was collected over a 72-h period. The serum and urine samples were analyzed by the COBAS INTEGRA Serum Benzodiazepines assay (SBENZ), the TDx serum and urine Benzodiazepines assay, and GC-MS. The GC-MS procedure was developed for analysis of FNP and metabolites in plasma and urine using an acid hydrolysis step resulting in the formation of specific benzophenones corresponding to FNP and its metabolites. The relative sensitivities of the assays for the detection of FNP and metabolites in serum and urine were GC-MS > SBENZ > TDx. The immunoassay results for serum samples showed peak concentrations of FNP metabolites at 8 h after FNP ingestion for three individuals and at about 1 h for the fourth individual. The GC-MS, SBENZ, and TDx urine immunoassays detected drug above the stated limit of detection (LOD) in 44, 41, and 35 serial FNP urine samples, respectively. FNP metabolites were detected in urine samples with all three assays for up to 72 h after a 2-mg dose. The improved detection rate with the SBENZ assay as compared to the TDx assay is likely explained by its higher cross-reactivity with the major metabolite, 7-amino-flunitrazepam (7-amino-FNP), and its lower LOD.

Administration, Oral↗

PubMedDate not supplied

Toxicological analysis of benzodiazepine-type compounds in post-mortem blood by gas chromatography.

Analytical methodology has been reviewed and investigated to present a rapid method for a qualitative screening and quantitation of a number of benzodiazepine compounds and metabolites. The procedure requires only one millilitre of blood for analysis by gas chromatography (ec). An optional step is included in order to confirm the identity of the compounds by formation of the benzophenone product. Qualitative and quantitative data of the benzodiazepines and related compounds are included.

Adult↗

PubMedDate not supplied

The determination of the triazolobenzodiazepine triazolam in post mortem samples.

A post mortem case involving the triazolobenzodiazepine triazolam is reported. Levels of 38 ng/g in the liver and 6.7 ng/mL in the blood were determined by reversed-phase high-performance liquid chromatography (HPLC) using an eluent of 0.06% acetic acid:acetonitrile (61:39) and ultraviolet detection at 221 nm. The presence of triazolam in the post mortem samples was verified by its oxidation to a benzophenone with potassium dichromate, followed by the analysis of the oxidized extract by HPLC using a silica column and an eluent of dichloromethane:methanol (97.5:2.5) at 250 nm.

Aged↗

PubMed1987

Photocross-linking from DNPated SH1 in myosin head. I. Cross-linking to the 50-kDa fragment.

When DNP-SH1-myosin, selectively dinitrophenylated at SH1 by 1,2,4-trinitrobenzene, was irradiated with a high-pressure mercury lamp equipped with a UV cut filter, a new 220-kDa band called the X-band appeared right above the heavy chain band (200 kDa) on SDS-PAGE (Laemmli). The time course of the X-band formation was composed of two phases, the initial one being rapid, and the second slow. Immune reaction experiments using antibodies specific for heavy or light chains indicated that the X-band in the initial phase contained heavy chain alone, but no light chains. Such an extra band (106 kDa) was also observed in the initial phase of photolysis of DNP-SH1-Subfragment-1 (heavy chain: 96 kDa) obtained from DNP-SH1-myosin. Trypsinolysis of the 106-kDa product generated a 83-kDa band. N-Terminal sequence analysis and the amino acid composition of the band revealed that the X-band is an intraheavy chain cross-linking product between the 20- and the 50-kDa fragments. This presents a striking contrast to the other cross-linking from SH1 using benzophenone-4-iodoacetamide which reacted with the 25-kDa fragment alone (Lu, R.C. et al. (1986) Proc. Natl. Acad. Sci. U.S. 83, 6392-6396). Based upon the result obtained, the spatial arrangement of the three tryptic domains around SH1 is discussed.

Amino Acid Sequence↗

PubMed1988

A novel anthraquinone ring cleavage enzyme from Aspergillus terreus.

An enzyme activity which catalyzes the ring cleavage of the anthraquinone questin to form benzophenone desmethylsulochrin was found in the cell-free extract of Aspergillus terreus, a (+)-geodin producer. The product was identified as desmethylsulochrin by high-resolution mass spectroscopy and chemical carrier dilution analysis. The enzyme showed an absolute requirement of NADPH and molecular oxygen. Therefore, the enzyme, named questin oxygenase, was considered to be classified as a monooxygenase. The optimum pH was around 7.5. The enzyme was very unstable and lost its activity completely after storage overnight at 4 degrees C in 0.05 M phosphate buffer, pH 7.5. The instability of the questin oxygenase was partially overcome by the addition of polyols and the non-ionic detergent Tween 80 to the buffer. By DEAE-cellulose column chromatography, two protein fractions, named DE-I and DE-II, were obtained. Neither fraction reacted with questin by itself. However, the combination of DE-I and DE-II reconstituted the questin oxygenase system to convert questin to desmethylsulochrin. This result suggested that the system is not a simple combination of oxygenase and hydrolase, but requires some additional factor(s) such as electron transfer protein.

Anthraquinones↗

PubMed2004

Interaction of polycyclic musks and UV filters with the estrogen receptor (ER), androgen receptor (AR), and progesterone receptor (PR) in reporter gene bioassays.

Two important ingredients of personal care products, namely polycyclic musk fragrances and UV filters, can be found in the environment and in humans. In previous studies, several compounds of both classes have been tested for their interaction with the estrogen receptor. Two polycyclic musk fragrances, namely AHTN and HHCB, turned out to be anti-estrogenic both in vitro and in vivo in a transgenic zebrafish assay. Several UV filters have been shown to exert estrogenic effects in vitro and in some in vivo studies. Here, we assessed the interaction of five polycyclic musk compounds and seven UV filters with the estrogen receptor (ER), androgen receptor (AR), and progesterone (PR) receptor, using sensitive and specific reporter gene cell lines. Four polycyclic musks (AHTN, HHCB, AETT, and AHMI) were found to be antagonists toward the ERbeta, AR and PR. The UV filters that showed estrogenic effects (benzophenone-3, Bp-3; 3-benzylidene camphor, 3-BC; homosalate, HMS; and 4-methylbenzylidene camphor, 4-MBC) were found to be antagonists toward the AR and PR. The ERalpha agonistic UV filter octyl-dimethyl-p-aminobenzoic acid (OD-PABA) did not show activity toward the AR and PR. Octyl methoxy cinnamate (OMC) showed weak ERalpha agonism, but potent PR antagonism. Butyl methoxydibenzoylmethane (B-MDM) only showed weak ERalpha agonism and weak AR antagonism. Most effects were observed at relatively high concentrations (above 1 muM); however, the anti-progestagenic effects of the polycyclic musks AHMI and AHTN were detected at concentrations as low as 0.01 muM. The activity of anti-progestagenic xenobiotics at low concentrations indicates the need to undertake more research to find out about the potential endocrine disrupting effects of these compounds in vivo.

Benzopyrans↗

PubMed2005

Endocrine disrupting chemical atrazine causes degranulation through Gq/11 protein-coupled neurosteroid receptor in mast cells.

We studied the effects of representative endocrine-disrupting chemicals on beta-hexosaminidase release from mast cells and their putative neurosteroid receptor involvement. Some endocrine-disrupting chemicals, such as amitrol, benzophenon, bisphenol A, pentachlorophenol, and tetrabromophenol A did not cause hexosaminidase release from RBL-2H3 cells, but they blocked the release by dehydroepiandrosterone sulfate, a representative neurosteroid agonist. On the contrary, atrazine, which is a widely used herbicide, caused a rapid and concentration-dependent degranulation in the range between 10 nM and 1 microM in RBL-2H3 and peritoneal mast cells. Atrazine-induced degranulation was also evaluated by Alexa 488-annexin V binding to the phosphatidylserine, which is externalized during degranulation, and these actions were blocked by BSA-conjugated (membrane-impermeable) progesterone (PROG-BSA). The atrazine-induced beta-hexosaminidase release was characterized by various inhibitors including antisense-oligodeoxynucleotide for Galpha(q/11), pertussis toxin, phospholipase C inhibitor U-73122, inositol 1,4,5-triphosphate receptor inhibitor xestospongin C and Ca(2+) channel blocker lanthanum chloride. These analyses revealed that the degranulation is mediated by putative metabotropic neurosteroid receptor, G(q/11), phospholipase C and Ca(2+) mobilization from intracellular stores. Having documented progesterone receptor-modulation of atrazine-induced mast cell degranulation in vitro, this response was evaluated in mice. Atrazine caused pain responses when injected in the foot pads of mice, and they were antagonized by local administration of PROG-BSA or diphenhydramine. Atrazine also caused PROG-BSA-reversible plasma extravasation. All these findings strongly suggest that herbicide atrazine exerts inflammatory activity through activation of putative G(q/11)-coupled neurosteroid receptor and phospholipase C.

Animals↗

PubMedDate not supplied

Basic fibroblast growth factor impregnated hydrogel microspheres for embolization of cerebral arteriovenous malformations.

To assess the prevention of recanalization at embolized sites in cerebral arteriovenous malformations, the authors devised a novel embolic material, hydrogel microspheres prepared from poly(ethylene glycol) diacrylate impregnated with basic fibroblast growth factor. In this article, preparation of the microspheres, and preliminary study of in vitro and in vivo performance are discussed. Poly(ethylene glycol) diacrylate, prepared from end capping of poly(ethylene glycol) (molecular weights, 1,000, 2,000, and 4,000) with acryloyl chloride and benzophenone derived poly(ethylene glycol), prepared from poly(ethylene glycol) (molecular weight, 2,000) with benzoyl benzoic acid chloride as a photoinitiator, were dissolved in a buffer solution with or without basic fibroblast growth factor. The mixed solution was dropped stepwise into liquid paraffin with stirring. Ultraviolet light irradiation resulted in the formation of relatively rigid hydrogel microspheres (diameter, 100-400 microm). The in vitro study showed that the higher the molecular weight of poly(ethylene glycol) diacrylate used, the faster the release rate of immobilized protein. Canine kidneys were embolized with these microspheres via the femoral artery using a microcatheter. Histologic examination showed that microspheres occluded arterioles. The degree of accumulation of fibroblasts and extracellular matrix were larger for basic fibroblast growth factor impregnated microspheres than for nonimpregnated ones. Basic fibroblast growth factor released from microspheres may help regenerate tissues at arteriovenous malformation sites, and recanalization is expected to be prevented.

Animals↗

PubMed1994

Dynamic association of proteins with the pre-mRNA branch region.

The association of proteins with the branch site region during pre-mRNA splicing was probed using a novel methodology to site-specifically modify the pre-mRNA with the photo-reagent benzophenone. Three sets of proteins were distinguished by the kinetics of their associations with pre-mRNAs, by their association with discrete splicing complexes, and by their differing factor requirements. An early U1 snRNP-dependent cross-link of the branch region to a p80 species was followed by cross-links to p14, p35, and p150 polypeptides associated with the U2 snRNP-pre-mRNA complex. Concomitant with formation of the spliceosome, a rearrangement of protein factors about the branch region occurred, in which the p35 and p150 cross-links were replaced by p220 and p70 species. These results establish that the branch region is recognized in a dynamic fashion by multiple distinct proteins during the course of spliceosomal assembly.

Base Sequence↗

PubMed2006

Cole-Cole law for critical dynamics in glass-forming liquids.

Within the mode-coupling theory (MCT) for glassy dynamics, the asymptotic low-frequency expansions for the dynamical susceptibilities at critical points are compared to the expansions for the dynamic moduli; this shows that the convergence properties of the two expansions can be quite different. In some parameter regions, the leading-order expansion formula for the modulus describes the solutions of the MCT equations of motion outside the transient regime successfully; at the same time, the leading- and next-to-leading-order expansion formulas for the susceptibility fail. In these cases, one can derive a Cole-Cole law for the susceptibilities; and this law accounts for the dynamics for frequencies below the band of microscopic excitations and above the high-frequency part of the alpha peak. It is shown that this scenario explains the optical-Kerr-effect data measured for salol and benzophenone (BZP). For BZP it is inferred that the depolarized light-scattering spectra exhibit a wing for the alpha peak within the Gigahertz band. This wing results from the crossover of the von Schweidler law part of the alpha peak to the high-frequency part of the Cole-Cole peak; and this crossover can be described quantitatively by the leading-order formulas of MCT for the modulus.

Journal Article↗

PubMed2004

Nearly logarithmic decay of correlations in glass-forming liquids.

Nearly logarithmic decay of correlations, which was observed for several supercooled liquids in optical-Kerr-effect experiments [Phys. Rev. Lett. 84, 2437 (2000)]; Phys. Rev. Lett. 90, 197401 (2003)]], is explained within the mode-coupling theory for ideal glass transitions as a manifestation of the beta-peak phenomenon. A schematic model, which describes the dynamics by only two correlators, one referring to density fluctuations and the other to the reorientational fluctuations of the molecules, yields for strong rotation-translation coupling response functions in agreement with those measured for benzophenone and Salol for the time interval extending from 2 ps to about 20 and 200 ns, respectively.

Journal Article↗

PubMed1993

Effects of sunscreens and a DNA excision repair enzyme on ultraviolet radiation-induced inflammation, immune suppression, and cyclobutane pyrimidine dimer formation in mice.

Exposure of skin to ultraviolet (UV) radiation inhibits the induction of delayed-type hypersensitivity (DTH) responses initiated at a distant, unirradiated site. Recent studies attributed this form of immune suppression to DNA damage in the form of cyclobutane pyrimidine dimers (CPD). In the present study, we investigated the protective defects of sunscreens on UV-induced systemic suppression of DTH to Candida albicans, inflammation, and DNA damage. The photoprotective effects of sunscreen preparations containing 8% octyl-N-dimethyl-p-aminobenzoate, 7.5% 2-ethylhexyl-p-methoxycinnamate, or 6% benzophenone-3 were studied in C3H mice exposed to a single dose of 500 mJ/cm2 UVB radiation from FS40 sunlamps. Inflammation was determined by the amount of skin edema at the site of UV irradiation, and DNA damage was assessed by measuring the frequency of endonuclease-sensitive sites in the epidermis. Application of the sunscreens before UV irradiation gave 75-97% protection against UV-induced edema, 67-91% protection against formation of CPD, but only 30-54% protection against suppression of DTH. In contrast, the topical application of liposomes containing a CPD-specific DNA repair enzyme immediately after UV irradiation resulted in 82% protection against suppression of DTH, but at best, 39% protection against skin edema. These findings demonstrate that sunscreens give less protection against UV-induced immune suppression than against skin edema and CPD formation. Furthermore, they suggest that less DNA damage is required to cause UV-induced immune suppression than to cause sunburn.

Animals↗

PubMed1993

Analysis of the protective effect of different sunscreens on ultraviolet radiation-induced local and systemic suppression of contact hypersensitivity and inflammatory responses in mice.

We investigated the capacity of three sunscreen compounds to protect mice from the inflammatory and immunosuppressive effects of ultraviolet radiation (UVR). The sunscreen preparations contained 7.5% 2-ethylhexyl-p-methoxycinnamate, 8% octyl-N-dimethyl-p-aminobenzoate, or 6% benzophenone-3 in an oil-in-water emulsion. Skin swelling was used as the measure of their effect on UVR-induced inflammation, and immunosuppression was assessed by contact sensitization with 2,4-dinitrofluorobenzene applied to UV-irradiated skin (local suppression) or a distant site (systemic suppression). The sunscreens were applied to the shaved dorsal skin of C3H mice, which were then given a single dose of UVR ranging from 2 to 32 kJ/m2 within the UVB (280-320 nm) region. All three sunscreens gave complete protection against local suppression of contact hypersensitivity caused by a dose of 2 kJ/m2 UVB. They also protected against both inflammation and systemic immunosuppression caused by UVR; however, protection was highly dependent on the UVR dose. Furthermore, the sunscreens were less effective in protecting against systemic immunosuppression than against inflammation. These results indicate that immunosuppression is less sensitive to the protective effects of the sunscreens than inflammation and that protection against UVR-induced inflammation does not necessarily imply prevention of immunologic alterations. In addition, these studies suggest that UVR-induced immunosuppression and inflammation may involve different mechanisms.

Animals↗

PubMed1992

Sunscreens protect epidermal Langerhans cells and Thy-1+ cells but not local contact sensitization from the effects of ultraviolet light.

This study compares the ability of two commonly used sunscreens--octyl dimethyl para-aminobenzoate (Padimate O) and 2-ethylhexyl-p-methoxycinnamate (2-EHMC)--to protect Langerhans cells (LC), Thy-1+ dendritic epidermal cells (Thy-1+ dEC), and local contact sensitivity (CS) from the effects of ultraviolet (UV) light. Chronic exposure of mice 5 d per week for 4 weeks with an intermediate dose of solar-simulated sunlight from which any UVC had been filtered reduced the LC and Thy-1+ dEC density of murine epidermis. This irradiation procedure was designed to simulate closely the daily exposure of humans to sunlight. This effect on LC and Thy-1+ dEC occurred in both albino and pigmented mice that develop a tan during the irradiation procedure, indicating that a tan does not protect these cells from the effects of UV light. Sunscreen preparations with Padimate O and 2-EHMC, both of which also contained benzophenone-3, as well as Padimate O or 2-EHMC in organic solvent, inhibited UV light from depleting LC from the epidermis of both mouse strains. Padimate O and 2-EHMC in organic solvent were used to ensure that these were the active ingredients in the sunscreen preparations. In contrast to the effects on LC, Padimate O, but not 2-EHMC, protected Thy-1+ dEC from UV exposure in both mouse strains, but neither protected against the development of local immunosuppression using a contact sensitivity model. Thus, even in a mouse strain that is sensitive to UV-induced immunosuppression, local immunosuppression can occur in the presence of normal densities of LC and Thy-1+ dEC.

Animals↗

PubMed1981

The effect of various sunscreen agents on skin damage and the induction of tumor susceptibility in mice subjected to ultraviolet irradiation.

Sunscreen preparations containing various chemical UV absorbers, para-aminobenzoic acid (PABA), 2 PABA derivatives, benzophenone or a combination of these were topically applied to the backs of C3H/HeN mice prior to their being irradiated with ultraviolet light in the UVB range. In all cases this treatment was effective in preventing the pathological skin changes associated with UVB irradiation. Histological evaluation of skin biopsies from mice treated with the sunscreen preparations and UVB irradiation showed little or no difference from normals in amount of hyperplasia, melanization or parakeratosis present. These histologic changes were observed in animals receiving UVB irradation in the absence of any sunscreen agent. Pretreatment with the various sunscreen agents did not, however, prevent the induction of tumor susceptibility as measured by the sustained growth of a UV-induced tumor which is immunologically rejected in normal syngeneic mice. These data show a clear distinction between the effects of UVB irradiation leading to histological changes in the epidermis and those leading to the state of tumor susceptibility in mice. The distinction was further corroborated by the finding that epidermal hyperplasia induced by repeated applications of croton oil had no significant enhancing or inducing effects on the induction of tumor susceptibility. In addition, the induction of tumor susceptibility. In addition, the induction of tumor susceptiblity is not due to wavelengths of light less than 320 nm since this effect was abrogated when the UVB radiation was filtered through glass. Possible mechanistic differences between the tumor susceptiblity generated in UVB and photoprotected UVB irradiated animals were observed, however, when we attempted to adoptively transfer the state of tumor susceptibility to normal animals. While it was readily transferable with splenic lymphoid cells from UVB irradiated animals, all attempts to transfer the tumor susceptibility from photoprotected animals have, to date, been unsuccessful.

Animals↗

PubMed1995

Sunscreens and T4N5 liposomes differ in their ability to protect against ultraviolet-induced sunburn cell formation, alterations of dendritic epidermal cells, and local suppression of contact hypersensitivity.

Exposure of skin to ultraviolet (UV) radiation can lead to diverse biologic effects, including inflammation, sunburn cell formation, alterations of cutaneous immune cells, and impaired induction of contact hypersensitivity responses. The molecular mechanisms of these UV-induced effects are not completely understood. We investigated the ability of sunscreens and liposomes containing the DNA excision repair enzyme T4 endonuclease V to prevent these effects of UV radiation. The use of T4N5 liposomes, which increase the repair of cyclobutyl pyrimidine dimers, provides an approach for assessing the role of DNA damage in the effects of UV radiation on the skin. Exposing C3H mice to 500 mJ/cm2 UVB radiation from FS40 sunlamps resulted in skin edema, sunburn cell formation, and morphologic alterations and decreased numbers of Langerhans cells and Thy-1+ dendritic epidermal T cells. In addition, the induction of contact hypersensitivity after application of 2,4-dinitrofluorobenzene on UV-irradiated skin was diminished by 80%. Applying sunscreens containing octyl-N-dimethyl-p-aminobenzoate, 2-ethylhexyl-p-methoxycinnamate, or benzophenone-3 before this dose of UV irradiation gave nearly complete protection against all of these effects of UV irradiation. In contrast, topical application of T4N5 liposomes after UV irradiation had no effect on UV-induced skin edema and only partially protected against sunburn cell formation and local suppression of contact hypersensitivity, although its ability to protect against alterations in dendritic immune cells was comparable to that of the sunscreens. These results suggest that DNA damage is involved in only some of the local effects of UV radiation on the skin. In addition, T4N5 liposomes may be a useful adjunct to sunscreens because they can reduce some of the deleterious effects of UV radiation on skin even after a sunburn has been initiated.

Animals↗