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'High' and 'low' temperature tars were evaluated on parakeratotic mouse tail skin, which was used as a model for the psoriatic keratinization process. The skin was examined histologically for signs of induced granular layers in previously scaly areas; epidermal thicknesses were also measured. It appears that the acidic (phenolic) fractions of coal tars induce granular layers and cause epidermal thickening, whereas neutral constituents alone only cause thickening. It is suggested that tar acids should be further investigated for anti-psoriatic activity.
Mice were exposed for 7 to 8 minutes on weekdays to fresh smoke from high-tar (HT) or low-tar (LT) cigarettes for varying periods of up to 36 weeks. Mice exposed to HT cigarettes exhibited more marked alterations in humoral immune responsiveness, hematological profiles, and pulmonary pathologic findings than those exposed to LT cigarettes. However, cell-mediated immune responsiveness to both bacterial and tumor-specific antigens was depressed similarly in animals exposed to HT or LT cigarettes. Furthermore, the growth rates of subcutaneously established tumors were enhanced similarly in the two groups, with respect to those in control animals.
Mouse tail scale epidermis was used as a model to evaluate anti-parakeratotic activity of tar oil acids (phenols) boiling between 175 and 400 degrees C. Lower boiling phenols seemed to cause more irritation, whereas high boiling phenols caused granular layer induction in formerly parakeratotic skin.
Twelve phenolic fractions of creosote and anthracene oils derived from a high temperature tar were applied in an ointment base to mouse tail skin. After treatment with the higher boiling acids, formerly parakeratotic scale areas underwent granular layer induction and 'basket-weave' keratin was produced. Changes in distribution of acid phosphatase and in horny layer fluorescence were consistent with the conversion to an orthokeratotic state. It is suggested that some of these phenols may be of value in the treatment of chronic psoriasis.
Twenty kinds of coal-tar dyes were subjected to median tolerance limit (TLm) test by use of Himedaka (Oryzias latipes) for the comparision of their acute toxicities. It became clear that 4 kinds of halogens substituted xanthene compounds dyes showed strong acute toxicities. From the fact that uranine had the lower acute toxicity than halogens substituted compounds and the toxicities of these 4 dyes increased through irradiation, it was assumed that halogen atoms in dyes might be responsible for these strong acute toxicities to fish.
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The toxicity of xanthene dyes were studied by various interaction between the dyes and the components in vital body. (1) An increase in the amount of Rose Bengale adsorbed on the gill of fish was followed by the increase in red corpuscle number, and it was assumed that the death of fish in xanthene dye solution was due to anoxemia. (2) Binding capacity of xanthene dyes with bovine serum albumin decreased in the following; Rose Bengale, Phloxine, Erythrosine, Eosine and Uranine. This order was quite coincident with the toxicity compared by TLm values. (3) From the results of rec-assay test by use of Bacillus subtilis, it was confirmed that Phloxine and Rose Bengale had DNA-damaging capacity related to the mutagenecity.
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Data on 1133 men and 1621 women who smoke solely cigarettes with a known tar yield are extracted from the baseline population survey of the Scottish Heart Health Study. The expired-air carbon monoxide (CO-E), serum thiocyanate and serum cotinine values are compared between smokers in three tar groups: low (below 13 mg/cig.), middle (14-15 mg/cig.) and high tar (above 15 mg/cig.). An index of tar consumption is calculated assuming that the intake of different smoke components relative to one another is in proportion to their concentration in the smoke. CO-E and cotinine are found to peak in the middle tar group. Thiocyanate only tends to increase from low to middle tar group for women and from middle to high tar group for men. Tar consumption increases with tar yield of the cigarette smoked, but the increase is much lower than would be expected. We conclude that the tar yield of a cigarette is not an accurate guide to the amount of smoke components consumed by its smoker. Health professionals should be aware of these limitations of tar yield as a measure of cigarette strength.
The photoxicity of coal tars was determined by comparing the ultraviolet light (UVL) energy required to produce erythema at tar treated sites (minimal phototoxic dose [MPD]) with the energy required to produce the same degree of erythema at untreated control sites (minimal erythema dose [MED]). The ratio of MED/MPD is the photoxic index (PI). Tars that were phototoxic had a PI of greater than 1. Using a UVA (320 to 400 nm) and a tuvb (290 to 320 nm) light source, 15 subjects and six tars were tested. All tars were phototoxic to UVA but not to UVB (P smaller than 0.0001). Although tar and UVL is a widely accepted treatment for psoriasis (Goeckerman therapy), the light sources employed at normal exposure times provide insufficient UVA energy to produce a phototoxic reaction to the tars are used. The therapeutic response seen in psoriatic patients treated with tar and UVL should therefore not be attributed to tar phototoxicity.
Acetonitrile extracts of cigarette tar inhibit state 3 and state 4 respiration of intact mitochondria. Exposure of respiring submitochondrial particles to acetonitrile extracts of cigarette tar results in a dose-dependent inhibition of oxygen consumption and reduced nicotinamide adenine dinucleotide (NADH) oxidation. This inhibition was not due to a solvent effect since acetonitrile alone did not alter oxygen consumption or NADH oxidation. Intact mitochondria are less sensitive to extracts of tar than submitochondrial particles. The NADH-ubiquinone (Q) reductase complex is more sensitive to inhibition by tar extract than the succinate-Q reductase and cytochrome complexes. Nicotine or catechol did not inhibit respiration of intact mitochondria. Treatment of submitochondrial particles with cigarette tar results in the formation of hydroxyl radicals, detected by electron spin resonance (ESR) spin trapping. The ESR signal attributable to the hydroxyl radical spin adduct requires the presence of NADH and is completely abolished by catalase and to a lesser extent superoxide dismutase (SOD). Catalase and SOD did not protect the mitochondrial respiratory chain from inhibition by tar extract, indicating that the radicals detected by ESR spin trapping are not responsible for the inhibition of the electron transport. We propose that tar causes at least two effects: (1) Tar components interact with the electron transport chain and inhibit electron flow, and (2) tar components interact with the electron transport chain, ultimately to form hydroxyl radicals.
Short basic peptides from the HIV Tat protein bind specifically to a bulge region in TAR RNA, with a single arginine residue providing the only sequence-specific contact. The free amino acid arginine also binds specifically to TAR. Previous circular dichroism (CD) experiments suggested that peptide binding induces a conformational change in TAR. Here we confirm this observation using single arginine-containing peptides and show that arginine or guanidine binding also induces a conformational change in TAR. A peptide containing a single arginine within a stretch of histidines (CYHHHRHHHHHA) shows pH-dependent binding and a corresponding change in TAR conformation, as detected by a decrease in the CD signal at 265 nm. Arginine and guanidine, which bind to TAR with apparent Kd's of approximately 1.5 mM, induce similar CD changes. In contrast, lysine, which does not bind specifically to TAR, has no effect. Mutants of TAR that abolish specific binding (a U-->C substitution in the three-nucleotide bulge, a deletion of the bulge, or an A-U to U-A base pair change above the bulge) show no change in the CD signal upon binding of peptides, arginine, or guanidine. The results suggest that binding of a single guanidinium group to a specific site in TAR induces a change in RNA conformation.
A specific RNA sequence located in the leader of all human immunodeficiency virus type 1 (HIV-1) mRNAs termed the transactivation response element, or TAR, is a primary target for induction of HIV-1 long terminal repeat activity by the HIV-1-derived trans-regulatory protein, Tat. Human neurotropic virus, JC virus (JCV), a causative agent of the degenerative demyelinating disease progressive multifocal leukoencephalopathy, contains sequences in the 5' end of the late RNA species with an extensive homology to HIV-1 TAR. In this study, we examined the possible role of the JCV-derived TAR-homologous sequence in Tat-mediated activation of the JCV late promoter (Tada et al., Proc. Natl. Acad. Sci. USA 87:3479-3483, 1990). Results from site-directed mutagenesis revealed that critical G residues required for the function of HIV-1 TAR that are conserved in the JCV TAR homolog play an important role in Tat activation of the JCV promoter. In addition, in vivo competition studies suggest that shared regulatory components mediate Tat activation of the JCV late and HIV-1 long terminal repeat promoters. Furthermore, we showed that the JCV-derived TAR sequence behaves in the same way as HIV-1 TAR in response to two distinct Tat mutants, one of which that has no ability to bind to HIV-1 TAR and another that lacks transcriptional activity on a responsive promoter. These results suggest that the TAR homolog of the JCV late promoter is responsive to HIV-1 Tat induction and thus may participate in the overall activation of the JCV late promoter mediated by this transactivation.