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{Bis(3,5-Di-tert-butyl-2-oxidobenzyl)[2-(N,N-dimethylamino)ethyl]amine-kappa(4)N,N',O,O'}zinc(II) and {bis(3-tert-butyl-5-methyl-2-oxidobenzyl)[2-(N,N-dimethylamino)ethyl]amine-kappa(4)N,N',O,O'}(tetrahdyrofuran)zinc(II).

The title zinc(II) complexes, [Zn(C(34)H(54)N(2)O(2))], (II), and [Zn(C(28)H(42)N(2)O(2))(C(4)H(8)O)], (III), were obtained as monomeric 1:1 complexes, in contrast with the calcium complexes supported by the same ligand class. Complex (II) crystallizes with two independent molecules in the asymmetric unit, which have similar geometric parameters. The donor atoms in (II) form a distorted trigonal-pyramidal arrangement around the zinc centre. Complex (III) contains a coordinated tetrahydrofuran molecule, resulting in a five-coordinate trigonal-bipyramidal arrangement around the Zn atom. The electron density provided by the coordination of this tetrahydrofuran molecule elongates the Zn-O and Zn-N bonds by approximately 0.07 and 0.10 A, respectively, in comparison with (II). Neither (II) nor (III) is active as an epsilon-caprolactone polymerization catalyst. The data presented here demonstrate that Zn may bind both an ONNO ligand and an additional oxygen-based ligand. The lack of activity is thus not due to steric hinderance at the metal atom.

Calcium↗

Crystal and molecular structure of the antimalarial agent 4-(tert-butyl)-2-(tert-butylaminomethyl)-6-(4-chlorophenyl)phenol dihydrogen phosphate (WR 194,965 phosphate).

WR 194,965 phosphate, a new antimalarial agent containing a biphenyl ring structure active against chloroquine-resistant Plasmodium falciparum, crystallized in ionic form with a positive charge on the quaternary nitrogen atom. The oxygen and nitrogen atoms of WR 194,965 were hydrogen bonded to the same phosphate group. The nitrogen atom was also hydrogen bonded to a second phosphate group. The phosphate ions formed discrete clusters of four phosphate moieties. The phosphate clusters contained fourfold inversion symmetry. The intramolecular N-O distance in WR 194,965 of 3.073 A (1 A = 0.1 nm) was close to the reported values for N-O distances in the active cinchona alkaloids and may be important for activity. A comparison of the crystalline structure of WR 194,965 with those of mefloquine and quinidine sulfate demonstrated that the regions of the three molecules in the vicinity of the aliphatic nitrogen atom and the oxygen atom superimpose. Much of the remainder of the WR 194,965 molecule spatially overlapped with the combined three-dimensional space defined by quinidine and mefloquine. The crystallographic parameters were: C21H29ClNO+.H2PO4-; Mr = 443.9; symmetry of unit cell, tetragonal; space group, I41/a; parameters of unit cell, a = b = 24.305 +/- 0.002 A, c = 17.556 +/- 0.003 A; V (volume of unit cell) = 10370.9 A3; Z (number of molecules per unit cell) = 16; Dx (calculated density) = 1.137 g cm-3; source of radiation, CuK alpha (lambda = 1.54178 A); mu (absorption coefficient) = 21.3 cm-1; F(000) (sum of atomic scattering factors at zero scattering angle) = 3,440; room temperature; final R = 8.2% for 2,508 reflections with [F0] greater than 3 sigma.

Animals↗

Proline-containing beta-turns. IV. Crystal and solution conformations of tert.-butyloxycarbonyl-L-prolyl-D-alanine and tert.-butyloxycarbonyl-L-prolyl-D-alanyl-L-alanine.

The conformations of the dipeptide t-Boc-Pro-DAla-OH and the tripeptide t-Boc-Pro-DAla-Ala-OH have been determined in the crystalline state by X-ray diffraction and in solution by CD, n.m.r. and i.r. techniques. The unit cell of the dipeptide crystal contains two independent molecules connected by intermolecular hydrogen bonds. The urethane-proline peptide bond is in the cis orientation in both the molecular forms while the peptide bond between Pro and DAla is in the trans orientation. The single dipeptide molecule exhibits a "bent" structure which approximates to a partial beta-turn. The tripeptide adopts the 4----1 hydrogen-bonded type II beta-turn with all trans peptide bonds. In solution, the CD and i.r. data on the dipeptide indicate an ordered conformation with an intramolecular hydrogen bond. N.m.r. data indicate a significant proportion of the conformer with a trans orientation at the urethane-proline peptide bond. The temperature coefficient of the amide proton of this conformer in DMSO-d6 points to a 3----1 intramolecular hydrogen bond. Taken together, the data on the dipeptide in solution indicate the presence (in addition to the cis conformer) of a C7 conformation which is absent in the crystalline state. The spectral data on the tripeptide indicate the presence of the type II beta-turn in solution in addition to the nonhydrogen-bonded conformer with the cis peptide bond between the urethane and proline residues. The relevance of these data to studies on the substrate specificity of collagen prolylhydroxylase is pointed out.

Circular Dichroism↗

Estrogenic effects in flounder Platichthys flesus orally exposed to 4-tert-octylphenol.

The estrogenic effect of dietary 4-tert-octylphenol in the flounder Platichthys flesus was investigated in the laboratory. In the first experiment male flounders were fed doses of 10, 50 and 100 mg 4-tert-octylphenol kg(-1) BW or 0.05 mg 17beta-estradiol kg(-1) BW every second day for 10 days. Increases in the plasma content of vitellogenin were observed on day 6 by the first sampling in all treated groups. An effect of octylphenol on the size of the liver and testis was only seen in one of the exposed group (50 mg 4-tert-octylphenol kg(-1) BW). An increase in the concentration of 4-tert-octylphenol was found in both liver and muscle tissues of all 4-tert-octylphenol treated fish. The concentration of 4-tert-octylphenol (ng g(-1) WW) in liver tissue was four to five times greater than the concentration in muscle tissue. Only about 8% of the 4-tert-octylphenol administered to the group receiving 50 mg 4-tert-octylphenol kg(-1) BW was retained in the liver and the muscles at the end of the experiment. In the second experiment male flounders were exposed to a low dose range of 4-tert-octylphenol (1 to 25 mg 4-tert-octylphenol kg(-1) BW) in order to establish the dose-response relationship of 4-tert-octylphenol when applied by feeding to flounder. Vitellogenin induction (LOED) occurred at 10 and 5 mg 4-tert-octylphenol kg(-1) BW after, respectively, 6 and 11 days of exposure. Based on a logistic regression analysis the effect dose (ED(50)) could be determined as 8.2 and 5.6 mg 4-tert-octylphenol kg(-1) BW on day 6 and 11, respectively. 4-tert-octylphenol accumulated in liver, muscle and testis tissue, and a significant accumulation in liver was found at 2.5 mg 4-tert-octylphenol kg(-1) BW and in muscle and testis at 5 mg 4-tert-octylphenol kg(-1) BW. Finally, a positive correlation between the plasma vitellogenin concentration and the liver tissue concentration of 4-tert-octylphenol was established as well as a positive correlation between the content of 4-tert-octylphenol in liver and muscle/testis tissue.

Animals↗

NTP technical report on the toxicity studies of p-tert-butylcatechol (CAS No. 98-29-3) administered in feed to F344/N rats and B6C3F1 mice.

[molecular structure: see text] p-tert-Butylcatechol is used as an antioxidant, stabilizer, and polymerization inhibitor for styrene, butadiene, neoprene, and other olefins and reactive monomers. p-tert-Butylcatechol was nominated by the National Cancer Institute and the U.S. Food and Drug Administration for testing based on reports of its increasing levels of production and use and to compare the toxicity of p-tert-butylcatechol with that of similar antioxidants, butylated hydroxyanisole and butylated hydroxytoluene, which are added to food. Male and female F344/N rats and B6C3F1 mice were exposed to p-tert-butylcatechol (greater than 99% pure) in feed for 15 days or 14 weeks. Genetic toxicology studies were conducted in Salmonella typhimurium, rat bone marrow cells, and mouse peripheral blood erythrocytes. In the 15-day studies, groups of five male and five female rats and mice were fed diets containing 0, 3,125, 6,250, 12,500, 25,000, or 50,000 ppm p-tert-butylcatechol (equivalent to average daily doses of approximately 290 to 2,470 mg p-tert-butylcatechol/kg body weight to rats and 590 to 8,200 mg/kg to mice). All animals in the 50,000 ppm groups were killed moribund on day 8 (rats) or by day 7 (mice). Mean body weights of all groups of rats exposed to 6,250 ppm or greater were significantly less than those of the controls. Mean body weights of male mice exposed to 12,500 or 25,000 ppm and of 25,000 ppm female mice were significantly less than those of the controls. Female rats, male and female mice in the 25,000 ppm groups, and 12,500 ppm male mice lost weight during the studies. Feed consumption by exposed rats generally decreased with increasing exposure concentration; feed consumption by exposed mice was similar to that by the controls. Thymus weights of 25,000 ppm rats and mice were significantly less than those of the controls. Gross findings noted at necropsy included thin carcasses for three male and all female rats in the 12,500 ppm groups and all male and female rats and mice in the 25,000 and 50,000 ppm groups. No exposure-related lesions were observed microscopically. In the 14-week studies, groups of 10 male and 10 female rats and mice were fed diets containing 0, 781, 1,562, 3,125, 6,250, or 12,500 ppm p-tert-butylcatechol (equivalent to average daily doses of approximately 70 to 1,030 mg/kg to rats and 135 to 2,815 mg/kg to mice). All animals survived to the end of the studies. Mean body weights of male rats exposed to 1,562 ppm or greater, female rats exposed to 3,125 ppm or greater, male mice exposed to 12,500 ppm, and female mice exposed to 6,250 or 12,500 ppm were significantly less than those of the controls. Feed consumption by male and female rats in the 6,250 and 12,500 ppm groups at week 1 and the 12,500 ppm groups at week 14 was less than that by the controls; feed consumption by exposed and control mice was similar. An erythrocytosis, indicated by increased hematocrit values, hemoglobin concentrations, and erythrocyte counts, was observed in 6,250 and 12,500 ppm rats on day 4 and in 12,500 ppm rats on day 22. At these time points, a transient hepatic effect was demonstrated by increases in alanine aminotransferase activities and bile salt concentrations in exposed rats. In 12,500 ppm male rats, absolute left cauda epididymis, epididymis, and testis weights were decreased by 15%, 10%, and 9%, respectively, compared to the controls. The number of spermatid heads per testis and epididymal sperm motility of male rats in the 12,500 ppm group were significantly less than those of the controls. The numbers of cycling female rats and females with regular estrous cycles were decreased in the 6,250 and 12,500 ppm groups. Exposed groups of females had significantly fewer estrous cycles than did the controls. Estrous cycle length increased with increasing exposure concentration; female rats in the 6,250 and 12,500 ppm groups had significantly longer cycles and spent more time in diestrus and less time in proestrus, estrus, and metestrus than did the controls. Female mice in the 12,500 ppm group had a significantly longer estrous cycle than did the controls. The incidences of hyperkeratosis of the forestomach epithelium were significantly increased in male and female rats in all exposed groups and in 12,500 ppm female mice. The incidences of hyperplasia of the forestomach epithelium were significantly increased in male and female rats exposed to 3,125 ppm or greater, male mice exposed to 12,500 ppm, and female mice exposed to 6,250 or 12,500 ppm. The severities of the forestomach lesions were minimal to moderate in male rats and minimal to mild in female rats and in mice. All male rats exposed to 6,250 or 12,500 ppm had minimal cytoplasmic alteration in the liver. The absorption, distribution, metabolism, and excretion of p-tert-butylcatechol following intravenous injection, gavage dosing, or dermal application were determined in male F344/N rats and B6C3F1 mice. The absorption of [(14)C]-p-tert-butylcatechol following gavage dosing or dermal application was high. The percent absorption following dermal application increased with increasing dose. Peak concentrations of [(14)C]-p-tert-butylcatechol equivalents in plasma were reached 1 hour after gavage dosing (200 mg/kg) and 2 hours after dermal application (60 mg/kg); no parent compound was detected in the plasma extracts. Regardless of route of administration, p-tert-butylcatechol derived radioactivity was readily excreted in the urine and was markedly nonpersistent in the tissues. p-tert- Butylcatechol was excreted as p-tert-butylcatechol sulfate and other polar metabolites that included predominately sulfate conjugates; it was not excreted as the parent compound. One metabolite was determined to be an O-methyl- ON-sulfate of p-tert-butylcatechol. p-tert-Butylcatechol (10 to 1,000 microg/plate) was not mutagenic in any of several strains of S. typhimurium with or without rat or hamster liver S9. Bone marrow micronucleus tests in which 125 to 500 mg/kg p-tert-butylcatechol was administered three times by intraperitoneal injection to male rats gave negative results. No increases in the frequencies of micronucleated normochromatic erythrocytes were observed in the peripheral blood of male or female mice administered p-tert-butylcatechol in feed for 14 weeks. No significant alteration in the percentage of polychromatic erythrocytes in mouse bone marrow was observed. In summary, the primary toxicity of p-tert-butylcatechol was to the forestomach of rats and mice. In the 14-week study in rats, forestomach toxicity was observed at all exposure concentrations, and the no-observed-adverse-effect level (NOAEL) was not reached for this effect. In the 14-week study in mice, the NOAEL for forestomach toxicity was 1,562 ppm.

Administration, Cutaneous↗

Sensitizing capacity of some trimers in p-tert-butylphenol-formaldehyde resin.

Contact allergy to p-tert-butylphenol formaldehyde resin (PTBP-F-R) is not rare. This resin consists of a large number of substances, most of which are still unknown. For diagnostic and preventive reasons the chemical identity of the sensitizers should be known, as well as their sensitizing capacities, cross-reaction patterns and presence in the environment. The aims of this study were to investigate the sensitizing capacities and potential cross-reacting patterns for 4-tert-butyl- 2,6-bis-(5-tert-butyl-2-hydroxy-3-hydroxymethyl-benzyloxymethyl)-phenol (XIII), 4-tert-butyl-2- (5 - tert - butyl - 2 - hydroxy-benzyloxymethyl) - 6 - (5 - tert - butyl - 2 - hydroxy - 3 - hydroxymethyl-benzyloxy methyl)-phenol (XIVa) and 7,15,23-tri-tert-butyl-25,26,27-trihydroxy-2,3,10,11,18,19-hexahomo-3,11,19-trioxacalix(3)arene (XVIII) by the guinea pig maximization test. 4-tert-Butyl-2,6-bis-hydroxymethyl-phenol, 4-tert-butylbenzene-1,2-diol, 4-tert-butyl-2-hydroxymethyl-phenol, 4-tert-butyl-phenol, 4-tert-butyl-2-(5-tert-butyl-2-hydroxy-3-hydroxymethyl-benzyloxymethyl)-6-hydroxymethyl-phenol, 4-tert-butyl-2-[5-tert-butyl-3-(5-tert-butyl-2-hydroxy-3-hydroxymethyl-benzyloxymethyl) - 2 -hydroxy-benzyloxymethyl] - 6 - (5 - tert-butyl- 2 -hydroxy- 3 -hydroxymethyl-benzyloxymethyl)- phenol and were used as potential cross-reacting substances. In this study it is strongly indicated that the linear trimer XIII has a sensitizing capacity in the guinea pig which was significant when compared to the controls (p = 0.024). No cross-reactions were detected in animals induced with the linear trimer XIII. The linear trimer XIVa and the cyclic trimer XVIII failed to induce sensitization.

Allergens↗

Metabolism of 3-tert-butyl-4-hydroxyanisole by microsomal fractions and isolated rat hepatocytes.

3-tert-Butyl-4-hydroxyanisole is oxidatively metabolized in the presence of rat liver microsomes, reduced nicotinamide adenine dinucleotide phosphate, and oxygen to yield tert-butylhydroquinone, tert-butylquinone, and a polar metabolite(s). In the presence of human and rat liver microsomes or eight purified cytochrome P-450 isozymes reconstituted with NADPH-cytochrome P-450 reductase, this phenolic antioxidant is converted to the oxidoreduction-active metabolite, tert-butylquinone, that can stimulate the NADPH oxidase activities of these preparations by 2- to 7-fold. The rate of formation of each of the metabolites of 3-tert-butyl-4-hydroxyanisole was increased by pretreatment of rats with either 5,6-benzoflavone or phenobarbital. In addition the tert-butylhydroquinone and tert-butylquinone concentrations in solution reached apparent steady-state levels during metabolism; the steady-state concentrations were also increased by various animal pretreatment regimens. Furthermore it was shown that the metabolism of 3-tert-butyl-4-hydroxyanisole yielded material which was covalently bound to protein. In the presence of glutathione the rates of formation of the polar metabolite(s) were enhanced 3- to 4-fold, while covalently bound products were nearly stoichiometrically decreased. The increase in the amount of polar metabolite was due to the formation of a 3-tert-butyl-4-hydroxyanisole-glutathione conjugate. 3-tert-Butyl-4-hydroxyanisole was also oxidatively metabolized by rat lung microsomes to yield the polar metabolite(s) and tert-butylhydroquinone. The polar metabolite(s), tert-butylquinone, and tert-butylhydroquinone were also shown to be formed in isolated hepatocyte suspensions. They could be found as either the free hydroquinone, the sulfate conjugate, the glucuronide conjugate, and polar metabolites, presumedly the 3-tert-butyl-4-hydroxyanisole-glutathione conjugate. The total tert-butylhydroquinone concentration attained a steady-state level in a manner similar to that seen with the microsomal suspensions. In addition 3-tert-butyl-4-hydroxyanisole itself formed sulfate and glucuronide conjugates, the glucuronide being the major product.

Animals↗

The effect of 2,5-di-(tert-butyl)-1,4-hydroquinone on force responses and the contractile apparatus in mechanically skinned muscle fibres of the rat and toad.

In this study, we investigated the effect of the Ca2+ pump inhibitor, 2,5-di-(tert-butyl)-1,4-hydroquinone on the function of the contractile apparatus, Ca2+ uptake, the permeability of the sarcoplasmic reticulum to Ca2+ and excitation-contraction coupling, in mechanically skinned muscle fibres of the rat and toad. 2,5-di-(tert-butyl)-1,4-hydroquinone had no significant effect on the maximum force and Ca2+ sensitivity of the contractile apparatus in rat and toad fibres at concentrations of 20 and 5 microM respectively. In rat fibres, 2,5-di-(tert-butyl)-1,4-hydroquinone was found to inhibit sarcoplasmic reticulum Ca2+ loading in a dose dependent manner, with a half maximal effect at 2 microM. In toad fibres, 5 microM 2,5-di-(tert-butyl)-1,4-hydroquinone completely blocked sarcoplasmic reticulum Ca2+ loading. Exposure to 5 mM BAPTA revealed a small resting sarcoplasmic reticulum Ca2+ leak in unstimulated rat fibres. This Ca2+ leak was not significantly affected by the presence of 20 microM 2,5-di-(tert-butyl)-1,4-hydroquinone, suggesting that 2,5-di-(tert-butyl)-1,4-hydroquinone does not substantially block or activate the sarcoplasmic reticulum Ca2+ release channels. Depolarisation-induced force responses elicited in rat and toad skinned fibres were not significantly affected by 0.5 microM 2,5-di-(tert-butyl)-1, 4-hydroquinone. In the rat fibres, 5 and 20 microM 2,5-di-(tert-butyl)-1,4-hydroquinone greatly increased the peak and duration of initial depolarisation-induced force responses, while subsequent responses were reduced. 2,5-di-(tert-butyl)-1,4-hydroquinone did not affect excitation contraction coupling, as depolarisation-induced force responses similar to initial controls could be elicited after 2,5-di-(tert-butyl)-1,4-hydroquinone exposure, provided that the initial Ca2+ release in 2,5-di-(tert-butyl)-1,4-hydroquinone was chelated with 0.5 mM EGTA (to prevent Ca(2+)-dependent damage) and the sarcoplasmic reticulum was reloaded with Ca2+. In the toad fibres, 5 microM 2,5-di-(tert-butyl)-1, 4-hydroquinone had a similar effect on depolarisation-induced force responses to that observed at 20 microM 2,5-di-(tert-butyl)-1, 4-hydroquinone in rat fibres. This study shows that 2,5-di-(tert-butyl)-1,4-hydroquinone specifically and reversibly inhibits the sarcoplasmic reticulum Ca2+ pump in skeletal muscle and therefore, 2,5-di-(tert-butyl)-1,4-hydroquinone could be a valuable tool for investigating the role of the sarcoplasmic reticulum in Ca2+ homeostasis in skeletal muscle.

Animals↗

Effects of phenyl N-tert-butyl nitrone and its derivatives on the early phase of hepatocarcinogenesis in rats fed a choline-deficient, L-amino acid-defined diet.

The present study examined the effects of various derivatives of a radical trapping agent, phenyl N-tert-butyl nitrone, on the early phase of hepatocarcinogenesis in male Wistar rats fed a choline-deficient, L-amino acid-defined diet for 16 weeks. The derivatives used were 4-hydroxyphenyl (a physiologically major metabolite), 3-hydroxyphenyl, 2-hydroxyphenyl and 2-sulfoxyphenyl N-tert-butyl nitrone, and their effects were studied in a comparison with those of the parent compound, phenyl N-tert-butyl nitrone. The sizes of putatively preneoplastic, glutathione S-transferase placental form-positive lesions and the levels of extra-nuclear oxidative injury of hepatocytes, using the formation of 2-thiobarbituric acid-reacting substances as a parameter, were decreased by all doses (0.009%, 0.045% and 0.090% in diet) of 4-hydroxyphenyl N-tert-butyl nitrone and only by the highest dose of 3-hydroxyphenyl N-tert-butyl nitrone and phenyl N-tert-butyl nitrone. While 4-hydroxyphenyl N-tert-butyl nitrone, 3-hydroxyphenyl N-tert-butyl nitrone and phenyl N-tert-butyl nitrone all enhanced and inhibited hepatocellular apoptosis in preneoplastic lesions and their surrounding tissue, respectively, only 4-hydroxyphenyl N-tert-butyl nitrone additionally inhibited hepatocyte proliferation both in preneoplastic lesions and their surrounding tissue. 2-Hydroxyphenyl or 2-sulfoxyphenyl N-tert-butyl nitrone did not exert any of the above effects. These results suggest that the selective induction of apoptosis in preneoplastic hepatocyte populations plays a crucial role in the inhibition of hepatocarcinogenesis derived by phenyl N-tert-butyl nitrone and its effective derivatives. Further, the metabolic conversion to 4-hydroxyphenyl N-tert-butyl nitrone may also be important for the inhibitory effects of phenyl N-tert-butyl nitrone on hepatocarcinogenesis.

Amino Acids↗

Non-telomeric function deficiency of TERT enhances pressure overload-induced mouse cardiac remodeling by activation of CNBP-mediated THBS3/ITGB1 pathway.

Recent studies show that telomerase reverse transcriptase (TERT) possesses important new biological functions in gene transcription regulation, signal transduction, tumorigenesis, vascular development and mitochondrial DNA protection independent of the maintenance of telomere length. In this study we investigated the role and mechanisms of TERT in regulating the gene expression and signal transduction during pressure overload-induced cardiac remodeling. The first-generation TERT knockout (Tert-/-) and wild-type littermate control (Tert+/+) male mice were subjected to transverse aortic constriction (TAC) surgery to establish a pressure overload-induced cardiac remodeling model. We showed that pressure overload significantly increased TERT expression in the hearts at 8 weeks after TAC, whereas TERT deficiency remarkably exacerbated pressure overload-induced cardiac dysfunction, cardiac hypertrophy and fibrosis, and reduced the survival rate of the mice. In contrast, TERT overexpression reversed phenylephrine (PE)-stimulated cardiomyocyte hypertrophy and fibrosis in neonatal rat ventricular myocytes (NRVMs). Ttranscriptomic and proteomic analyses revealed that extracellular matrix (ECM)-receptor interaction was a key Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway regulated by TERT in hemodynamic overload-induced cardiac remodeling. TERT knockdown greatly enhanced, while TERT overexpression inhibited the activation of the THBS3/ITGB1 signaling pathway, in which transcription factor cellular nucleic acid-binding protein (CNBP) played a pivotal mediating role by interacting with TERT. In conclusion, the non-telomeric function of TERT in gene transcription regulation and signaling transduction plays an important role during pressure overload-induced myocardial remodeling via modulating CNBP-mediated THBS3/ITGB1 signaling pathway, which provides new targets and strategies for the prevention and treatment of pressure overload-induced cardiac remodeling.

Animals↗

Low-molecular-weight contact allergens in p-tert-butylphenol-formaldehyde resin.

BACKGROUND: p-tert-Butylphenol-formaldehyde resin (PTBPFR) is a contact allergen that is included in most standard patch test series. This resin consists of a large number of substances most of which are unknown. OBJECTIVE: The aim of this study was to investigate if allergens in PTBPFR are molecules mainly of low (MW < 250), medium, or high molecular weight (MW > 1,000); to isolate and identify some of the low molecular weight components of the resin; and for new substances to determine if these were allergens. METHODS: Gel permeation chromatography, patch testing, high-pressure liquid chromatography, mass spectrometry, and nuclear magnetic resonance spectrometry were used. RESULTS: Patch test reactions indicated allergens in low-, medium-, and high-molecular-weights fractions. The strongest patch test reactivity was seen to a medium molecular weight fraction constituting only 6% wt/wt of the resin for 4 of the patients. Two patients reacted positively to low molecular weight fractions, and one of these patients reacted only to these fractions. The following substances were isolated: 4-tert-butyl-[1,2]benzoquinone, 4-tert-butyl-2,6-bis-hydroxymethyl-phenol, 4-tert-butylbenzene-1,2-diol, 4-tert-butyl-2-hydroxymethyl-phenol, 5-tert-butyl-2-hydroxy-3-hydroxymethyl-benzaldehyde, 4-tert-butyl-2-hydroxymethyl-6-methoxymethyl-phenol, and p-tert-butylphenol. Patients reacted positively to 5-tert-butyl-2-hydroxy-3-hydroxymethyl-benzaldehyde and 4-tert-butyl-2-hydroxymethyl-6-methoxymethyl-phenol but not to 4-tert-butyl-[1,2]benzoquinone. CONCLUSION: Two new allergens in PTBPFR were found: 5-tert-butyl-2-hydroxy-3-hydroxymethyl-benzaldehyde and 4-tert-butyl-2-hydroxymethyl-6-methoxymethyl-phenol.

Allergens↗

Sensitizing capacity of two monomeric aldehyde components in p-tert-butylphenol-formaldehyde resin.

Contact allergy to p-tert-butylphenol-formaldehyde resin is not rare. This resin consists of a large number of substances, most of which are unknown. For diagnostic and preventive reasons, the chemical identity of the sensitizers should be known as well as their sensitizing capacities, cross-reaction patterns and presence in the environment. The aim of this study was to investigate the sensitizing capacities and cross-reaction patterns for 5-tert-butyl-2-hydroxy-3-hydroxymethyl-benzaldehyde and 5-tert-butyl-2-hydroxy-benzaldehyde in the guinea pig maximization test. 2,6-Dimethylol p-tert-butylphenol, p-tert-butylcate chol, 2-methylol p-tert-butylphenol, p-tert-butylphenol, 4-tert-butyl-2-(5-tert-butyl-2-hydroxy-3-hydroxymethyl-benzyloxymethyl)-6-hydroxymethyl-phenol and 4-tert-butyl-2-(5-tert-butyl-2-hydroxy-benzyloxymethyl)-phenol were used as potential cross-reacting substances. 5-tert-Butyl-2-hydroxy-3-hydroxymethyl-benzaldehyde was shown to be a sensitizer (p = 0.041). In animals induced with this compound no cross-reactions to the putative cross-reacting substances were seen. In contrast, 5-tert-butyl-2-hydroxy-benzaldehyde failed to induce sensitization and no cross-reactions were detected.

Allergens↗

The telomerase RNA component Terc is required for the tumour-promoting effects of Tert overexpression.

A role for the telomerase reverse transcriptase subunit (Tert) in tumorigenesis independent of telomere length is emerging. K5-Tert mice, which overexpress Tert in the skin, show increased tumorigenesis and faster wound healing than wild-type controls. Here, we demonstrate that the telomerase RNA component Terc is necessary to mediate these effects of Tert overexpression. In contrast to K5-Tert mice, K5-Tert mice in a Terc-deficient background, K5-Tert/Terc-/-, do not show increased tumorigenesis or increased wound healing compared with wild-type controls. Indeed, K5-Tert/Terc-/- mice show a reduction in tumour growth compared with Terc-/- controls, indicating an inhibitory effect of Tert overexpression in the absence of Terc. These results indicate that the tumour-promoting effects of Tert overexpression require the formation of Tert-Terc complexes. In addition, we show that the increased expression of Tert in the absence of Terc has an inhibitory effect on tumorigenesis, independently of telomere length and telomerase activity. These findings highlight Terc as a target for telomerase-based anticancer therapies.

Animals↗

TERT promoter mutations and recurrence patterns in differentiated thyroid carcinoma.

Telomerase reverse transcriptase promoter mutations (TERT) are known prognostic factors associated with poor outcomes in differentiated thyroid carcinoma (DTC). We analyzed differences in DTC recurrence patterns over time according to TERT. A retrospective review was conducted on DTC patients who achieved remission after total thyroidectomy and/or radioactive iodine treatment at Samsung Medical Center between 1994 and 2004. The sites and patterns by time of recurrence in the patients were reviewed. In total, 367 patients with a median follow-up of 14 years (interquartile range, 12-17 years) were included. Recurrence occurred in 91 patients, wherein 56 had lymph node recurrence and 35 had either local or distant recurrence. TE RT and tumor size <2 cm were independent factors for recurrence in the Cox proportional hazards analysis. In cases of TERT-wild type (WT), the recurrence rate decreased significantly over time after diagnosis, whereas in TERT-mutant type (MT), a consistently high recurrence rate was observed. In the Kaplan-Meier analysis, TERT-MT exhibited a significantly poorer disease-free survival, with continuous recurrence over time, whereas in TERT-WT, the curve showed a gradual decline. Further analysis of the overall survival among the 91 patients revealed that TERT-MT was significantly associated with a higher risk of mortality, whereas TERT-WT exhibited a slowly decreasing curve. In conclusion, TERT-MT was a significant adverse prognostic factor wherein continuous recurrence necessitates long-term follow-up. For TERT-WT, the recurrence rate decreased compared to TERT-MT, and even in cases of recurrence, the treatment outcomes are favorable.

Humans↗