The minimum effective amount of uncouplers for rat liver mitochondria.
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Adenosine Triphosphate↗
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Results for “Benzylidene Compounds”
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Sodium benzylideneascorbate induces apoptosis in HIV-replicating U1 cells.
U1 cells, a subclone of U937 cells chronically infected with human immunodeficiency virus type 1 (HIV-1), produced HIV-1 only in the presence of inducers such as 12-O-tetradecanoxylphorbol 13-acetate (TPA) or tumor necrosis factor (TNF)-alpha. The expression of HIV-antigen on U1 cells induced by TPA or TNF-alpha was found to be prevented by sodium 5,6-benzylidene-L-ascorbate (SBA) in a concentration-dependent manner. Treatment of U1 cells with SBA in the presence of inducers resulted in cell death with cell shrinkage, chromatin condensation and DNA fragmentation into nucleosomal oligomers, characteristics of apoptosis. In contrast, SBA had scarcely any apoptotic effect on U1 cells in the absence of inducers. SBA did not also induce apoptosis in parental U937 cells in the presence or absence of inducers. These results suggest that HIV-replicating U1 cells selectively undergo apoptosis on treatment with SBA.
Antiviral Agents↗
The p15 matrix protein of moloney murine leukemia virus is a phosphotyrosine protein.
Retroviruses have been etiologically implicated with leukemia in humans and animals. Understanding the virus life cycle, the proteins and enzymes involved in its replication, is essential for developing potent anti-viral drugs. Phosphorylation of retroviral proteins may alter their shape in such a way as to increase or inhibit their biological activities and thus influence the replication and pathogenic potential of the retroviruses. In our previous work, we demonstrated that non-cytotoxic doses of tyrphostins (protein tyrosine kinase blockers) inhibit moloney murine leukemia virus (Mo-MuLV) replication in acutely and chronically infected cells. In an attempt to understand their mode of action as anti-MoMuLV drugs, we examined the possibility that a viral protein is phosphorylated in tyrosine. Indeed, in our present work, we show that the p15 matrix protein (MA) of Mo-MuLV is a phosphotyrosine protein and is the only viral protein which is phosphorylated on tyrosine. Moreover, treatment of Mo-MuLV/NIH/3T3 chronically infected cells with tyrphostin AG-555 specifically inhibits the synthesis of p15 and other viral proteins but does not affect the synthesis of cellular proteins. Our results suggest that tyrosine phosphorylation of p15 MA protein may play a pivotal role in Mo-MuLV replication.
3T3 Cells↗
Spinal delta 2 but not delta 1 opioid receptors are involved in intracerebroventricular beta-endorphin-induced antinociception in the mouse.
The antinociception induced by beta-endorphin given intracerebroventricularly (i.c.v.) has been previously demonstrated to be mediated by the release of Met-enkephalin and subsequent stimulation of delta receptors in the spinal cord for antinociception. The present study was designed to determine what type of opioid receptor, delta 1 or delta 2, in the spinal cord is involved in i.c.v. beta-endorphin-induced antinociception. Antinociception was assessed by the tail-flick test in male ICR mice. NTB (0.2-20 nmol) and NTI (0.22-2.2 nmol), selective delta 2 receptor antagonists, given intrathecally (i.t.) dose-dependently attenuated i.c.v. beta-endorphin-induced inhibition of the tail-flick response. On the other hand, BNTX (0.02-2.2 nmol), a selective delta 1 receptor antagonist, given i.t., did not block i.c.v. beta-endorphin-induced antinociception. The tail-flick inhibition induced by DAMGO, a mu receptor agonist, or U50,488H, a kappa receptor agonist, was not blocked by i.t. BNTX, NTB or NTI. It is concluded that delta 2 but not delta 1 receptors in the spinal cord are involved in i.c.v. beta-endorphin-induced antinociception.
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
7-Benzylidenenaltrexone (BNTX): a selective delta 1 opioid receptor antagonist in the mouse spinal cord.
Recent reports provided evidence that at least two delta opioid receptors may mediate antinociception in mice. In this study, we studied further the involvement of delta opioid receptor subtypes in mediating antinociception at spinal sites in mice using subtype selective agonists and antagonists. The antinociceptive ED50 values (95% C.I.) of i.t. administered DPDPE [(D-Pen2, D-Pen5)enkephalin] (delta 1 receptor agonist) and DELT II [(D-Ala2)deltorphin II] (delta 2 receptor agonist) were 6.3 (5.2-7.6) and 6.4 (5.4-7.7) nmol/mouse, respectively. Administration of BNTX, s.c. increased the antinociceptive ED50 value of DPDPE 5.9-fold whereas that of DELT II was not changed significantly. On the other hand administration of naltriben (NTB, the benzofuran derivative of naltrindole), s.c. increased the antinociceptive ED50 value of DELT II 12.5-fold but did not alter that of DPDPE. Similarly administration of BNTX, i.t. increased the antinociceptive ED50 value of DPDPE 4-fold without altering significantly that of DELT II. NTB given i.t. enlarged the antinociceptive ED50 of DELT II 11-fold without affecting significantly that of DPDPE. BNTX, s.c. did not alter the antinociceptive ED50 values of the mu-agonists, DAMGO [(D-Ala2,MePhe4,Gly-ol5) enkephalin] and morphine or that of the kappa-agonist, U50,488H [trans(+/-)-3,4-dichloro-N-methyl-N-[2-(1- pyrrolidinyl-cyclohexyl]benzeneacetamide] These results demonstrate that BNTX is highly selective for delta 1 opioid receptors at spinal sites. Also, the present data provide for the involvement of both delta 1 and delta 2 opioid receptors in mediating antinociception at spinal sites in mice.
Analgesics↗
The mixed antinociceptive agonist-antagonist activity of beta-endorphin(1-27) in mice.
beta-Endorphin(1-27) (i.c.v.) has been reported to inhibit the antinociceptive activity of i.c.v. administered beta-endorphin in mice. In this study the antagonist activity of beta-endorphin(1-27) has been confirmed and the antagonism appears to be mediated at delta 1 opioid receptors. At higher doses than that used for antagonism, i.c.v. administered beta-endorphin(1-27) was a full antinociceptive agonist. The antinociceptive activity of beta-endorphin is attributed to the release of met-enkephalin in the spinal cord and is antagonized by the selective delta 2 opioid receptor antagonist, naltriben (NTB) but not by the selective delta 1 opioid receptor antagonist, 7-benzylidenenaltrexone (BNTX). In contrast, the antinociceptive activity of i.c.v. administered beta-endorphin(1-27) was not affected by either NTB or BNTX administered i.c.v. or i.t. Also, the antinociceptive activity of beta-endorphin(1-27) was unaffected by the selective mu opioid receptor antagonist, beta-funaltrexamine (beta-FNA) or the selective kappa opioid receptor antagonist, norbinaltorphimine (norBNI). Thus, beta-endorphin(1-27) appears to mediate antinociception supraspinally through the interaction of a unique receptor, i.e. a receptor that is different from mu, kappa, delta 1 or delta 2 opioid receptors. Alternatively, a non-opioid mechanism may be considered.
Animals↗
Evidence for delta opioid receptor subtypes regulating adenylyl cyclase activity in rat brain.
Opioid agonists selective for mu- or delta opioid receptors inhibit adenylyl cyclase in membranes from rat caudate-putamen and nucleus accumbens. The presence of subtypes of delta opioid receptors has been suggested. In both brain regions we have found that the inhibition of adenylyl cyclase by DPDPE was more readily antagonized by 7-benzylidenenaltrexone (BNTX), than by naltriben. In contrast, the inhibitory effects of deltorphin-II and DSLET were more readily antagonized by naltriben, than by BNTX. Neither naltriben nor BNTX significantly antagonized the effect of a mu selective agonist. These results suggest that inhibition of adenylyl cyclase in caudate-putamen and nucleus accumbens is regulated by two forms of delta-opioid receptor with ligand selectivities similar to those two forms proposed to mediate analgesic effect.
Adenylyl Cyclase Inhibitors↗
Supraspinal delta receptor subtype activity of heroin and 6-monoacetylmorphine in Swiss Webster mice.
The purpose of this study was to determine which delta (delta) opioid receptor subtype, delta 1 or delta 2, was involved in producing the antinociceptive action of heroin and 6-monacetylmorphine (MAM) in Swiss Webster mice. Previous work from this laboratory established that heroin and MAM, given intracerebroventricularly (i.c.v.) in Swiss Webster mice, produce antinociception through activation of supraspinal delta receptors. Naltrindole, but not naloxone or nor-binaltorphimine, antagonizes the inhibitory action of heroin and MAM in the tail-flick test. Recent literature documents the occurrence of subtypes of the delta opioid receptor and the availability of selective antagonists. 7-Benzylidenenaltrexone (BNTX) antagonizes the antinociception induced by delta 1 receptor agonists without affecting that induced by delta 2 receptor agonists. Naltriben (NTB) selectively inhibits delta 2- but not delta 1-induced antinociception. In the present study BNTX and NTB were administered i.c.v. with heroin and MAM to determine the delta receptor subtype responsible for inhibition of the tail-flick response in Swiss Webster mice. The ED50 for heroin-induced antinociception was increased 19-fold by BNTX and was not altered by NTB administration. On the other hand, the ED50 value of MAM was increased 3-fold by NTB and was not altered by BNTX administration. These results suggest that heroin activated supraspinal delta 1 receptors and MAM acted on supraspinal delta 2 receptors to produce antinociception in Swiss Webster mice.
Animals↗
The role of delta-opioid receptor subtypes in cocaine- and methamphetamine-induced place preferences.
The effects of delta-receptor antagonists on cocaine- and methamphetamine-induced place preferences were examined in rats. Cocaine- and methamphetamine-induced place preferences were significantly attenuated by naltrindole (NTI: a non-selective delta-opioid receptor antagonist). Furthermore, naltriben (NTB: a selective delta 2-opioid receptor antagonist), but not 7-benzylidenenaltrexone (BNTX: a selective delta 1-opioid receptor antagonist), attenuated the cocaine- and methamphetamine-induced place preferences. These results suggest that delta-opioid receptors, particularly delta 2-opioid receptors, may be involved in the reinforcing effects of cocaine and methamphetamine.
Animals↗
Streptozotocin-induced diabetes selectively enhances antinociception mediated by delta 1- but not delta 2-opioid receptors.
We assessed the effect of diabetes on antinociception produced by intracerebroventricular injection of delta-opioid receptor agonists [D-Pen2,5]enkephalin (DPDPE) and [D-Ala2]deltorphin II. The antinociceptive effect of DPDPE (10 nmol), administered i.c.v., was significantly greater in diabetic mice than in non-diabetic mice. The antinociceptive effect of i.c.v. DPDPE was significantly reduced in both diabetic and non-diabetic mice following pretreatment with 7-benzylidenenaltrexone (BNTX), a selective delta 1-opioid receptor antagonist, but not with naltriben (NTB), a selective delta 2-opioid receptor antagonist. There were no significant differences in the antinociceptive effect of [D-Ala2]deltorphin II (3 nmol, i.c.v.) in diabetic and non-diabetic mice. Furthermore, the antinociceptive effect of i.c.v. [D-Ala2]deltorphin II was significantly reduced in both diabetic and non-diabetic mice following pretreatment with NTB, but not with BNTX. In conclusion, mice with diabetes are selectively hyper-responsive to supraspinal delta 1-opioid receptor-mediated antinociception, but are normally responsive to activation of delta 2-opioid receptors.
Analgesia↗
Differential mediation of cold water swim stress-induced antinociception by delta-opioid receptor subtypes in diabetic mice.
The involvement of delta-opioid receptor subtypes in cold water swim stress (CWSS)-induced antinociception in diabetic mice was compared with that in non-diabetic mice. Three-minute swim stress produced significant antinociception in both diabetic and non-diabetic mice as determined by the tail-pinch test. However, the extent of CWSS-induced antinociception in diabetic mice was significantly greater than that in non-diabetic mice. Pretreatment with naltriben, a selective delta 2-opioid receptor antagonist, significantly attenuated CWSS-induced antinociception in both non-diabetic and diabetic mice. In contrast, although 7-benzylidenenaltrexone, a selective delta 1-opioid receptor antagonist, significantly attenuated CWSS-induced antinociception in diabetic mice, it had no effect in non-diabetic mice. These results suggest that CWSS-induced antinociception in non-diabetic mice is mediated by delta 2-opioid receptors, whereas CWSS-induced antinociception in diabetic mice is mediated by both delta 1- and delta 2-opioid receptors. Furthermore, the enhanced CWSS-induced antinociception in diabetic mice may be due to the activation of delta 1-opioid receptors.
Analgesia↗
In vivo labeling of delta opioid receptors in mouse brain by [3H]benzylidenenaltrexone, a ligand selective for the delta 1 subtype.
(E)-7-Benzylidenenaltrexone (BNTX) is a selective ligand for the putative delta 1 (delta 1) opioid receptor. To explore the feasibility of labeling delta 1 sites in vivo; we determined the cerebral distribution of radioactivity after systemic administration of [3H]BNTX to CD1 mice. Uptake was highest in striatum and lowest in cerebellum throughout the 4 hr time course. Specific radioligand binding, approximated as the difference in radioactivity concentrations between striatum and cerebellum, peaked at 0.32 percent injected dose/g at 30 min and comprised a modest 23% of total striatal radioactivity. For seven brain regions, radioactivity concentrations correlated with delta site densities known from prior in vitro studies (rS = 0.79, p = 0.03), and also with the uptake of N1'-([11C]methyl)naltrindole in vivo (rS = 0.78, p = 0.04) in mice. Specific binding in striatum, olfactory tubercles and cortical regions was saturable by BNTX, and was inhibited stereoselectively by the optical isomers of naloxone. Naltrindole and naltriben (NTB), delta antagonists, blocked 65-99% of [3H]BNTX specific binding at a dosage of 5.0 mumol/kg. Similar doses of the mu antagonist cyprodime, or the kappa agonist U50,488H, did not inhibit binding. Adjusted for the four-fold greater brain penetration of NTB relative to BNTX, dose-response studies suggested that delta 1 selective BNTX (ED50 = 1.51 mumol/kg) was 50% more potent than delta 2 selective NTB (ED50 = 0.56 mumol/kg) in blocking specific [3H]BNTX binding in striatum. In CXBK mice, a strain with functional delta 1 but not delta 2 receptors in antinociceptive assays, radioligand uptake and distribution proved similar to that in CD1 mice. In sum, [3H]BNTX labels murine delta opioid receptors in vivo with a low extent of specific binding. The data is consistent with, but not conclusive for, selective labeling of the delta 1 subtype.
Animals↗
Use of antisense oligodeoxynucleotide to determine delta-opioid receptor involvement in [D-Ala2]deltorphin II-induced locomotor hyperactivity.
Intracerebroventricularly (i.c.v.)-administered [D-Ala2]deltorphin II (20 micrograms) produced a marked locomotor hyperactivity in male ICR mice. The locomotor hyperactivity induced in response to i.c.v. [D-Ala2]deltorphin II (20 micrograms) was suppressed by pretreatment with naltriben (NTB, 10 micrograms) but not 7-benzylidene naltrexone (BNTX, 1 microgram) and D-Phe-Cys-Tyr-D-Try-Orn-Thr-Phe-Thr-NH2 (CTOP, 100 ng). The influence of antisense oligodeoxynucleotide to delta-opioid receptor mRNA (delta-AS oligo) or a mismatch oligodeoxynucleotide (MM oligo) on the locomotor hyperactivity induced by [D-Ala2]deltorphin II was determined. Groups of mice pretreated i.c.v. with delta-AS oligo (1 microgram), MM oligo (1 microgram) or saline (4 microliters) once a day for 3 days, were injected i.c.v. [D-Ala2]deltorphin II (10 or 20 micrograms) and the locomotor response to [D-Ala2]deltorphin II was measured. The locomotor hyperactivity of i.c.v. [D-Ala2]deltorphin II (10 or 20 micrograms) were significantly suppressed by i.c.v. pretreatment with delta-AS oligo but not MM oligo. The present results indicate that pretreatment with delta-AS oligo suppresses mouse locomotor hyperactivity produced by stimulation of delta 2-opioid receptors in the brain.
Amino Acid Sequence↗
Effect of methylmercury on brain acetylcholine concentration and turnover in mice.
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Acetylcholine↗
The effect of a new non-steroidal anti-inflammatory agent, sulindac, on platelet function.
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Anti-Inflammatory Agents↗
The sensitization potential of some perfume ingredients tested using a modified draize procedure.
A modified Draize procedure was used to test 23 natural and 46 synthetic perfume ingredients for their potential to induce allergic contact dermatitis in guinea pigs. Fifty-three ingredients did not induce sensitization. Two synthetic ingredients showed a strong sensitization potential and 14 ingredients, 7 natural and 7 synthetic, showed a weak sensitization potential. The findings indicate that there is little risk of sensitization in man to most of these perfume ingredients.
Animals↗
Spectral properties of chlorophyll a in liquid crystal.
Solution of chlorophyll a in liquid crystals mixture (MBBA + EBBA) was investigated. Chl molecules are in LC in low electric field oriented. They can be divided into two groups: one strongly interacting with LC and subjected to reorientation by the electric field, and another weakly interacting with the solvent and insensitive to the voltage applied. The emission spectrum of the first type of chlorophyll is strongly perturbed. At higher voltages, the pigment molecules orientation in the plane of the electrode is another. Pigment absorption and emission anisotropy provides information about the reorientation of LC molecules. Even at high (10(-3)M) Chl concentration and regular pigment array, the interaction between the pigment and solvent exceeds pigment-pigment interaction because the solvent appears to have a stronger influence on the Chl spectrum.
Benzylidene Compounds↗
Resonance Raman spectra of chlorophylls dissolved in liquid crystal matrices. I. The interaction between chlorophylls and a liquid crystalline MBBA + EBBA mixture.
The resonance Raman (RR) spectra of chlorophyll (Chl) a, Chl b and pheophytin a dissolved in a liquid-crystalline MBBA + EBBA mixture were measured. The RR frequencies of chlorophylls in the liquid crystal (LC) are compared with those of solutions of various chlorophyll monomers and aggregates taken from the literature. It is concluded that Chl a and Chl b in LC exist largely as the solvated monomers, even at high concentration. The magnesium atoms in both Chl a and Chl b are pentacoordinated.
Benzylidene Compounds↗