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PubMed1996

Reactivation of denatured proteins by 23S ribosomal RNA: role of domain V.

Escherichia coli ribosome, its 50S subunit, or simply the 23S rRNA can reactivate denatured proteins in vitro. Here we show that protein synthesis inhibitors chloramphenicol and erythromycin, which bind to domain V of 23S rRNA of E. coli, can inhibit reactivation of denatured pig muscle lactate dehydrogenase and fungal glucose-6-phosphate dehydrogenase by 23S rRNA completely. Oligodeoxynucleotides complementary to two regions within domain V (which cover sites of chloramphenicol resistant mutations and the putative A site of the incoming aminoacyl tRNA), but not to a region outside of domain V, also can inhibit the activity. Domain V of 23S rRNA, therefore, appears to play a crucial role in reactivation of denatured proteins.

Animals↗
PubMed2000

Comparison of oxime-initiated reactivation of organophosphorous-inhibited acetylcholinesterase in brains of avian embryos.

Organophosphorous (OP) insecticide-induced inhibition and oxime reactivation of acetylcholinesterase (AChE) was determined in whole-brain homogenates prepared from 15-d-old chick embryos. Doses of chlorpyrifos, parathion, acephate, and trichlorfon that inhibited AChE >70% were administered to the embryos. Following insecticide exposure, an in vitro system compared the capability of the oximes pralidoxime (2-PAM), obidoxime, TMB-4, and HI-6 to reactivate the OP-inhibited AChE. Concentration-related increases in AChE activities were noted in embryo brains reactivated with 2-PAM, TMB, and HI-6. 2-PAM was the most effective reactivator of trichlorfon-inhibited AChE; 2-PAM and obidoxime were relatively similar in effectiveness for reactivation of AChE inhibited with the other OP insecticides used as test agents. All oximes were similarly effective against acephate, but HI-6 was the least effective reactivator of AChE in chick embryo brain homogenates inhibited by the other OP insecticides. These results suggest that both the OP insecticide inhibiting AChE and the oxime reactivating this enzyme can contribute to the effectiveness of the avian brain AChE reactivation.

Acetylcholinesterase↗
PubMed1988

Sulfur derivatives of 2-oxopropanal oxime as reactivators of organophosphate-inhibited acetylcholinesterase in vitro: synthesis and structure-reactivity relationships.

We have prepared four new oximes, 1b-e, which conform to the general structure RCH2COCH = NOH where R = CH3S, CH3SO, CH3SO2, and (CH3)2S+, respectively, and have the same E configuration as the parent 2-oxopropanal oxime 1a (R = H, MINA). The pKa values range from 6.54 (1e) to 8.16 (1b), as compared with 8.30 for 1a. Rates of reaction (kappa 1) with 4-nitrophenyl acetate indicate that the oximate anions have a much higher nucleophilicity than common oxyanions of similar basicities: the alpha effects measured for 1a-e are of the order of 200-250. The abilities of 1b-e to reactivate acetylcholinesterase (AChE) inhibited by organophosphates have been evaluated. In vitro experiments reveal a significant reactivation potency of 1b-e against VX-, sarin-, and paraoxon-inhibited immobilized eel AChE. The highly lipophilic methylthio oxime 1b (log P greater than 1) is intrinsically (kappa 2) 3 times more reactive than the more basic MINA (log P less than 1). The sulfonium oxime 1e is a potent reactivator against paraoxon. Interestingly, both 1b and 1e have a low toxicity and they exhibit a significant antidotal effect at a relative low dose against paraoxon in rats.

Acetylcholinesterase↗
PubMed1979

Leukocyte migration inhibition assay in patients with bladder cancer.

The leukocyte migration inhibition assay has demonstrated successfully tumor-associated antigenic activity in protein extracts of cell culture lines of a number of neoplasms. Our data have shown a high degree of leukocyte migration inhibition reactivity with protein extracts from the well characterized T-24 transitional carcinoma cell line. Thus, the leukocyte migration inhibition assay may prove a valuable method of in vitro assessment of the cell-mediated immunity of bladder cancer patients and as a method to monitor attempts at further purification of tumor-associated antigens.

Antigens, Neoplasm↗
PubMed2006

Inhibition of sulfotransferases by xenobiotics.

The sulfotransferase (SULT) family comprises important phase II conjugation enzymes for the detoxification of xenobiotics and modulation of the activity of physiologically important endobiotics such as thyroid hormones, steroids, and neurotransmitters. SULT enzymes catalyze the transfer of a sulfuryl group, donated by 3'-phosphoadenosine-5'-phosphosulfate (PAPS), to an acceptor substrate that may be a hydroxy group or an amine group in a process originally called sulfation, but more correctly referred to as sulfonation or sulfurylation. SULT activity may be inhibited when humans are exposed to certain xenobiotics including drugs (mefenamic acid, salicylic acid, clomiphene, danazol etc.), dietary chemicals (catechins, food colorants, flavonoids and phytoestrogens etc.), and environmental chemicals (hydroxylated polychlorinated biphenyls, hydroxylated polyhalogenated aromatic hydrocarbons, pentachlorophenol, triclosan and bisphenol A, etc.). Inhibition of individual SULT isoforms may cause adverse effects on human health. For example, hydroxylated polychlorinated biphenyls have been shown to interfere with the transport of thyroid hormones, inhibit estradiol sulfonation, and inhibit thyroid hormone sulfonation, thereby potentially disrupting the thyroid hormone system. Formation of sulfate conjugates of toxic xenobiotics usually decreases their toxicity, so inhibition of this pathway may lead to prolonged exposure to the compounds. Conversely, some sulfate conjugates are chemically reactive, inhibition of their formation may protect from toxicity. This manuscript will review the literature concerning the inhibition of SULTs by xenobiotics including isoform-selective effects, inhibition kinetics and health effects resulting from the inhibition.

Animals↗
PubMedDate not supplied

Oxime-induced reactivation of carboxylesterase inhibited by organophosphorus compounds.

A structure-activity analysis of the ability of oximes to reactivate rat plasma carboxylesterase (CaE) that was inhibited by organophosphorus (OP) compounds revealed that uncharged oximes, such as 2,3-butanedione monoxime (diacetylmonoxime) or monoisonitrosoacetone, were better reactivators than cationic oximes. Cationic oximes that are excellent reactivators of OP-inhibited acetylcholinesterase, such as pyridine-2-aldoxime or the bis-pyridine aldoximes, HI-6 and TMB-4, produced poor reactivation of OP-inhibited CaE. The best uncharged reactivator was 2,3-butanedione monoxime, which produced complete reactivation at 0.3 mM in 2 h of CaE that was inhibited by phosphinates, alkoxy-containing phosphates, and alkoxy-containing phosphonates. Complete reactivation of CaE could be achieved even after inhibition by phosphonates with highly branched alkoxy groups, such as sarin and soman, that undergo rapid aging with acetylcholinesterase. CaE that was inhibited by phosphonates or phosphates that contained aryloxy groups were reactivated to a lesser extent. The cause of this decreased reactivation appears to be an oxime-induced aging reaction that competes with the reactivation reaction. This oxime-induced aging reaction is accelerated by electron-withdrawing substituents on the aryloxy groups of phosphonates and by the presence of multiple aryloxy groups on phosphates. Thus, reactivation and aging of OP-inhibited CaE differ from the same processes for OP-inhibited acetylcholinesterase in both their oxime specificity and inhibitor specificity and, presumably, in their underlying mechanisms.

Animals↗
PubMed1987

Sequence of protective epitopes of streptococcal M proteins shared with cardiac sarcolemmal membranes.

Synthetic peptide fragments spanning the entire amino acid sequence of pep M5 were used to detect epitopes cross-reactive with heart tissue components other than myosin. Heart-cross-reactive pep M5 antibodies were affinity purified by absorption to and elution from purified sarcolemmal membranes. Only one of the synthetic peptides, SM5(164-197)C, inhibited reactivity of the affinity-purified antibodies with pep M5 by ELISA. SM5(164-197)C linked to KLH evoked both opsonic and heart-cross-reactive antibodies in rabbits. In addition to type 5, the immune sera opsonized M types 6, 18, 19, and 49 streptococci. The antisera reacted strongly with isolated cardiac sarcolemmal membranes by immunofluorescence. In Western blots of cardiac tissue, the anti-SM5(164-197)C reacted with a 40 kDa protein but not with myosin. The reaction was inhibited by pep M5 and SM5(164-197)C but not by any of the other peptides spanning pep M5. The cross-reactive anti-SM5(164-197)C affinity purified on sarcolemmal membranes opsonized types 5, 6, and 19 but not type 24 streptococci. These results indicate that SM5(164-197)C contains heart-cross-reactive, opsonic epitopes that are shared among heterologous serotypes of group A streptococci.

Amino Acid Sequence↗
PubMed2001

Cryptic epitopes in N-terminally truncated prion protein are exposed in the full-length molecule: dependence of conformation on pH.

Prion diseases are diseases of protein conformation. Structure-dependent antibodies have been sought to probe conformations of the prion protein (PrP) resulting from environmental changes, such as differences in pH. Despite the absence of such antibodies for full-length PrP, a recombinant Fab (D13) and a Fab derived from mAb 3F4 showed pH-dependent reactivity toward epitopes within the N-terminus of N-terminally truncated PrP(90-231). Refolding and maintaining this protein at pH > or =5.2 before immobilization on an ELISA plate inhibited reactivity relative to protein exposed to pH < or =4.7. The reactivity was not affected by pH changes after immobilization, showing retention of conformation after binding to the plate surface, although guanidine hydrochloride at 1.5-2 M was able to expose the cryptic epitopes after immobilization at pH > or =5.2. The alpha-helical CD spectrum of PrP(90-231) refolded at pH 5.5 was reduced somewhat by these pH changes, with a minor shift toward beta-sheet at pH 4 and then toward coil at pH 2. No covalent changes were caused by the pH differences. This pH dependence suggests titration of an acidic region that might inhibit the N-terminal epitopes. A similar pH dependence for a monoclonal antibody reactive to the central region identified an acidic region incorporating Glu152 as a significant participant.

Amino Acid Sequence↗
PubMed1998

Effects of vitamin E and/or C on reactive oxygen species-related lead toxicity in the rat sperm.

This study was undertaken to investigate whether treatment with vitamin E (VE) and/or vitamin C (VC) protects rat sperm by inhibiting reactive oxygen species generation induced by lead (Pb) exposure. Male Sprague-Dawley rats were assigned to the following five groups: vitamin-unsupplemented; 150 mg VE/kg chow supplemented; 300 mg VE/kg chow supplemented; 500 mg VC/l drinking water supplemented and 150 mg VE/kg chow + 500 mg VC/l drinking water supplemented group. Rats in each group were divided into Pb-unexposed and Pb-exposed subgroups, received weekly intraperitoneal injection of 10 mg sodium acetate or 10 mg Pb acetate/kg for 6 weeks, respectively. The blood and sperm Pb levels were analyzed by graphite furnace atomic absorption spectrophotometer. Chemiluminescence was measured to evaluate the generation of sperm reactive oxygen species (ROS). Motility and sperm-oocyte penetration rate (SOPR) were measured. In Pb-unexposed rats, epididymal sperm counts, motility, ROS, and SOPR were not different in the five supplemented groups. Lead exposure might decrease the defense capacity of sperm to the oxidative stress and therefore elevate the ROS generation, reduce sperm motility, and reduce SOPR. Supplementation with VE and/or VC reduced ROS generation, prevented loss of motility and capacity of oocyte penetration in Pb-exposed rats. This study suggests that supplementation with VE and/or VC inhibits Pb-related ROS generation, protects spermatozoa from loss of motility and oocyte penetration capability.

Animals↗
PubMed1998

Thermal injury induces macrophage hyperactivity through pertussis toxin-sensitive and -insensitive pathways.

C57BL/6 mice were subjected to a full thickness scald thermal injury covering 25% of their total body surface area, and thioglycollate elicited peritoneal macrophages (Mphi were isolated 4 days later. Mphi from injured mice produced significantly greater amounts of reactive nitrogen intermediates and tumor necrosis factor-alpha in response to lipopolysaccharide and lipid A. Pertussis toxin (PTX) treatment of Mphi dose-dependently inhibited reactive nitrogen intermediate production in Mphi from sham-treated mice; however, Mphi from injured mice were insensitive to PTX-mediated inhibition. Conversely, tumor necrosis factor-alpha production was enhanced by PTX treatment, with Mphi from injured mice being more sensitive than Mphi from sham-treated mice to this effect of PTX. These results indicate that thermal injury increases Mphi sensitivity to lipopolysaccharide by a mechanism that is both PTX sensitive and PTX insensitive, thereby suggesting a role for G proteins in the modulation of Mphi activity after thermal injury.

Animals↗
PubMedDate not supplied

Oligodendrocyte precursor cells: reactive cells that inhibit axon growth and regeneration.

Oligodendrocyte precursor cells (OPCs) are a newly recognized glial component of the adult central nervous system of unknown function. Antibodies against the NG2 chondroitin sulfate proteoglycan have been useful tools to identify these cells in intact tissue. Here we review studies that show that OPCs react to several types of experimentally induced brain injury. Injury stimulates OPCs to re-enter the cell cycle, divide, and accumulate at the site of damage. OPCs, together with microglia and astrocytes, form the glial scar. Glial scars are thought to inhibit or prevent axonal regeneration and reactive OPCs contribute to this inhibition by producing growth-inhibiting chondroitin sulfate proteoglycans, particularly NG2. In developing animals, NG2 is found in areas, such as the perinotochordal mesenchyme, that are avoided by growing motor and sensory axons. Within the developing CNS, NG2-expressing cells surround the developing optic chiasm and tract and separate it from the overlying diencephalon. Thus, NG2-expressing cells are well positioned to inhibit axonal growth from developing as well as regenerating neurons.

Animals↗
PubMed1977

Migration inhibition by an agarose microdroplet assay: monitoring of tumor-associated antigens on a simian virus 40-induced sarcoma.

Macrophage migration inhibition assays, with a direct agarose microdroplet method, were used to monitor TAA activity of preparations of SV-40-induced mKSA cells. These preparations included cell-free crude membranes, papain-solubilized and NP40 detergent-solubilized membrane extracts from mKSA tumor cells. The assay was extremely sensitive and could detect migration inhibition reactivity with all three types of antigenic preparations with concentrations as low at 250 ng protein/ml. The reactivities were quite reproducible from experiment to experiment using the same or different lots of these antigen preparations, and the reactivities were specific in that peritoneal exudate cells from BALB/c mice, immunized with antigenically unrelated but syngeneic plasmacytomas, were not inhibited by these antigens. The results demonstrated the usefulness of this assay in rapidly detecting small concentrations of partially purified TAA preparations by using small number of immune cells.

Animals↗
PubMed1980

The sex difference in rotary pursuit performance: aptitude or inhibition?

This study examined the hypothesis that male dominance in the acquisition and performance of rotary pursuit skill reflects a lower male proclivity for the generation and accumulation of reactive inhibition rather than some innately superior ability to profit from practice. On this hypothesis, the magnitude of male dominance should decline as the length of the intertrial interval increases. The experimental sample consisted of 120 Caucasian subjects (60 of each sex) who were given sixty 30-sec trials on rotary pursuit with intertrial intervals ranging from 0 to 40 sec. The principal finding was that the magnitude of the sex difference depended significantly upon the length of the intertrial interval, as hypothesized. When the interval was 10 sec or longer, performance levels of the sexes were essentially equal. The sex variance was reduced to insignificance even on the first trial when allowance was made for the inhibitory effect of practice. Thus, male dominance in rotary pursuit skill appears to be a procedural effect mediated by and inhibitory mechanism rather than a consequence of differential endowments of learning ability.

Journal Article↗
PubMed2005

Antioxidant and DNA protecting properties of anti-fatigue herb Trichopus zeylanicus.

Chronic fatigue is considered a complex symptom for which currently there is no curative treatment available. Oxidative stress plays an important role in the etiology of fatigue and antioxidant treatment might be a valuable therapeutic approach. The Kani, a tribal high altitude living population in southern India, traditionally use the seeds of Trichopus zeylanicus to combat fatigue. In this study, the antioxidant properties of Trichopus zeylanicus were established on free radicals (DPPH and ABTS), its ability to reduce iron, lipoxygenase activity and hydrogen peroxide-induced lipid peroxidation. The effects of Trichopus zeylanicus on reactive oxygen species induced plasmid DNA (pBR322) cleavage were also investigated. Trichopus zeylanicus significantly scavenged free radicals, reduced lipid peroxidation and inhibited lipoxygenase activity. Trichopus zeylanicus also exhibited iron-chelating activity and inhibited reactive oxygen species induced DNA damage. Trichopus zeylanicus contains NADH, polyphenols and sulfhydryl compounds, which have the ability to scavenge reactive oxygen species suggesting that the antioxidant activity may be an important mechanism of action of Trichopus zeylanicus to combat fatigue.

Animals↗
PubMed1993

Retinoic acid is a negative regulator of the Epstein-Barr virus protein (BZLF1) that mediates disruption of latent infection.

Disruption of latent Epstein-Barr virus (EBV) infection is induced by the key immediate-early protein BZLF1 (or Z, a member of the basic leucine-zipper family), which transactivates the viral early promoters. Viral reactivation is marked by renewed synthesis of early gene products such as EBV early antigen-diffuse (EA-D). Retinoic acid has been previously shown to inhibit reactivation of EBV infection. Retinoic acid responsive receptors are known to act as positively regulating transcription factors but can also negatively regulate AP-1 responsive genes. Here we demonstrate that the retinoic acid receptor alpha (RAR alpha) and retinoid X receptor alpha (RXR alpha) inhibit the ability of the Z protein to transactivate the viral early promoter BMRF1, which directs transcription of EA-D. Z can also reciprocally inhibit RAR alpha- and RXR alpha-induced activation of an autoregulated cellular promoter for the RAR beta gene (BRE) through a non-DNA binding mechanism. RXR alpha inhibits Z from binding to the AP-1 motif in the BMRF1 promoter and, reciprocally, Z inhibits RAR alpha from binding to its retinoic acid response element in the BRE promoter. Furthermore, a glutathione-S-transferase-RXR alpha fusion protein can interact directly with the Z protein. These results suggest that a direct protein-protein interaction between Z (the viral protein) and RAR alpha and RXR alpha (cellular proteins) can modulate the reactivation of latent EBV infection.

Animals↗
PubMedDate not supplied

Links between systems of inhibition from infancy to preschool years.

Links between early and late emerging inhibitory characteristics of young children are poorly understood. Based on existing evidence, this study proposed an indirect link between reactive inhibition to novelty (fearfulness) and later emerging effortful inhibition of prepotent response tendencies. A model was tested that posits that fearful children have opportunistic advantages in developing a nonimpulsive approach style in contexts that are not imbued with salient novelty cues. That nonimpulsive approach style, in turn, facilitates future effortful inhibition. Longitudinal panel data, all based on observational measures, at 9, 14, 22, 33, and 45 months were used to support the proposed indirect link. The implications for understanding regulatory influences of fearful behavior and developmental complexity in child characteristics are discussed.

Child, Preschool↗
PubMed2006

4-O-methylgallic acid down-regulates endothelial adhesion molecule expression by inhibiting NF-kappaB-DNA-binding activity.

We here investigated the functional effect of 4-O-methylgallic acid (4-OMGA), a major metabolite of gallic acid abundant in red wine, on vascular inflammation and its action mechanism. 4-OMGA inhibited the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis factor-alpha (TNF-alpha), resulting in the suppression of leukocyte adhesion to HUVECs. In addition, 4-OMGA inhibited the promoter activities of ICAM-1 and VCAM-1 and the activity of nuclear factor-kappaB (NF-kappaB) without affecting cytosolic IkappaB kinase (IKK) activation, inhibitor of kappaB (IkappaB) phosphorylation and degradation, and nuclear translocation of NF-kappaB. This compound did not alter nitric oxide (NO) generation, but inhibited reactive oxygen species (ROS) production in TNF-alpha-stimulated HUVECs, suggesting that NO and ROS are not involved in 4-OMGA-mediated inhibition of NF-kappaB activity. Moreover, 4-OMGA directly blocked the binding activity of NF-kappaB to its consensus DNA oligonucleotide, when pre-incubated with the nuclear extract from TNF-alpha-stimulated HUVECs, but not with the oligonucleotide alone. This inhibition was completely abolished by the addition of dithiothreitol. 4-OMGA exhibits an anti-inflammatory property by interfering with the formation of the NF-kappaB-DNA complex in the nuclei through direct and redox-sensitive interactions and may play an important role in the prevention of inflammatory responses such as the atherosclerotic process.

Anti-Inflammatory Agents↗