RESUMEN
Humic substances (HS) have been reported to possess anti-inflammatory as well as pro-inflammatory properties. The anti-inflammatory activity was demonstrated in the rat paw edema model and we found a preliminary explanation in the 5-lipoxygenase inhibitory effect of humic acids (HA). The pro-inflammatory activity is reflected by the production and release of pro-inflammatory cytokines in HA-treated neutrophilic granulocytes. With regard to the potential use of HA as antiviral and UV-protective agents it appears advisable to investigate the role of HS in the inflammation process in more detail. Hence we tested four different HS preparations - two naturally occurring HA from the Altteich peatland in Germany, one fulvic acid (FA) preparation from a Finnish spruce forest and a synthetic HA-like polymer (caffeic acid oxidation product, KOP) for their influence on the lipopolysaccharide (LPS)-induced TNF-alpha release in human U937 cells. In addition, the cytotoxicity of HS was determined. The results demonstrate a concentration-dependent bimodal effect of HA on the TNF-alpha release of differentiated LPS-stimulated U937 cells for both the natural black peat HA from the Altteich peatland and the HA-like polymer KOP. Low HA concentrations (10-80 microg/ml) enhanced the TNF-alpha release by up to threefold (pro-inflammatory activity), while HA concentrations >100 microg/ml reduced it about 10-fold (anti-inflammatory activity). FA failed to enhance TNF-alpha release, but reduced it at higher concentrations (>200 microg/ml) by the half. Brown water HA did not exert any significant effect on TNF-alpha release. No HS-stimulated TNF-alpha release was also observed in the absence of exogenously supplied LPS. This means that HS, unlike endotoxin, are no inflammation-causing agents for LPS-untreated cells. Differences in the effect of individual HS on TNF-alpha release are discussed in connection with the polyanionic character of HS, their molecular mass distribution and the hitherto imperfectly known chemical structure.
Asunto(s)
Antiinflamatorios/farmacología , Benzopiranos/farmacología , Sustancias Húmicas , Factor de Necrosis Tumoral alfa/metabolismo , Antiinflamatorios/efectos adversos , Benzopiranos/efectos adversos , Ácidos Cafeicos/metabolismo , Relación Dosis-Respuesta a Droga , Humanos , Sustancias Húmicas/efectos adversos , Lipopolisacáridos/toxicidad , Plantas , Suelo , Células U937RESUMEN
A panel of ten humic-acid-like polymers was synthesized by oxidation of p-diphenolic compounds and characterized by relative molecular weights, FT-IR spectra and functional group analysis. Using the XTT-based tetrazolium reduction assay EZ4U, both the low-molecular starting compounds and the synthesized polymers were examined for antiviral and cytotoxic activities in HSV-1-infected Vero cells. With the exception of hydroquinone, 2,5-dihydroxytoluene and 2,5-dihydroxybenzoquinone, the starting compounds failed to inhibit herpesvirus replication. The polymeric oxidation products, however, developed anti-HSV-1 activity with EC50 values in the range of 0.65 (2,5-DHPOP) and 322 microg/ml (2,5-DHBQOP). The CC50 values of the polymers varied among 32.0 (TMHYDROP) and >512 microg/ml (2,5-DHBQOP, HYDSULFOP). The most effective polymers were found to be 2,5-DHPOP 2,5-DHTOP and GENOP (EC50: 0.65, 1.6 and 2.2 microg/ml, respectively, and SI: > or = 400, > or = 80 and > or = 58, respectively). Functional group analysis revealed that increasing numbers of carboxyl groups together with a high content of hydroxyl groups tend to enhance the antiviral activity of polymers derived from p-diphenolic compounds.
Asunto(s)
Antivirales/farmacología , Herpesvirus Humano 1/efectos de los fármacos , Sustancias Húmicas/farmacología , Fenoles/química , Polímeros/farmacología , Animales , Antivirales/química , Chlorocebus aethiops , Relación Dosis-Respuesta a Droga , Herpesvirus Humano 1/crecimiento & desarrollo , Humanos , Sustancias Húmicas/química , Dosificación Letal Mediana , Peso Molecular , Oxidación-Reducción , Fenoles/farmacología , Polímeros/química , Espectroscopía Infrarroja por Transformada de Fourier , Relación Estructura-Actividad , Células Vero/efectos de los fármacos , Células Vero/virología , Ensayo de Placa ViralRESUMEN
Two drug formulations of povidone-iodine (PVP-I)--an aqueous PVP-I solution (Betaisodona) and a liposomal PVP-I formulation--were tested for their virucidal activity and cytotoxicity in cell culture. As to the virudical activity against influenza A virus, herpes simplex virus type 1, adenovirus type 8 and human rhinovirus type 14, the liposomal formulation of PVP-I proved to be approximately as active as the aqueous one. Half maximum cytotoxic PVP-I concentrations were 0.01-0.07% for aqueous PVP-I and 0.03-0.27% for the liposomal PVP-I formulation (XTT reduction assay EZ4U). The detection of lactate dehydrogenase (LDH) release, DNA fragmentation (ELISA) and DNA strand breakage (TUNEL assay) after 24 h exposure of human embryonic lung fibroblasts to PVP-I revealed that necrosis predominates in cells treated with aqueous 0.08-0.32% PVP-I solutions, whereas apoptosis was the predominant type of cell death in cells treated with equivalent concentrations of liposomal PVP-I formulation. The favorable virucidal efficiency together with the preferred apoptotic route of cell death makes the liposomal PVP-I formulation a promising candidate for topical use in prevention and treatment of infections of the eye and the upper respiratory tract.
Asunto(s)
Antivirales/administración & dosificación , Antivirales/toxicidad , Yodóforos/administración & dosificación , Yodóforos/toxicidad , Povidona Yodada/administración & dosificación , Povidona Yodada/toxicidad , Adenoviridae/efectos de los fármacos , Administración Tópica , Animales , Apoptosis/efectos de los fármacos , Células Cultivadas , Chlorocebus aethiops , Cricetinae , Perros , Herpesvirus Humano 1/efectos de los fármacos , Humanos , Etiquetado Corte-Fin in Situ , Virus de la Influenza A/efectos de los fármacos , L-Lactato Deshidrogenasa/análisis , Liposomas , Pulmón/citología , Pulmón/efectos de los fármacos , Necrosis , Conejos , Rhinovirus/efectos de los fármacosRESUMEN
The in vitro antiviral activity of a new series of cycloSal-pro-nucleotides derived from the acyclic nucleoside analogues aciclovir and penciclovir against herpes simplex virus type 1 (HSV-1), thymidine kinase deficient (TK-) HSV-1, and Epstein-Barr virus (EBV) was evaluated. Using the XTT-based tetrazolium reduction assay EZ4U, the cycloSal derivatives were examined for their antiviral and cytotoxic effects in HSV-1 as well as HSV-1-TK--infected Vero cells. The anti-EBV activity was assessed by means of an EBV DNA hybridization assay using a digoxigenin-labeled probe specific for the Bam H1-W-fragment of the EBV genome and by measuring viral capsid antigen (VCA) expression in P3HR-1 cells by indirect immunofluorescence. Among the new cycloSal-phosphotriesters the three aciclovir monophosphates proved to be potent and selective inhibitors of HSV-1 replication, EBV DNA synthesis and EB-VCA expression. Of interest is the retention of activity of the aciclovir monophosphates in HSV-1-TK--infected cells. Particularly 3-methyl-cycloSal-aciclovir monophosphate retained the same effectiveness, as compared to the wild type virus strain. In contrast to the aciclovir pro-nucleotides the penciclovir cycloSal-phosphotriesters exhibited at best only a marginal antiviral effect on HSV and EBV replication.
Asunto(s)
Aciclovir/análogos & derivados , Antivirales/farmacología , Proteínas de la Cápside , Herpesvirus Humano 1/efectos de los fármacos , Herpesvirus Humano 4/efectos de los fármacos , Aciclovir/química , Aciclovir/farmacología , Animales , Antígenos Virales/biosíntesis , Antivirales/química , Células Cultivadas , Chlorocebus aethiops , ADN Viral/biosíntesis , Guanina , Herpesvirus Humano 1/metabolismo , Herpesvirus Humano 4/metabolismo , Timidina Quinasa/metabolismo , Células Vero , Replicación Viral/efectos de los fármacosRESUMEN
Povidone-iodine (PVP-I) is a broad-spectrum microbicide with in vitro activity against bacteria, viruses, fungi and protozoans. A 5% solution of PVP-I proved to be highly effective in ophthalmic surgery for the prophylaxis of endophthalmitis. For the antiseptic treatment of eye infections a novel application form of PVP-I has been developed by using a PVP-I liposome complex which demonstrated an excellent antimicrobial efficacy. In this study it could be shown that the novel liposomal formulations containing 2.5 or 5% PVP-I were as active as the aqueous solution against herpes simplex virus type 1, adenovirus type 8, coxsackievirus A9 and Chlamydia trachomatis in cell culture referring to equal PVP-I concentrations. Long-term cytotoxicity experiments demonstrated a moderate cytotoxicity for both formulations with a better tolerability of the liposomal PVP-I formulation compared with the aqueous solution. There is no evidence for a genotoxic activity of these agents.
Asunto(s)
Adenovirus Humanos/efectos de los fármacos , Antiinfecciosos Locales/farmacología , Chlamydia trachomatis/efectos de los fármacos , Enterovirus/efectos de los fármacos , Herpesvirus Humano 1/efectos de los fármacos , Soluciones Oftálmicas/farmacología , Povidona Yodada/farmacología , Animales , Chlorocebus aethiops , Relación Dosis-Respuesta a Droga , Humanos , Liposomas , Masculino , Conejos , Células VeroRESUMEN
We studied the genotoxic and apoptosis-inducing properties of ganciclovir (GCV) and penciclovir (PCV) using Chinese hamster ovary cells stably transfected with the thymidine kinase (tk) gene of herpes simplex virus-1 (HSV-1). Cells expressing HSVtk were 300 and 100 times more sensitive than their isogenic HSVtk- counterparts to the cytotoxic effects of GCV and PCV, respectively. Using radiolabeled drugs, GCV was found to be incorporated into the genomic DNA much more effectively than PCV. GCV was highly potent in inducing chromosomal aberrations compared with PCV, which provoked less sister chromatid exchanges and chromosomal changes using equimolar or equitoxic doses. For both agents, apoptosis was shown to be the major route of cell killing. Time course experiments revealed that neither genotoxicity nor apoptosis were induced within the cell cycle exposed to the drug; they are late events provoked in the following cell cycle(s). This indicates that the incorporation/exposure step of GCV or PCV into DNA is not decisive for triggering genotoxicity and apoptosis, but that events occurring subsequently, presumably during replication of a DNA containing the nucleotide analogs, are of major importance. Because PCV, unlike GCV, induced highly effectively apoptosis without exerting much genotoxicity, the use of PCV as a relatively safe alternative drug for suicide gene therapy of malignant diseases is recommended.
Asunto(s)
Aciclovir/análogos & derivados , Apoptosis , Ganciclovir/farmacología , Terapia Genética , Timidina Quinasa/genética , Aciclovir/metabolismo , Aciclovir/farmacología , Animales , Células CHO , Ciclo Celular/efectos de los fármacos , Cricetinae , ADN/metabolismo , Replicación del ADN/efectos de los fármacos , Ganciclovir/metabolismo , Guanina , Herpesvirus Humano 1/enzimología , Pruebas de Mutagenicidad , Necrosis , Intercambio de Cromátides Hermanas/efectos de los fármacos , Timidina Quinasa/metabolismo , TransfecciónRESUMEN
The three anti-herpes nucleoside analogues ganciclovir, penciclovir and aciclovir were investigated as to their recombinogenic [sister chromatid exchange (SCE) inducing] and clastogenic activity in CHO cells expressing the thymidine kinase gene of HSV-1, which is a precondition of therapeutic activity of these drugs. The compounds were applied for the duration of one cell cycle and cytogenetic end-points were measured between 0 and 42 h after exposure. Although the nucleoside analogues are quite similar with respect to chemical structure, they differ basically in their genotoxic potency, aberration types induced as well as the time course of chromosomal damage. Aciclovir induced SCEs and chromosomal aberrations immediately after exposure but only in a concentration range much higher than that reached in blood plasma during anti-herpes therapy. The direct genotoxic activity is explained by the obligate chain terminating property of aciclovir upon incorporation into genomic DNA. On the other hand, genotoxic damage caused by ganciclovir and penciclovir is of the delayed type requiring at least one post-exposure cell cycle for its expression. Unlike aciclovir, ganciclovir is an extremely potent inducer of SCEs and chromosome breaks and translocations at concentrations far below those impairing the proliferative activity and triggering apoptosis of the target cells (as shown by our previous investigation). Penciclovir is essentially devoid of genotoxic activity. It induces SCEs only at cytotoxic/apoptotic concentrations, is only weakly clastogenic and induces premature chromosome condensation which appears to result from uncoupling of karyokinesis and cytokinesis. The genotoxic activity of ganciclovir is explained as due to repair processes triggered in the second post-exposure replication cycle at the sites of nucleoside analogue incorporation into genomic DNA. The findings have considerable implications with respect to the use of ganciclovir or other antiviral drugs in suicide gene therapy of malignant diseases.
Asunto(s)
Aciclovir/análogos & derivados , Aciclovir/toxicidad , Antivirales/toxicidad , Ganciclovir/toxicidad , Herpesvirus Humano 1/metabolismo , Timidina Quinasa/metabolismo , Animales , Células CHO , Cromosomas/efectos de los fármacos , Cricetinae , Relación Dosis-Respuesta a Droga , Guanina , Mutágenos/toxicidad , Intercambio de Cromátides Hermanas/efectos de los fármacos , Timidina Quinasa/genética , Factores de TiempoRESUMEN
The synthesis of different cycloSal-phosphotriesters of the acyclic nucleoside analogues acyclovir (ACV), penciclovir (PCV) and T-penciclovir (T-PCV) as potential new lipophilic, membrane-soluble pronucleotides is described. The introduction of the cycloSal moiety was achieved by using reactive cyclic chlorophosphane reagents. In addition to the cycloSal-PCV monophosphate (MP) phosphotriesters, a second derivative bearing an acetyl group at the second primary alcohol function was prepared. In hydrolysis studies the cycloSal-ACVMPs showed the expected range of hydrolytic stability dependent on the substituent in the masking group (8-17 h). In contrast, the cycloSal-PCVMP derivatives exhibited a 11- to 15-fold increase in hydrolytic lability as compared to the corresponding cycloSal-ACVMP derivatives. We demonstrated that the free primary alcohol group is responsible for this rate acceleration because cycloSal-OAc-PCVMP, in which the hydroxyl group was blocked by acetylation, did not show the aforementioned acceleration. Unexpectedly, the hydrolysis product was not PCVMP but according to NMR and mass spectrometry it was cycloPCVMP (cPCVMP). The title compounds were evaluated in vitro for their ability to inhibit herpes simplex virus type 1 (HSV-1) and thymidine kinase-negative (TK-) HSV-1 replication in Vero cells. The cycloSal-ACVMP compounds exhibited high antiviral activity in HSV-1-infected cells. More importantly, one derivative retained all activity from the wild-type virus strain in HSV-1/TK(-)-infected Vero cells. The PCV derivatives were markedly less active. The reason for the failure of the cycloSal-PCVMPs seems to be due to the formation of cPCVMP instead of the desired PCVMP.
Asunto(s)
Aciclovir/análogos & derivados , Antivirales/síntesis química , Herpesvirus Humano 1/efectos de los fármacos , Nucleósidos/síntesis química , Nucleótidos/síntesis química , Aciclovir/farmacología , Animales , Antivirales/farmacología , Chlorocebus aethiops , Guanina , Espectroscopía de Resonancia Magnética , Nucleósidos/farmacología , Nucleótidos/farmacología , Células Vero , Replicación Viral/efectos de los fármacosRESUMEN
After incubation of highly enriched neurons from rat cerebral cortex with the HIV-1 coat protein gp120 for 18 h, cells showed fragmentation of DNA at internucleosomal linkers followed by NMDA receptor-mediated neurotoxicity. We report that in response to exposure to gp120 cells react with an increased release of arachidonic acid (AA) via activation of phospholipase A2. This process was not inhibited by NMDA receptor antagonists. To investigate the role of AA on the sensitivity of the NMDA receptor towards its agonist, low concentrations of NMDA were co-administered with AA. This condition enhanced the NMDA-mediated cytotoxicity. Administration of mepacrine reduced cytotoxicity caused by gp120. We conclude that gp120 causes an activation of phospholipase A2, resulting in the increased release of AA, which may in turn sensitize the NMDA receptor.
Asunto(s)
Ácido Araquidónico/metabolismo , Proteína gp120 de Envoltorio del VIH/farmacología , VIH-1 , Neuronas/efectos de los fármacos , Neuronas/metabolismo , Neurotoxinas/farmacología , Receptores de N-Metil-D-Aspartato/fisiología , Animales , Ácido Araquidónico/antagonistas & inhibidores , Muerte Celular , Células Cultivadas , Daño del ADN/efectos de los fármacos , Neuronas/fisiología , Quinacrina/farmacología , Ratas , Ratas Wistar , Receptores de N-Metil-D-Aspartato/antagonistas & inhibidoresRESUMEN
The release of arachidonic acid (AA) from membrane phospholipids is part of a signal system with which cells respond to environmental changes of various kinds. Using the promonocytic cell line U937, the kinetics of AA release was studied in [(3)H]AA-labelled U937 cells under the influence of various chemicals. Membrane-toxic agents such as lysolecithin and sodium dodecyl sulfate (SDS) cause pronounced enhancement of [(3)H]AA release in U937 cells. The effect occurred immediately after exposure and proved to be dose-dependent, non-enzymatic and irreversible. With regard to mean [(3)H]AA-releasing rate in untreated U937 cells, the following maximum tolerable concentrations were found: lysolecithin, 0.5 mug/ml; SDS, 2 mug/ml; dimethoate, 31.3 mug/ml; chloramine, 160 mug/ml; 2,4-dichlorophenoxyacetic acid (2,4-D), 1 mg/ml; formamide, 50 mg/ml and dimethyl sulfoxide, 100 mg/ml. AA release represents a highly sensitive bioindicator for the membrane-toxic effect of a chemical substance.
RESUMEN
Infection of monocytes with human immunodeficiency virus type 1 (HIV-1) (strain Ada-M) caused increased levels of leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) in vitro. These two products result from the activities of the two enzymes cyclooxygenase and 5-lipoxygenase. The addition of the sesquiterpenoid hydroquinone Avarol, an HIV inhibitor, strongly reduced the levels of LTB4 and PGE2 via inhibition of both cyclooxygenase and lipoxygenase in monocytes. The 50% inhibition concentrations (IC50) for the enzymes were determined to be 2.26 microM (cyclooxygenase) and 1.97 microM (lipoxygenase). A 50% reduction of the extent of PGE2 and LTB4 production in HIV-infected monocytes was measured at a concentration of 0.9 microM Avarol, a dose which caused an 80% anti-HIV effect in vitro (50% inhibition of virus release from infected cells: 0.3 microM). We conclude that Avarol inhibits the enzymes cyclooxygenase and lipoxygenase and suggest that, in general, inhibitors of these enzymes are promising anti-HIV compounds.
Asunto(s)
Antivirales/farmacología , Dinoprostona/metabolismo , VIH-1/fisiología , Leucotrieno B4/metabolismo , Monocitos/microbiología , Sesquiterpenos/farmacología , Araquidonato 5-Lipooxigenasa/metabolismo , Inhibidores de la Ciclooxigenasa/farmacología , VIH-1/efectos de los fármacos , Inhibidores de la Lipooxigenasa/farmacología , Monocitos/metabolismo , Prostaglandina-Endoperóxido Sintasas/metabolismoRESUMEN
Polyhydroxycarboxylates (MW: 3,800-14,000) derived from phenolic (PDP) compounds have been found to inhibit the cytopathicity of HIV-1 and HIV-2 in MT-4 cells at concentrations that are not toxic to the host cells. The PDP compounds also inhibited syncytium formation in cocultures of MOLT-4 cells with HIV-1- or HIV-2-infected HUT-78 cells. They also interfered with the binding of OKT4A/leu3a monoclonal antibody (mAb) to the CD4 receptor, the binding of anti-gp120 mAb to HIV-1 gp120, and attachment of HIV-1 virions to MT-4 cells. The anti-HIV activity in this series of compounds can be ascribed to inhibition of the gp120-CD4 interaction and seems to depend on the presence of the anionic carboxylate groups. Their mechanism of action is similar to that of the heterogeneous polymer aurintricarboxylic acid (ATA).
Asunto(s)
Antivirales/farmacología , Ácidos Carboxílicos/química , VIH-1/efectos de los fármacos , VIH-2/efectos de los fármacos , Fenoles/química , Replicación Viral/efectos de los fármacos , Adsorción , Anticuerpos Monoclonales/inmunología , Antígenos CD4/inmunología , Linfocitos T CD4-Positivos/inmunología , Ácidos Carboxílicos/farmacología , Células Cultivadas , Células Gigantes/microbiología , Proteína gp120 de Envoltorio del VIH/inmunología , VIH-1/crecimiento & desarrollo , VIH-1/inmunología , VIH-2/crecimiento & desarrollo , VIH-2/inmunología , Fenoles/farmacología , Receptores de Antígenos de Linfocitos T/inmunologíaRESUMEN
Various polymeric oxidation products of polyphenols strongly inhibited the purified lipoxygenase of rabbit reticulocytes, whereas the prostaglandin H synthase of sheep vesicular gland was only weakly inhibited. The oxidized polymeric preparations of caffeic acid, 2,5-dihydroxytoluene and 3,4-dihydroxytoluene were the most potent lipoxygenase inhibitors. Since such preparations are also known to inhibit herpes simplex virus in an early stage of the virus-cell interaction it is proposed that lipoxygenase metabolites are involved in virus-induced changes in the cell metabolism.
Asunto(s)
Antivirales/farmacología , Flavonoides , Inhibidores de la Lipooxigenasa/farmacología , Fenoles/metabolismo , Polímeros/metabolismo , Prostaglandinas H/antagonistas & inhibidores , Animales , Antivirales/metabolismo , Ácidos Cafeicos/metabolismo , Ácidos Cafeicos/farmacología , Catecoles/metabolismo , Catecoles/farmacología , Hidroquinonas/metabolismo , Hidroquinonas/farmacología , Oxidación-Reducción , Fenoles/farmacología , Polímeros/farmacología , Conejos , Reticulocitos/enzimología , OvinosRESUMEN
The influence of (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU), caffeic acid oxidation product (KOP), and trisodiumphosphonoformate (TPF) on the course of the primary cutaneous herpes simplex virus infection was investigated by means of a guinea pig test model. The antiviral substances were applied in an ointment with 10% urea as a penetration mediator. When the treatment was initiated 15 minutes after virus inoculation, 3% BVDU effectively inhibited the development of herpetic vesicles and 0.1% BVDU prevented the appearance of herpetic satellites. Under the same conditions 1% and 3% KOP ointments inhibited the appearance of satellites; and 0.5% TPF ointment completely inhibited the development of cutaneous herpes lesions. Prophylactic drug administration given 24, 20, and 4 hours before virus inoculation was without any protective effect.
Asunto(s)
Antivirales/uso terapéutico , Bromodesoxiuridina/análogos & derivados , Ácidos Cafeicos/uso terapéutico , Cinamatos/uso terapéutico , Herpes Simple/tratamiento farmacológico , Compuestos Organofosforados/uso terapéutico , Ácido Fosfonoacético/uso terapéutico , Animales , Bromodesoxiuridina/uso terapéutico , Femenino , Foscarnet , Cobayas , Humanos , Masculino , Oxidación-Reducción , Ácido Fosfonoacético/análogos & derivados , Simplexvirus/aislamiento & purificaciónRESUMEN
Phenolic polymers synthesized by enzymatic oxidation of coffeic acid, chlorogenic acid, and gentisinic acid were found to strongly inhibit RNA-dependent DNA polymerase (revertase) of retroviruses. Except of two type C retroviruses inhibition became reversible by the addition of bovine serum albumin to the exogenous revertase test. The phenolic polymers tested did not influence the propagation of retroviruses in the cell culture. The replication of Rauscher leukemia virus in mice was diminished by a short-time preincubation of virus suspension with coffeic acid polymer (KOP). In contrast, the preincubation of a virus-containing serum with KOP increased the leukemogenic effect of the virus. KOP given to mice at a high dose subsequently to virus inoculation resulted in high revertase activities and in an elevation of spleen weights too.
Asunto(s)
Flavonoides , Fenoles/síntesis química , Polímeros/síntesis química , Retroviridae/efectos de los fármacos , Animales , ADN Viral/biosíntesis , Depresión Química , Ratones , Inhibidores de la Síntesis del Ácido Nucleico , Oxidación-Reducción , Fenoles/farmacología , Polímeros/farmacología , Polifenoles , Retroviridae/fisiología , Proteínas Virales/biosíntesis , Replicación Viral/efectos de los fármacosRESUMEN
The virucidal effect, the inhibition of virus adsorption and penetration and the influence on later phases of replication of human pathogenic viruses were studied. The compounds showed a significant virucidal effect to enveloped viruses (measles virus, herpes virus type 1 and 2), whereas the compounds were ineffective against nonenveloped viruses (Coxsackie virus A9 and B1, attenuated poliovirus type 1, adenovirus type 1). Interactions with the viral envelope are supposed.