RESUMEN

The influence of He-Ne laser radiation on the formation of new blood vessels in the bone marrow compartment of a regenerating area of the mid-cortical diaphysis of the tibiae of young adult rats was studied. A small hole was surgically made with a dentistry burr in the tibia and the injured area received a daily laser therapy over 7 or 14 days transcutaneously starting 24 h from surgery. Incident energy density dosages of 31.5 and 94.5 Jcm(-2) were applied during the period of the tibia wound healing investigated. Light microscopic examination of histological sections of the injured area and quantification of the newly-formed blood vessels were undertaken. Low-level energy treatment accelerated the deposition of bone matrix and histological characteristics compatible with an active recovery of the injured tissue. He-Ne laser therapy significantly increased the number of blood vessels after 7 days irradiation at an energy density of 94.5 Jcm(-2), but significantly decreased the number of vessels in the 14-day irradiated tibiae, independent of the dosage. These effects were attributed to laser treatment, since no significant increase in blood vessel number was detected between 8 and 15 non-irradiated control tibiae. Molecular mechanisms involved in low-level laser therapy of angiogenesis in post-traumatic bone regeneration needs further investigation.

Asunto(s)

Terapia por Láser , Terapia por Luz de Baja Intensidad , Neovascularización Fisiológica/efectos de la radiación , Tibia/lesiones , Animales , Helio , Masculino , Neón , Ratas , Ratas Wistar , Tibia/irrigación sanguínea , Factores de Tiempo , Cicatrización de Heridas/efectos de la radiación

RESUMEN

We investigated whether veratrine (5 microl, 10 ng/kg) injected into the mouse extensor digitorum longus (EDL) (fast-twitch) and soleus (SOL) (slow-twitch) muscles provokes distinctive ultrastructural disturbances 15, 30 and 60 min later. The mitochondria in SOL were affected earlier (within 15 min) than in EDL. Swelling of the sarcoplasmic reticulum terminal cisternae was more marked in EDL than in SOL and caused distortion of sarcomeres so that fragmentation of myofilaments was more pronounced in EDL. Hypercontracted sarcomeres were seen mainly in SOL and veratrine caused infoldings of the sarcolemma only in this muscle. In both muscles, the T-tubules remained unaffected and by 60 min after veratrine most of the above alterations had reverted to normal. Pretreatment with tetrodotoxin prevented the alterations induced by veratrine. This suggests that most of the alterations resulted from the enhanced influx of Na+ into muscle fibers. These results emphasize the importance of considering the type of muscle when studying the action of myotoxic agents.

Asunto(s)

Músculo Esquelético/efectos de los fármacos , Enfermedades Musculares/inducido químicamente , Veratrina/toxicidad , Animales , Antagonismo de Drogas , Masculino , Ratones , Ratones Endogámicos BALB C , Mitocondrias/efectos de los fármacos , Mitocondrias/ultraestructura , Fibras Musculares de Contracción Rápida/efectos de los fármacos , Fibras Musculares de Contracción Rápida/ultraestructura , Fibras Musculares de Contracción Lenta/efectos de los fármacos , Fibras Musculares de Contracción Lenta/ultraestructura , Músculo Esquelético/ultraestructura , Enfermedades Musculares/patología , Sarcómeros/efectos de los fármacos , Sarcómeros/ultraestructura , Tetrodotoxina/farmacología

RESUMEN

Bothropstoxin-I (BthTX-I), the principal myotoxin of Bothrops jararacussu venom, is devoid of phospholipase A(2) (PLA(2)) activity but capable of blocking neuromuscular transmission in mouse nerve-muscle preparations. In this study, the ability of crotoxin antiserum and heparin in preventing the neurotoxic and myotoxic effects of BthTX-I was investigated. Phrenic nerve-diaphragm preparations (PND) stimulated indirectly with supramaximal stimuli (0.2 ms, 0.1 Hz) were incubated with BthTX-I (20 microg/ml) alone or with BthTX-I preincubated with antiserum or heparin for 30 min at 37 degrees C prior to testing. Control preparations were incubated with Tyrode solution, antiserum or heparin alone. BthTX-I (20 microg/ml) produced 50% neuromuscular blockade in the PND preparations in 31+/-4min, with complete blockade occurring in 120 min. The antiserum and heparin significantly prevented the neuromuscular blockade caused by BthTX-I (84 +/- 4% and 100% protection, respectively). Light microscopy examination of the muscles at the end of the 120 min incubation showed that BthTX-I damaged 48 +/- 6% of the fibers. Preincubating the toxin with antivenom significantly reduced the extent of this damage (only 15 +/- 4% of fibers affected, corresponding to 69% protection, P<0.01) whereas heparin offered no protection (34 +/- 7% of fibers affected, not significantly different from that seen with toxin alone). These results show that the antivenom was more effective in neutralizing the myotoxic effects of BthTX-I than was heparin.

Asunto(s)

Antivenenos/farmacología , Venenos de Crotálidos/antagonistas & inhibidores , Crotoxina/antagonistas & inhibidores , Inmunoglobulina G/análisis , Músculo Esquelético/efectos de los fármacos , Nervio Frénico/efectos de los fármacos , Animales , Antivenenos/inmunología , Antivenenos/uso terapéutico , Bothrops , Venenos de Crotálidos/inmunología , Venenos de Crotálidos/toxicidad , Crotoxina/inmunología , Crotoxina/toxicidad , Estimulación Eléctrica , Electroforesis en Gel de Poliacrilamida , Heparina/uso terapéutico , Inmunoglobulina G/sangre , Inmunoglobulina G/aislamiento & purificación , Técnicas In Vitro , Inyecciones Subcutáneas , Masculino , Ratones , Músculo Esquelético/patología , Músculo Esquelético/fisiología , Bloqueo Neuromuscular , Unión Neuromuscular/efectos de los fármacos , Unión Neuromuscular/patología , Unión Neuromuscular/fisiología , Pruebas de Neutralización , Nervio Frénico/fisiología , Conejos , Factores de Tiempo

RESUMEN

The histopathological changes induced in avian kidney by the intramuscular injection of Bothrops insularis (jararaca ilh a) venom and its phospholipase A2 (PLA2)-containing fraction were examined. Acute experiments (3 h and 24 h) with B. insularis crude venom (20 microg and 80 microg) or its PLA2-contaning fraction (10 microg and 40 microg) resulted in significant structural damage to the kidneys of 5-12-day-old chicks. Histopathological analysis indicated that the venom and its fraction acted on the renal tubules and glomeruli. The morphological changes, although widespread, varied in intensity from cell to cell, and from tubule to tubule in venom-injected chicks. The tubular and glomerular changes produced by the venom and its PLA2-containing fraction may be the result of a direct cytotoxic effect potentiated by ischemia-related disturbances in the regional hemodynamics. The venom and its fraction affected more segments along reptilian-type nephrons than along mammalian ones. This divergent sensitivity to the venom and its fraction may reflect the species-specific characteristics of B. insularis snake, an example of geographical isolation influencing its diet which is almost exclusively avian.

Asunto(s)

Bothrops , Pollos/fisiología , Venenos de Crotálidos/toxicidad , Riñón/patología , Fosfolipasas A/toxicidad , Animales , Conducta Animal/efectos de los fármacos , Venenos de Crotálidos/administración & dosificación , Venenos de Crotálidos/enzimología , Inyecciones Intramusculares , Masculino , Adhesión en Parafina , Fosfolipasas A/administración & dosificación , Fosfolipasas A2 , Insuficiencia Respiratoria/inducido químicamente , Insuficiencia Respiratoria/patología , Factores de Tiempo , Uréter/patología

RESUMEN

Bothrops jararacussu venom and its major toxin, bothropstoxin-I (BthTX-I), possess myotoxic and neurotoxic activities. The ability of commercial equine antivenom to neutralize these activities was studied in mouse isolated phrenic nerve-diaphragm (PND) and extensor digitorum longus (EDL) preparations by indirect stimulation (0.1 HZ, 0.2 ms). The time required to produce 50% neuromuscular blockade in the PND and EDL preparations was, respectively, 70 +/- 11.5 min and 58 +/- 8 min for B. jararacussu venom (50 microg/mL), and 31 +/- 6 min and 30 +/- 3 min for BthTX-I (20 microg/mL). After a 120-min incubation, the creatine kinase (CK) concentrations in the EDL preparations were 3464 +/- 346 U/L and 3422 +/- 135 U/L following exposure to venom (50 microg/mL) and BthTX-I (20 microg/mL), respectively. Antivenom neutralized the neuromuscular blockade induced by the venom and toxin in PND preparations in a dose-dependent fashion, but only partially neutralized this effect in EDL. Antivenom also effectively prevented the venom- and toxin-induced release of CK from EDL. In contrast, histological analysis showed that the morphological damage caused by B. jararacussu venom and BthTX-I in the EDL was only partially prevented by the anti- venom. These results indicate that commercial equine antiserum fully protects against the neurotoxic action of B. jararacussu and BthTX-I in PND preparations, but only partially protects against the neurotoxic and myotoxic actions of the venom and its toxin in EDL preparations. Care must therefore be exercized in extrapolating results from different preparations even when similar pharmacological or physiological responses are involved.

Asunto(s)

Antivenenos/farmacología , Venenos de Crotálidos/toxicidad , Músculo Esquelético/efectos de los fármacos , Unión Neuromuscular/efectos de los fármacos , Nervio Frénico/efectos de los fármacos , Animales , Bothrops , Diafragma/efectos de los fármacos , Diafragma/patología , Diafragma/fisiología , Estimulación Eléctrica , Técnicas In Vitro , Masculino , Ratones , Músculo Esquelético/patología , Músculo Esquelético/fisiología , Unión Neuromuscular/fisiología , Nervio Frénico/fisiología

RESUMEN

Phoneutria nigriventer (Labidognatha, Ctenidae) is a spider found in the warm regions of South America. Bites by this species cause intense local pain, autonomic dysfunction and paralysis. PhTx2, a neurotoxic fraction of the venom of this species, interferes with the physiology of sodium channel function. The present study describes the morphological changes in mouse phrenic nerve and diaphragm muscle after 15, 30, 45 and 60 min of incubation with 1 microg of PhTx2/ml. Light and transmission electron microscopy showed that PhTx2 caused progressive myonecrosis which involved swelling of the sarcoplasmic reticulum, mitochondrial damage, disorganization of the sarcomeres, zones of hypercontracted myofibrils and rupture of the plasma membrane. The intramuscular fascicles of the phrenic nerve showed vacuolated myelinated axons and Schwann cells. The neuromuscular junctions had vesicle-depleted nerve terminals with swollen mitochondria. The axolema was frequently invaginated and sequestered portions of the axoplasm, or was sometimes interrupted at the site of the synaptic gutter. The post-synaptic junctional folds were shallow and disperse. These morphological alterations in the muscle and nerve fibres were similar to those caused by osmotic disturbances and agree with the ability of PhTx2 to increase the permeability of sodium channels. An increase in sodium influx would probably be accompanied by an influx of water and an elevation in the concentration of cytosolic calcium as a result of calcium release by the sarcoplasmic reticulum and/or mitochondria and the entry of extracellular calcium. The morphological effects caused by PhTx2 were comparable to those seen with Phoneutria nigriventer whole venom which is known to activate and to delay the inactivation of sodium channels. We conclude that PhTx2 is probably the main toxic fraction responsible for such morphological alterations.

Asunto(s)

Diafragma/efectos de los fármacos , Neuropéptidos/toxicidad , Neurotoxinas/toxicidad , Venenos de Araña/toxicidad , Animales , Diafragma/inervación , Diafragma/ultraestructura , Masculino , Ratones , Microscopía Electrónica , Unión Neuromuscular/efectos de los fármacos , Nervio Frénico/efectos de los fármacos , Nervio Frénico/ultraestructura , Factores de Tiempo

RESUMEN

The ability of snake venoms to increase vascular permeability and to induce oedema through the release of pharmacologically active substances is well known. We have studied the oedema and vascular permeability induced by Bothrops lanceolatus venom in male Swiss white mice. Paw oedema was induced by the subplantar injection of B. lanceolatus venom (125-1000 ng/paw) and was quantified as the increase in paw weight. Changes in vascular permeability were assessed by measuring the amount of Evans blue dye extravasation. The oedema and the increase in vascular permeability were maximal within 2 h and had resolved after 24 h. The administration of the vasodilator iloprost (20 ng/paw) immediately after B. lanceolatus venom potentiated the oedema and the increase in vascular permeability by approximately four-fold. Pretreating the mice with indomethacin, dexamethasone, NDGA or BW A4C inhibited the venom-induced oedema and the increase in vascular permeability. In contrast, histamine, serotonin and PAF-acether antagonists (mepyramine, cyproheptadine and WEB 2086, respectively) were ineffective. Histological examination showed that B. lanceolatus venom (250 ng and 500 ng/paw) caused thickening of the inner dermal layers which was accompanied by extensive intercellular spaces indicative of oedema. In addition, there was a marked infiltration of inflammatory cells, particularly neutrophils, into the underlying muscle layer. The latter, however, remained morphologically unaffected during the 3 h of observation. Venom doses larger than 500 ng/paw produced intense haemorrhage. These results indicate that B. lanceolatus venom induces oedema and increases vascular permeability in the mouse hind paw. The principal mediators of this inflammatory response are cyclooxygenase and lipoxygenase products.

Asunto(s)

Permeabilidad Capilar , Venenos de Crotálidos/toxicidad , Edema/etiología , Animales , Antiinflamatorios/farmacología , Ácido Araquidónico/metabolismo , Azepinas/farmacología , Edema/patología , Masculino , Ratones , Triazoles/farmacología

RESUMEN

Acute renal failure (ARF) is the main cause of death following snake bites by Bothrops species. In this study, we investigated the morphologic and functional renal disturbances caused by Bothrops moojeni venom in rats. Renal function was assessed based on creatinine and lithium clearances and on histologic examination of renal tissue 5 hr after the intravenous administration of 0.2 mg of venom/kg and 5 hr, 16 hr, and 48 hr after 0.4 mg of venom/ kg. A venom dose of 0.4 mg/kg produced renal tubule disturbances, including acute impairment of proximal and post-proximal tubule sodium handling associated with acute tubule necrosis. The glomerular filtration rate (GFR) decreased significantly and was accompanied by severe morphologic disturbances in the renal glomeruli. These functional and morphologic findings were observed in the absence of any change in mean arterial blood pressure. The decrease in GFR was not related to the presence of fibrin deposits in the glomerular capillary loops. These results suggest an early nephrotoxic action of B. moojeni venom involving significant morphologic and functional changes similar to those observed in snakebite-induced ARF in humans.

Asunto(s)

Lesión Renal Aguda/inducido químicamente , Bothrops , Venenos de Crotálidos/toxicidad , Mordeduras de Serpientes/fisiopatología , Lesión Renal Aguda/patología , Lesión Renal Aguda/fisiopatología , Animales , Presión Sanguínea , Creatinina/sangre , Creatinina/orina , Pruebas de Función Renal , Glomérulos Renales/patología , Glomérulos Renales/fisiopatología , Túbulos Renales Proximales/patología , Túbulos Renales Proximales/fisiopatología , Litio/sangre , Litio/orina , Masculino , Potasio/sangre , Potasio/orina , Ratas , Ratas Wistar , Mordeduras de Serpientes/patología , Sodio/sangre , Sodio/orina

RESUMEN

The effects of Bothrops pirajai snake venom on the mouse extensor digitorum longus (EDL) preparation were examined using myographic, histopathological and biochemical approaches. B. pirajai venom (10, 25 or 50 microg/ml) dose dependently and irreversibly blocked the contractile response of indirectly stimulated EDL muscle. Histopathological analysis of EDL muscle incubated with venom showed dose-dependent damage with a loss of the normal tissue structure and the appearance of highly dark, edematous fibers together with myofibrils in various stages of condensation. At high doses of venom (50 microg/ml), loss of muscle cells was observed. In non-stimulated EDL, B. pirajai venom (10 and 50 microg/ml) caused a time-dependent release of CK which was maximal after 120 min. These results suggest that a component(s) present in the B. pirajai venom has a direct myolytic action on the skeletal muscle.

Asunto(s)

Bothrops/fisiología , Creatina Quinasa/metabolismo , Contracción Muscular/efectos de los fármacos , Músculo Esquelético/efectos de los fármacos , Venenos de Serpiente/toxicidad , Animales , Relación Dosis-Respuesta a Droga , Estimulación Eléctrica , Técnicas In Vitro , Ratones , Músculo Esquelético/química , Músculo Esquelético/patología , Miografía

RESUMEN

MP-III 4R PLA2 was purified from the venom of Bothrops pirajai venom (Bahia's jararacussu) after three chromatographic steps which started with RP-HPLC. The complete amino acid sequence of MP-III 4R PLA2 from Bothrops pirajai was determined by amino acid sequencing of reduced and carboxymethylated MP-III 4R and the isolated peptides from clostripain and protease V8 digestion. MP-III 4R is a D49 PLA2 with 121 amino acid residues and has a molecular weight estimated at 13,800 Da, with 14 half-cysteines. This protein showed moderate PLA2 and anticoagulant activity. This PLA2 does not have a high degree of homology with other bothropic PLA2-like myotoxins (approximately 75%) and nonbothropic myotoxins (approximately 60%). MP-III 4R is a new PLA2, which was isolated using exclusively analytical and preparative HPLC methods. Based on the N-terminal sequence and biological activities, MP-III 4R was identified as similar to piratoxin-III (PrTX-III), which was isolated by conventional chromatography based on molecular exclusion ion exchange chromatography. Clinical manifestations indicate that at the site of toxin injection, there may be pain of variable intensity, because animals continue to lick the limb. No clinical sign indicating general toxicity was noticed. Myotoxicity was observed in gastrocnemius muscle cells after exposure to MP-III 4R, with a high frequency (70%) of affected muscle fibers.

Asunto(s)

Bothrops/metabolismo , Fosfolipasas A/química , Fosfolipasas A/aislamiento & purificación , Venenos de Serpiente/química , Venenos de Víboras , Secuencia de Aminoácidos , Animales , Anticoagulantes/química , Cromatografía Líquida de Alta Presión , Cromatografía por Intercambio Iónico , Fosfolipasas A2 Grupo II , Ratones , Datos de Secuencia Molecular , Músculo Esquelético/química , Músculo Esquelético/citología , Péptidos/metabolismo , Fosfolipasas A2 , Proteínas de Reptiles , Análisis de Secuencia , Homología de Secuencia de Aminoácido , Venenos de Serpiente/toxicidad , Factores de Tiempo , Toxinas Biológicas/química

RESUMEN

Micrurus nigrocinctus is the most abundant coral snake in Central America. The venom of this specie induced a concentration-dependent (10-20 micrograms/ml) depolarization in the isolated mouse phrenic nerve-diaphragm preparations incubated at 37 degrees C. d-Tubocurarine (10 micrograms/ml) and (alpha beta ungarotoxin (3-5 micrograms/ml) were able to partially protect against the depolarization induced by the venom (10 micrograms/ml), suggesting the involvement of subsynaptic cholinergic receptors. This venom (10 micrograms/ml) also increased the frequency and amplitude of miniature end-plate potentials (mepps) during the first 10-20 min of incubation. Subsequently, the mepps progressively decreased and disappeared after 60 min. These responses were accompanied by ultrastructural changes involving the nerve terminals, the subsynaptic junctional folds and the muscle mitochondria. The synaptic gutter was shallow and, very often, "shrunken" terminals with omega-shaped axolemmal indentations and a decreased number of synaptic vesicles were present. A common finding was the presence of numerous finger-like, membrane-bounded bodies interposed between the terminal and the Schwann cells or postsynaptic sarcolemma. The preincubation of the venom with specific antivenom or the incubation of the preparations at room temperature (24-26 degrees C) reduced the number and intensity of the ultrastructural alterations. The last finding suggests the involvement of a enzymatic process, probably a phospholipase A2, present in the venom. There was a good correlation between the electrophysiological and ultrastructural effects induced by the venom which allow us to conclude that M. nigrocinctus venom has a presynaptic action in the initial stages of intoxication followed by sub- and postsynaptic effects, the last being the most important cause of neuromuscular blockade. A direct action of the venom on muscle fibers may also contributes to the irreversible blockade.

Asunto(s)

Venenos Elapídicos/toxicidad , Elapidae , Bloqueo Neuromuscular , Nervio Frénico/efectos de los fármacos , Animales , Diafragma/efectos de los fármacos , Diafragma/inervación , Diafragma/ultraestructura , Relación Dosis-Respuesta a Droga , Electrofisiología , Masculino , Ratones , Fármacos Neuromusculares Despolarizantes/toxicidad , Unión Neuromuscular/efectos de los fármacos , Unión Neuromuscular/fisiología , Nervio Frénico/fisiopatología , Nervio Frénico/ultraestructura , Ratas , Ratas Wistar , Transmisión Sináptica/efectos de los fármacos

RESUMEN

The 'armed' spider Phoneutria nigriventer is responsible for most human accidents involving spiders in Brazil. The effects of fraction Tx1 (PhTx1) from the venom of this spider were investigated by physiological and morphological methods using the mouse phrenic nerve-diaphragm preparation. PhTx1 (1 and 5 microg) did not affect the twitch tension of muscle fibers under indirect electrical stimulation. At this same concentration, PhTx1 also did not alter the miniature end-plate potential (mepp) frequency and amplitude, nor did it change the resting membrane potential 60 min after addition to the preparation. Light microscopy (LM) revealed that in muscles incubated with PhTx1 a number of fibers were morphologically altered, as evidenced by microvacuolization and myofibril hypercontraction and loss within 15 min after toxin administration. Transmission electron microscopy (TEM) showed sarcoplasmic reticulum swelling, disorganization of the sarcomeres and mitochondrial damage, and occasionally, sarcolemmal discontinuities with a persisting basal membrane. The intra-muscular fascicles of the phrenic nerve showed myelinated axons with vacuolated myelin sheaths as well as peri- and intra-axoplasmic vacuoles. The neuromuscular junction changes were variable, but were rarely severe. Thus, although PhTx1 did not depolarize or hyperpolarize the neuromuscular junction, it was nevertheless toxic to a restricted number of muscle fibers and nerve structures. The site of action of PhTx1 may involve the sarcolemma and axolemma as suggested by the morphological abnormalities which could reflect hydroelectrolytic disturbances.

Asunto(s)

Músculo Esquelético/efectos de los fármacos , Músculo Esquelético/patología , Neuropéptidos/toxicidad , Venenos de Araña/toxicidad , Arañas , Animales , Diafragma/inervación , Estimulación Eléctrica , Técnicas In Vitro , Masculino , Potenciales de la Membrana/fisiología , Ratones , Microscopía Electrónica , Mitocondrias/efectos de los fármacos , Mitocondrias/ultraestructura , Unión Neuromuscular/efectos de los fármacos , Unión Neuromuscular/patología , Unión Neuromuscular/fisiología , Nervio Frénico/efectos de los fármacos , Nervio Frénico/fisiología , Vesículas Sinápticas/efectos de los fármacos , Vesículas Sinápticas/ultraestructura

RESUMEN

Trypanosoma cruzi-infected mice show disturbance in the peripheral immune system such as polyclonal lymphocyte activation, autoantibody production, and immunosuppression of T lymphocytes. Previous observations in our laboratory showed that some stocks of T. cruzi can be contaminated with mouse hepatitis virus type 3 (MHV-3). Literature has shown that MHV-3 infection induces immunologic disorders characterized by thymic involution with marked cell depletion. However, the effects of interactions between MHV-3 and the parasite on the immune system are not well understood. In the present study specific-pathogen-free CBA mice were inoculated with MHV-3, alone or associated with different stocks of T. cruzi. Concurrent murine virus infection resulted in increased pathogenicity of T. cruzi infection shown by profound thymic atrophy; loss of cortical thymocytes; depletion of Thy1.2+, CD4+, and CD8+ cells; enhancement of in situ labeling of nuclear DNA fragmentation; and eventually, death of the animals. Such lines of evidence show that the mechanism underlying this thymic atrophy is associated with apoptosis. These results also suggest that MHV-3 can account for the increased immunosuppression observed during experimental infection with the parasite.

Asunto(s)

Apoptosis/inmunología , Enfermedad de Chagas/inmunología , Hepatitis Viral Animal/inmunología , Terapia de Inmunosupresión , Virus de la Hepatitis Murina/inmunología , Timo/inmunología , Trypanosoma cruzi/inmunología , Animales , Autoanticuerpos/inmunología , Ratones , Ratones Endogámicos CBA , Timo/patología

RESUMEN

The benzidine technique for histochemical detection of the SO4 ion was studied analytically on filter paper strips loaded with 0.02 ml of solutions of sulfate containing and sulfate free substances. The influence of the benzidin solution pH on the SO4 and PO4 ion precipitation was analysed and the experimental condition where the SO4 ion was specifically precipitated was established. In basis on this study a benzidine histochemical technique suitable to detect the SO4 ion without interference of the PO4 ion was proposed for tissue sections. This technique has some advantages on the other benzidin techniques previously proposed mainly concerning its specificity.

Asunto(s)

Bencidinas , Sulfatos , Aniones , Precipitación Química , Histocitoquímica , Fosfatos