Cell accumulation and antileishmanial effect of exogenous and endogenous protoporphyrin IX after photodynamic treatment / Acumulación celular y efecto anti- Leishmania de la protoporfirina IX exógena y endógena después del tratamiento fotodinámico

Introduction: Photodynamic therapy (PDT) using 5-aminolevulinic acid-induced protoporphyrin IX (ALA-PpIX) constitutes an interesting alternative for cutaneous leishmaniasis treatment. Objective: To evaluate the production of PpIXbased on the administration of ALA and MAL and the effect of ALA-PDTat cellular level on non-infected and infected THP-1 cells using Leishmania ( Viannia ) panamensis or Leishmania ( Leishmania ) infantum (syn Leishmania chagasi ) parasites. Materials and methods: Protoporphyrin IX (PpIX) production and mitochondrial colocalization were evaluated by confocal microscopy. Cell toxicities were evaluated after treatment with the compounds, followed by light irradiation (597-752 nm) at 2.5 J/cm 2 fluency using a colorimetric MTT assay for THP-1 cells and a standard microscopic analysis of parasites. Results were expressed as compound concentration activity against 50% of cells or parasites (CC 50 or IC 50 ). Results: ALA or MAL induced an endogenous PpIX with a red fluorescence localized mainly in the mitochondria inside human cells. ALA and MAL-PDT induced a similar range of toxicities on THP-1 cells (CC 50 0.16±0.01mM and 0.33±0.019 mM, respectively) without any apparent inhibition of intracellular parasites in the infected cells as compared to untreated controls. Exogenous PpIX-PDT was toxic to THP-1 cells (CC 50 0.00032±0.00002 mM), L. (L.) infantum (IC 50 0.003±0.0001 mM) and L. (V.) panamensis (IC 50 0.024±0.0001 mM) promastigotes. Conclusions: Despite the effectiveness of exogenous PpIX on promastigotes and the production of PpIX by human infected cells, treatment with ALA or MAL before irradiation was unable to completely destroy L. (L.) infantum or L. (V.) panamensis intracellular amastigotes.

Introducción. El tratamiento fotodinámico con ácido 5-aminolevulínico como inductor de la protoporfirina IX (ALA-PpIX) constituye una alternativa interesante en el tratamiento de la leishmaniasis cutánea. Objetivo. Evaluar la producción de protoporfirina IX (PpIX) a partir de la administración de ALA o MAL y el efecto de la PDT con ALA a nivel celular en células THP-1 no infectadas e infectadas con Leishmania ( Viannia ) panamensis o Leishmania ( Leishmania ) infantum (syn. Leishmania chagasi ). Materiales y métodos. La producción de protoporfirina IX y su ‘colocalización´ mitocondrial se evaluaron mediante microscopía ‘confocal´. Se evaluó la toxicidad celular después del tratamiento con los compuestos y la aplicación de irradiación de luz (597-752 nm) en una fluencia de 2,5 J/cm 2 mediante el empleo de la prueba colorimétrica con metil-tiazol-tetrazolio (MTT) en las células, y de métodos microscópicos estándar en los parásitos. Los resultados se expresaron como la concentración del compuesto activo en el 50 % de las células o parásitos (CC 50 o CI 50 ). Resultados. El ácido aminolevulínico o el metil-5-aminolevulinato indujeron la protoporfirina IX endógena en células humanas, y se observó fluorescencia de color rojo en las mitocondrias. La actividad del ácido aminolevulínico y del metil-5-aminolevulinato utilizados con terapia fotodinámica fue similar en las células THP-1 (CC 50 0,16±0,01 mM y 0,33±0,019 mM, respectivamente) y, aparentemente, no inhibió los parásitos en las células infectadas, en comparación con los controles. El tratamiento exógeno con protoporfirina IX y terapia fotodinámica fue tóxico para las células THP-1 (CC 50 0,00032 ±0,00002 mM) y para los promastigotes de L. (L .) infantum (IC 50 0,003±0,0001 mM) y L. ( V .) panamensis (CI 50 0,024±0,0001 mM). Conclusiones. A pesar de la ‘fotoactividad´ del tratamiento con protoporfirina IX en promastigotes y de su producción después del tratamiento con ácido aminolevulínico y metil-5-aminolevulinato en las células infectadas con Leishmania , no se observó daño en los amastigotes presentes en las células de L. ( L .) infantum o L . ( V .) panamensis .

Trypanosoma cruzi: prevalencia y factores de riesgo de seropositividad en donantes de sangre del Hemocentro y Unidad de Aféresis, Valledupar, Colombia, 2013-2014 / Trypanosoma cruzi: prevalence and risk factors for seropositivity in blood donors of Hemocentro y Unidad de Aféresis, Valledupar, Colombia, 2013-2014

Introducción: La transmisión de Trypanosoma cruzi por transfusiones sanguíneas representa la segundalínea de infección después de la vectorial, lo que hace necesario identificar algunas particularidadessocioepidemiológicas en los donantes que permitan predecir la infección por Trypanosoma cruzi. Objetivo: Determinar la prevalencia de anticuerpos anti-Trypanosoma cruzi y los factores de riesgo de seropositividad en donantes de sangre voluntarios del Hemocentro y Unidad de Aféresis de Valledupar, Colombia. Materiales y métodos: Se realizó un estudio descriptivo de corte transversal en 170 donantes de sangre voluntarios reclutados entre 2013 y 2014. La detección de anticuerpos IgG anti-Trypanosoma cruzi se realizó mediante pruebas serológicas. Las variables que predicen la seropositividadpara Trypanosoma cruzi se indagaron mediante un cuestionario socioepidemiológico y un posterioranálisis bivariado y de regresión logística...

Introduction: Transmission of Trypanosoma cruzi through blood transfusions represents the second most frequent mechanism after the vectorial transmission. Therefore, it is necessary to identify some socioepidemiological characteristics that allow predicting the Trypanosoma cruzi infection on the donors. Objective: To determine the prevalence of anti-Trypanosoma cruzi and risk factors for seropositivity in voluntary blood donors at the Hemocentro y Unidad de Aferesis de Valledupar, Colombia. Materialsand methods: A descriptive cross-sectional study was conducted in 170 volunteer blood donors recruited between 2013 and 2014. Detection of IgG antibodies anti-Trypanosoma cruzi was performed by serological tests. The inquiry about the predictors of seropositivity for Trypanosoma cruzi was made through a socioepidemiological questionnaire, followed by a bivariate analysis and logistic regression...

Leprosy type 1 reactions and erythema nodosum leprosum: [review]

Leprosy reactions are a major cause of nerve damage and morbidity in a significant proportion of leprosy patients. Reactions are immunologically mediated and can occur even after successful completion of multi-drug therapy. This review focuses on the epidemiology, pathology and treatment of leprosy type 1 reactions, erythema nodosum leprosum and silent neuropathy.

As reações hansênicas são a principal causa de dano e morbidade neural em grande parte dos pacientes hansênicos. São imunomediadas e podem ocorrer mesmo após o término bem sucedido da poliquimioterapia. Esta revisão enfoca a epidemiologia, a patologia e o tratamento das reações hansênicas do tipo 1, do eritema nodoso hansênico e da neuropatia silenciosa.

Sublethal toxicity of deltamethrin in relation to sex: Enzymatic studies in the freshwater fish Channa punctatus.

One of the most widely used active ingredients in the world (for pest control) is deltamethrin, a synthetic pyrethroid. Deltamethrin is popular not only because of its effectiveness, but also for characteristics that allow the insecticide to work efficiently at low doses. Deltamethrin is a Type-II pyrethroid compound that is however highly toxic to fish, while being less toxic to birds and mammals. In the present study, Channa punctatus was used as an animal model to determine the toxicity of deltamethrin. Males weighing 10 ± 2g and females weighing 12 ± 2g were divided into groups of ten each and were exposed to different concentrations of deltamethrin ranging from 0.02 ppm to 0.2 ppm, for five exposure periods, i.e., 1, 7, 15, 20 and 30 days. The acetylcholinesterase (AChE) activity and actylcholine (ACh) content were estimated. The levels of AChE activity rose at 24 h relative to control in all the organs, whereas the ACh content dipped. Thereafter, the levels of AChE activity progressively decreased through 7 days, and continued upto the 15th day, mirroring the steady increase in ACh. From 15th day onwards, the levels of AChE activity gradually increased, and approached that of the control at 30 day exposure, whereas the levels of ACh content displayed an opposite trend.