Assessment of genotoxicity induced by helminthes parasites in freshwater fishes of river Ganges

Several parasites have been shown to induce genotoxicity in humans and fish are important intermediate hosts for completing the life cycle of many parasites, posing a huge economic loss worldwide through the ecosystem food chain. In the present study, we assessed the genotoxic potential of helminth Rostellascaris sp. through a benchmark of comet assay and micronucleus (MNi) tests on the hepatocytes, muscle, and whole blood of infected fish Bagarius bagarius (Hamilton) collected from different sites of the river Ganges. The percentage of the mean tail length of the comet was 10.28±0.36 in the reticulocytes of the infected fish which was significantly (P ?0.05) longer compared to the control (2.86±0.12). Similarly, a significantly (P ?0.05) higher DNA damage was observed in hepatocytes of parasite-infected fish (12.15±0.24) when compared to the control (3.024±0.013). A comparatively higher DNA damage was observed in the hepatocytes than the reticulocytes, indicative of tissue-specific DNA damage as hepatocytes are the biomarkers of metabolic functions prone toward biotic stress. A higher induction of MN was observed in infested fish (0.18±0.07) as compared to the control. Our results suggest that parasites contribute to the induction of cellular and DNA damage in fish during the progression of the host-parasite interaction.

Expression of CRELD2 in mouse tissues / 药学实践杂志

Objective To explore the expression of CRELD2 at the gene and protein levels of mouse tissues, and to provide a reference for studying the biological function of CRELD2 in various tissues. Methods The expression level of CRELD2 in the liver, pancreas, stomach, and lung of C57BL/6J mice was determined by real-time PCR and Western Blot. Results RT-PCR and WB showed that CRELD2 was expressed in mouse liver, pancreas, stomach, and lung. The relative expression levels of CRELD2 from high to low were pancreas, stomach, liver, and lung at the gene level, and pancreas, liver, stomach, and lung at protein level respectively. The result suggested that the relative expression levels of the CRELD2 gene and protein in different tissues were not completely consistent, suggesting that it is related to transcriptional regulation. Conclusion CRELD2 is expressed in mouse liver, pancreas, stomach, and lung, and the relative expression levels of CRELD2 are not completely parallel at the gene and protein level.

Tissue-specific Role of CX₃CL1 Expressing Immune Cells and Their Relationships with Human Disease

Chemokine (C-X3-C motif) ligand 1 (CX₃CL1, also known as fractalkine) and its receptor chemokine (C-X3-C motif) receptor 1 (CX₃CR1) are widely expressed in immune cells and non-immune cells throughout organisms. However, their expression is mostly cell type-specific in each tissue. CX₃CR1 expression can be found in monocytes, macrophages, dendritic cells, T cells, and natural killer (NK) cells. Interaction between CX3CL1 and CX₃CL1 can mediate chemotaxis of immune cells according to concentration gradient of ligands. CX₃CL1 expressing immune cells have a main role in either pro-inflammatory or anti-inflammatory response depending on environmental condition. In a given tissue such as bone marrow, brain, lung, liver, gut, and cancer, CX₃CL1 expressing cells can maintain tissue homeostasis. Under pathologic conditions, however, CX₃CL1 expressing cells can play a critical role in disease pathogenesis. Here, we discuss recent progresses of CX3CL1/CX₃CL1 in major tissues and their relationships with human diseases.

Structure and Expression Analyses of SVA Elements in Relation to Functional Genes

SINE-VNTR-Alu (SVA) elements are present in hominoid primates and are divided into 6 subfamilies (SVA-A to SVA-F) and active in the human population. Using a bioinformatic tool, 22 SVA element-associated genes are identified in the human genome. In an analysis of genomic structure, SVA elements are detected in the 5' untranslated region (UTR) of HGSNAT (SVA-B), MRGPRX3 (SVA-D), HYAL1 (SVA-F), TCHH (SVA-F), and ATXN2L (SVA-F) genes, while some elements are observed in the 3'UTR of SPICE1 (SVA-B), TDRKH (SVA-C), GOSR1 (SVA-D), BBS5 (SVA-D), NEK5 (SVA-D), ABHD2 (SVA-F), C1QTNF7 (SVA-F), ORC6L (SVA-F), TMEM69 (SVA-F), and CCDC137 (SVA-F) genes. They could contribute to exon extension or supplying poly A signals. LEPR (SVA-C), ALOX5 (SVA-D), PDS5B (SVA-D), and ABCA10 (SVA-F) genes also showed alternative transcripts by SVA exonization events. Dominant expression of HYAL1_SVA appeared in lung tissues, while HYAL1_noSVA showed ubiquitous expression in various human tissues. Expression of both transcripts (TDRKH_SVA and TDRKH_noSVA) of the TDRKH gene appeared to be ubiquitous. Taken together, these data suggest that SVA elements cause transcript isoforms that contribute to modulation of gene regulation in various human tissues.

Altered vascular reactivity induced by malaria parasites / Reactividad vascular alterada inducida por los parásitos de la malaria

OBJECTIVES: In this study, we have examined the possibility that there is altered vascular reactivity due to the direct interaction between parasitized erythrocytes and vascular endothelial cells. METHOD: Ring preparations of rat aorta were studied using standard in vitro techniques, the rings were mounted in 20 ml organ baths containing PSS under an initial load of 1g, maintained at 37ºC atpH 7.4 and isometric contractions were recorded electronically. Rings were allowed 90 minutes to equilibrate before the commencement of the various protocols: * Dose responses to phenylephrine (PE) and other vasoactive agents (high-K+) * Acetylcholine (Ach) -induced relaxation in phenylephrine-contracted rings (pre-contraction was induced by EC70 concentration of phenylephrine) * Ach-induced relaxation in PE-precontracted, endothelium-denuded rings * Also, relaxation responses to acetylcholine was investigated through application ofa single (EC7o) concentration of acetylcholine in rings exposed to blood with varying concentrations and dilutions ofparasitized blood and varying durations ofexposure. RESULTS: Incubation with parasitized blood resulted in a significant increase in maximum contractile response to phenylephrine in the rat aortic rings (p < 0.05) but no effect to the base line. Analysis of the whole dose-response curve (using paired t-test) showed a significant left-ward shift following the addition of parasitized blood (p < 0.05), EC70 (M) values increasing from 7 x 10-7 to 5 x 10-6M. Following exposure to parasitized blood, the magnitude ofAch-induced relaxation responses reduced signi ficantlyfrom 73 ± 3.6 to 24.75 ± 7.25% in rat aortic rings (p < 0.05). Ach relaxations were significantly enhanced (p < 0.05) at 5-minute exposure; however at longer durations, Ach-relaxations were variable and inconsistent. The lesser the dilution, due to increased volume of parasitized blood, the lesser the relaxation response. Following endothelium removal, there was a marked impairment in endothelium-dependent relaxation responses to ACh in both the control and incubated vessels. Exposure to parasitized blood did not significantly alter contractile responses induced by potassium depolarization. CONCLUSIONS: This gives evidence in support of an endothelium-dependent action of malaria parasites as vascular effects ofmalaria parasites are mediated, at least in part, via endothelium-dependent mechanism(s).

OBJETIVO: En este estudio, hemos examinado la posibilidad de que exista una reactividad vascular alterada debido a la interacción directa entre los eritrocitos parasitados y las células endoteliales vasculares. MÉTODO: Se estudiaron preparaciones de anillo de aorta de rata usando técnicas in vitro estándar. Los anillos fueron montados en baños de órgano de 20 ml que contenían solución salina fisiológica (SSF) con una carga inicial de 1g, mantenida a 37ºC con un pH de 7.4, y las contracciones isométricas fueron registradas electrónicamente. A los anillos se les dio un tiempo de 90 minutos para permitir que se equilibraran, antes del comienzo de los varios protocolos. * Respuestas a la dosis de fenilefrina (FE) y otros agentes vasoactivos (K+ alto) * Relajación inducida mediante acetilcolina (Ac) en los anillos contraídos con fenilefrina (la precontracción fue inducida mediante una concentración EC70 de fenilefrina) * Relajación inducida mediante Ac en anillos despojados de endotelio. Pre-contraídos con FE. * También, se investigaron las respuestas de relajación a la acetilcolina a través de la aplicación de una sola concentración (EC70) de acetilcolina en anillos expuestos a la sangre con diversas concentraciones y diluciones de sangre parasitada y distintas duraciones de exposición. RESULTADOS: La incubación con sangre parasitada tuvo como resultado un aumento significativo en la respuesta contráctil máxima a la fenilefrina en los anillos aórticos de las ratas (p < 0.05) pero ningún efecto a la línea de base. El análisis de toda la curva de respuesta a la dosis (usando la prueba t pareada) mostró un desplazamiento significativo hacia la izquierda tras la adición de sangre parasitada (p < 0.05), EC70 (M), aumentado los valores de 7 x 10-7 a 5 x 10-6M. Tras la exposición a la sangre parasitada, la magnitud de las respuestas a la relajación inducida por Ac se redujo significativamente de 73 ± 3.6 a 24.75 ± 7.25% en los anillos aórticos de ratas (p < 0.05). Las relajaciones por Ac mejoraron significativamente (p < 0.05) a los 5 minutos de exposición. Sin embargo, a duraciones más largas, las relajaciones por Ac fueron variables e inconstantes. Mientras menor era la dilución, debido al aumento de volumen de la sangre parasitada, menor era la respuesta de relajación. Una vez retirado el endotelio, se producía un marcado deterioro en las respuestas de relajación dependiente del endotelio, ante el Ac, tanto en los recipientes de control como en los encubados. La exposición a la sangre parasitada no alteró de manera significativa las respuestas contráctiles inducidas por la despolarización del potasio. CONCLUSIONES: Esto provee evidencias en apoyo a una acción dependiente del epitelio, por parte de los parásitos de la malaria, por cuanto los efectos vasculares de los parásitos de la malaria se hallan mediados, al menos en parte, por los mecanismos dependientes del endotelio.

Tissue-specific Expression of DNA Repair Gene, N-Methylpurine-DNA Glycosylase (MPG) in Balb/c Mice without External Damage

The N-methylpurine-DNA glycosylase (MPG), a ubiquitous DNA repair enzyme, removes N-methylpurine and other damaged purines induced in DNA. Tissue-specific mRNA levels of the N-methylpurine-DNA glycosylase (MPG) were investigated in Balb/c mice of four different growing stages; newborn, 1, 4 and 8-weeks postpartum. MPG expressions in the newborn and the 8-week-old mice were the highest in thymus and testis, respectively. The tested tissues of the newborn mice had consistently higher MPG mRNA level than 8-week-old adults except in testis and thymus. The MPG mRNA level in testis was the lowest in the newborn mice, but it attained the highest in the 8-week-old mice. The levels of MPG mRNA among the different tissues in the newborn and the 8-week-old mice were more than 9.0 and 19.0-fold respectively. These results suggest that the of MPG expression was dependent on the growing stage and had tissue-specificity.