CDH with analgesic overuse is a common disorder in the general population, mainly in women in their fifties, in whom 5% meet its diagnostic criteria.

We present here the cloning and characterization of the EhPgp1 multidrug resistance gene promoter isolated from the Entamoeba histolytica drug-resistant mutant clone C2. The EhPgp1 promoter lacks the typical TATA box and the transcriptional initiation sequences described for other E. histolytica promoters. The major transcription initiation site of the EhPgp1 gene was located at the ATG start codon. The EhPgp1 core promoter located within the first 244 base pairs showed a higher chloramphenicol acetyltransferase expression in the transfected trophozoites of clone C2 than in those of the sensitive clone A. Gel shift assays revealed three specific DNA-protein complexes (Ia, IIa, and IIIc) using nuclear extracts from clone C2, whereas three main complexes (If, IIf, and IIg) were limited to clone A. Competition assays suggested the presence of C/EBP-like and OCTlike proteins in complexes Ia and IIa, respectively, probably involved in the expression of the EhPgp1 gene, whereas complex IIIc was competed by GATA-1, C/EBP, OCT, and HOX oligonucleotides. Thus, differential DNAprotein complexes may be formed by transcriptional factors involved in the regulation of the EhPgp1 gene expression.

This study presents morphological and biochemical evidence of programmed cell death (PCD) in Entamoeba histolytica induced by exposure of trophozoites to the aminoglycoside antibiotic G418. Morphological characteristics of PCD, including cell shrinkage, reduced cellular volume, nuclear condensation, DNA fragmentation and vacuolization were observed, with preservation of trophozoite membrane integrity. PCD is orchestrated biochemically by alterations in intracellular ion fluxes. In G418-treated trophozoites, overproduction of reactive oxygen species (ROS), decreased intracellular K + , increased cytosolic calcium, and decreased intracellular pH levels were observed. However, externalization of phosphatidylserine was not detected. These results suggest that amoebae can undergo PCD under stress conditions, and that this PCD shares several properties with PCD reported in mammals and in a variety of unicellular organisms. INTRODUCTIONEntamoeba histolytica, the causal agent of amoebiasis, is a protozoan parasite that resides in the colon of infected humans. The invasive trophozoites adhere to mucus and epithelial cells, proliferate by binary fusion, and release proteolytic factors that destroy the intestinal mucosa, resulting in amoebic dysentery. In one in 10 patients with intestinal E. histolytica infection, the trophozoites migrate through the portal vein to the liver and give rise to amoebic abscesses, the main cause of death by this parasite (Espinosa-Cantellano & Martínez-Palomo, 2000). The apoptosis of host cells such as macrophages induced by contact with E. histolytica trophozoites has been widely studied, and it is considered an important feature of the host-parasite relationship (Ragland et al., 1994;Berninghausen & Leippe, 1997).Programmed cell death (PCD) has been considered a critical mechanism of development, differentiation and control of cellular proliferation in metazoans. However, increasing evidence indicates that PCD is also present in unicellular organisms. Forms of PCD such as apoptosis, apoptosis-like processes and necrosis-like processes have been identified in several bacteria (Lewis, 2000), yeast (Madeo et al., 1999), the slime mould Dictyostelium discoideum (Cornillon et al., 1994), the dinoflagellate Peridinium gatunense (Vardi et al., 1999), the euglenoid Euglena gracilis (Scheuerlein et al., 1995), the ciliate Tetrahymena thermophila (Christensen et al., 1995), and the protozoan parasites Trypanosoma, Leishmania (Nguewa et al., 2004) and Plasmodium (Al-Olayan et al., 2002). Recently, results reported by Ramos et al. (2007) have suggested the induction of an apoptotic-like process by nitric oxide species in E. histolytica. Apoptosis is the result of a genetic program that induces cellular and biochemical changes, including caspase activation, externalization of phosphatidylserine (PS), an increase in intracellular Ca 2+ and mitochondrial dysfunction, as well as physical changes such as cell shrinkage, alteration in cell volume, cytoplasmic blebbing and vacuolization, chromatin conden...

By understanding structure–function relationships of active biopolymers (e.g. enzymes and nucleic acids) in green non-conventional media, sustainable chemical processes may be developed.

Infections with protozoa parasites are associated with high burdens of morbidity and mortality across the developing world. Despite extensive efforts to control the transmission of these parasites, the spread of populations resistant to drugs and the lack of effective vaccines against them contribute to their persistence as major public health problems. Parasites should perform a strict control on the expression of genes involved in their pathogenicity, differentiation, immune evasion, or drug resistance, and the comprehension of the mechanisms implicated in that control could help to develop novel therapeutic strategies. However, until now these mechanisms are poorly understood in protozoa. Recent investigations into gene expression in protozoa parasites suggest that they possess many of the canonical machineries employed by higher eukaryotes for the control of gene expression at transcriptional, posttranscriptional, and epigenetic levels, but they also contain exclusive mechanisms. Here, we review the current understanding about the regulation of gene expression in Plasmodium sp., Trypanosomatids, Entamoeba histolytica and Trichomonas vaginalis.