Universidad Juárez del Estado de Durango

About: Universidad Juárez del Estado de Durango is a education organization based out in Durango, Mexico. It is known for research contribution in the topics: Population & Biodiversity. The organization has 1209 authors who have published 1404 publications receiving 12999 citations. The organization is also known as: Universidad Juarez del Estado de Durango & Juarez University of the State of Durango.

Arsenic Exposure and Cognitive Performance in Mexican Schoolchildren

Abstract: Recent studies indicate that in several regions of the world, arsenic concentration in water is much higher than accepted levels (Smedley and Kinniburgh 2002). The concern with As contamination of drinking water is that consumption and use of this water in cooking can increase As exposure in humans (Del Razo et al. 2002). In Mexico, the amount of this contaminant in ground water varies from 10 to 5,000 μg/L (Del Razo et al. 1990). Del Razo et al. (1990; 1994) reported on the problem of As-contaminated groundwater in the Lagunera Region of northern Mexico, with > 50% of samples having As concentrations > 50 μg/L, which was the former level of reference set by the World Health Organization (International Programme on Chemical Safety 2001). The predominant type of As in 90% of the samples was pentavalent arsenic. In 1977, the presence of As in potable water was reported in the city of Torreon, the main city in the Region Lagunera and the site of the most important metallurgic complex of Mexico. As concentration in Torreon’s water was up to 4–6 mg/L, far above the present 10-μg/L limit (Cebrian et al. 1994; Mandal and Suzuki 2002). Benin et al. (1999) evaluated heavy metal contamination of soil in three residential areas that surround the smelter and found that As levels had a median of 113 μg/g, and ranged from 78 to 287 μg/g. These levels exceeded the level at which the U.S. Environmental Protection Agency (EPA) designated cleanup goals for Superfund sites, 5–65 μg/g (U.S. EPA 1997). Approximately 60–90% of the soluble inorganic arsenic (InAs) components are absorbed through the gastrointestinal tract (Hall 2002). In humans, InAs metabolism involves at least five metabolites that can exert toxic effects (Valenzuela et al. 2005). The measure of urinary As (UAs) excretion is a good biomarker for chronic exposure via drinking water [Agency for Toxic Substances and Disease Registry (ATSDR) 2000]. As concentration in urine, normally < 10 μg/L, can reach as high as 50 μg/L in adults and children living close to metal foundries (Carrizales et al. 2006; Polissar et al. 1990). The negative consequences of As exposure in humans include respiratory, gastrointestinal, hematologic, hepatic, renal, dermic, neurologic, and immunologic effects (ASTDR 2000; Garcia-Vargas and Hernandez-Zavala 1996; International Programme on Chemical Safety 2001), many of which continue even after the contaminant source is controlled (Diaz-Barriga et al. 1997). As can also have detrimental effects on the central nervous system and cognitive development in children (International Programme on Chemical Safety 2001). Acute As exposure affects sensory nerves as well as the long axon neurons, which results in the clinical manifestation of numb extremities. Neurologic tests have shown nerve axonophathy and demyelination (Franzblau and Lilis 1989; Rodriguez et al. 2003; Yung 1984). As also affects the content of brain monoamines, and the concentrations of dopamine and serotonin in the hippocampus, hypothalamus, cerebral cortex, and the striatum (Itoh et al. 1990; Mejia et al. 1997; Rodriguez et al. 2003). Few reports have suggested a detrimental effect of As exposure on cognitive development and function, including disturbed visual perception, problems with visuomotor integration, psychomotor speed, attention, speech, and memory. (Calderon et al. 2001; Rodriguez et al. 2003; Tsai et al. 2003). In this regard, the effects of As are similar to and could be confounded with the effects of other environmental contaminants such as lead. In fact, in many regions of the world, As exposure co-occurs with exposure to other contaminants such as lead (Carrizales et al. 2006; Diawara et al. 2006). Poorer performance on a range of cognitive tests has been reported in children with low to moderate lead exposure in Torreon (Kordas et al. 2004) and other settings (Canfield et al. 2003; De Burbure 2006; Lanphear et al. 2000). In this study we identified demographic and nutritional factors that are associated with UAs concentration in school-age children. We also investigated the influence of As exposure on cognitive function in these children.

Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic.

Abstract: Arsenic is a ubiquitous element found in several forms in foods and environmental media such as soil, air, and water; the predominant form in drinking water is inorganic As (iAs), which is both highly toxic and readily bioavailable. iAs is a recognized carcinogen in humans [National Research Council (NRC) 2001]. Chronic ingestion of iAs-contaminated drinking water is therefore considered the major pathway behind the risk to human health. It has been estimated that 200 million people worldwide are at risk from health effects associated with high concentrations of As in their drinking water (NRC 2001). Several other regions in the world are exposed to levels above the maximum permissible limit recommended by the World Health Organization (WHO 1993). In humans, the chronic ingestion of iAs (> 500 μg/day As) has been associated with cardiovascular, nervous, hepatic, and renal alterations and diabetes mellitus as well as cancer of the skin, bladder, lung, liver, and prostate [Agency for Toxic Substances and Disease Registry (ATSDR) 2000]. Characteristic features of arseniasis include skin manifestations, such as hyperpigmentation, hypopigmentation, and hyperkeratosis on the palms and soles, and skin cancer at later stages (Cebrian et al. 1983; Schwartz 1997; Tseng et al. 1968). In humans, the mechanism by which iAs exerts its toxic effects is very complex because its metabolism involves at least five metabolites that can exert toxic effects. The scheme for the stepwise conversion of arsenite (iAsIII) into mono-, di-, and trimethylated products is as follows: Briefly, the metabolic process is carried out in two processes: a) the reactions of reduction that convert the pentavalent species to trivalency, and b) reactions of oxidative methylations where iAs is converted to mono-, di-, and trimethyl arsenic forms (MAs, DMAs, and TMAsO, respectively). Thus, both pentavalent methylarsenic (MAsV) and trivalent methylarsenic (MAsIII) forms are intermediates or products of this pathway (Lin et al. 2002; Thomas et al. 2004). Using S-adenosylmethionine as a methyl group donor, As methyltransferase (Cyt19, EC 2.1.1.138) has been shown to catalyze reactions, reduction and oxidative methylation, in rodents and humans (Waters et al. 2004). Other studies have shown the capacity of two mammalian proteins to reduce iAsV, glutathione S-transferase omega (GST Ω, EC 2.5.1.18) (Zakharyan et al. 2001) and the purine nucleoside phosphorylase (PNP, EC 2.4.2.1) (Nemeti et al. 2003; Radabaugh et al. 2002). Urinary As is generally regarded as the most reliable indicator of recent exposure to iAs and is used as the main biomarker of exposure (Mushak and Crocetti 1995). In addition, the urinary profiles of iAs metabolites have frequently been used in epidemiologic studies to assess the capacity of exposed individuals to methylate iAs. During almost 20 years, the methylation of iAs has been generally evaluated using urinary measurement of iAs (III + V), MAs (III + V), and DMAs (III + V) in people exposed to As. Nevertheless, the differentiation of the trivalent intermediaries of As metabolism is important because the trivalent methylated arsenicals, MAsIII and DMAsIII, are more potent than either iAsIII or iAsV in cytotoxicity (Styblo et al. 2000), genotoxicity (Mass et al. 2001; Nesnow et al. 2002), and inhibition of enzymes with antioxidative functions (Lin et al. 2001; Styblo et al. 1997). Therefore, the formation of MAsIII and DMAsIII in the methylation pathway for iAs may play a significant role in the induction of toxic effects associated with exposures to iAs. The goal of this study was to assess the urinary pattern of As methylation, including trivalent methylated metabolites, in an As-endemic population using freshly collected samples analyzed as soon as possible to avoid the oxidation of MAsIII and DMAsIII, even at temperatures < 0°C (Del Razo et al. 2001; Gong et al. 2001). Additionally, we compared the pattern of urinary trivalent methylated metabolites between persons with and without skin lesions associated with arsenicism in an endemic Mexican area.

Exposure to arsenic in drinking water is associated with increased prevalence of diabetes: A cross-sectional study in the Zimapán and Lagunera regions in Mexico

Abstract: Human exposures to inorganic arsenic (iAs) have been linked to an increased risk of diabetes mellitus. Recent laboratory studies showed that methylated trivalent metabolites of iAs may play key roles in the diabetogenic effects of iAs. Our study examined associations between chronic exposure to iAs in drinking water, metabolism of iAs, and prevalence of diabetes in arsenicosis-endemic areas of Mexico. We used fasting blood glucose (FBG), fasting plasma insulin (FPI), oral glucose tolerance test (OGTT), glycated hemoglobin (HbA1c), and insulin resistance (HOMA-IR) to characterize diabetic individuals. Arsenic levels in drinking water and urine were determined to estimate exposure to iAs. Urinary concentrations of iAs and its trivalent and pentavalent methylated metabolites were measured to assess iAs metabolism. Associations between diabetes and iAs exposure or urinary metabolites of iAs were estimated by logistic regression with adjustment for age, sex, hypertension and obesity. The prevalence of diabetes was positively associated with iAs in drinking water (OR 1.13 per 10 ppb, p < 0.01) and with the concentration of dimethylarsinite (DMAsIII) in urine (OR 1.24 per inter-quartile range, p = 0.05). Notably, FPI and HOMA-IR were negatively associated with iAs exposure (β -2.08 and -1.64, respectively, p < 0.01), suggesting that the mechanisms of iAs-induced diabetes differ from those underlying type-2 diabetes, which is typically characterized by insulin resistance. Our study confirms a previously reported, but frequently questioned, association between exposure to iAs and diabetes, and is the first to link the risk of diabetes to the production of one of the most toxic metabolites of iAs, DMAsIII.

Comparison of the value of PCNA and Ki-67 as markers of cell proliferation in ameloblastic tumors.

Abstract: Objectives: The aim of this study was to compare among PCNAand Ki-67 as the most reliable immunohisto chemical marker for evaluating cell proliferation in ameloblastic tumors Study Design: Observational, retrospective, and descriptive study of a large series of ameloblastic tumors, com- D esign: Observational, retrospective, and descriptive study of a large series of ameloblastic tumors, com- esign: Observational, retrospective, and descriptive study of a large series of ameloblastic tumors, com posed of 161 ameloblastomas and four ameloblastic carcinomas, to determine and compare PCNA and Ki-67 expression using immunohistochemistry techniques Results: When analyzing Ki-67 positivity, the desmoplastic ameloblastoma demonstrated a significantly lower proliferation rate (19%) compared with the solid/multicystic and unicystic ameloblastomas and ameloblastic car cinomas (p<005), whereas the ameloblastic carcinomas displayed a significantly higher rate compared with all of the other ameloblastomas (487%) (p<005) When analyzing cell proliferation with PCNA, we found significant differences only between the ameloblastic carcinomas (933%) and the desmoplastic ameloblastomas (p<005) When differences between the immunopositivity for PCNA and Ki-67 were compared, the percentages were higher for PCNA in all types of ameloblastomas and ameloblastic carcinomas In all cases, the percentages were greater than 80%, whereas the immunopositivity for Ki-67 was significantly lower; for example, the ameloblastic carcinoma expressed the highest positivity and only reached 487%, compared to 933% when we used PCNA Conclusions: In the present study, when we used the proliferation cell marker Ki-67, the percentages of positiv ity were more specific and varied among the different types of ameloblastomas, suggesting that Ki-67 is a more specific marker for the proliferation of ameloblastic tumor cells