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1.
Ear Hear ; 45(2): 329-336, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-37700446

RESUMEN

OBJECTIVES: To evaluate the extent of hearing loss among pottery workers in Mexico exposed to lead. DESIGN: The authors conducted a cross-sectional study including 315 adult pottery workers. Auditory function was evaluated by air conduction pure-tone audiometry (pure-tone average) and distortion-product otoacoustic emission (DPOAE) levels (amplitude and signal-to-noise ratio). Lead exposure was assessed with a single blood sample test and classified as low, medium, and high according to blood lead tertiles. Logistic regression models were calculated for the association between blood lead levels, pure-tone average, and DPOAE records. RESULTS: Median (25th-75th) blood lead levels were 14 µg/dL (7.5-22.6 µg/dL). The audiometric pattern and DPOAE records were similar across blood lead levels groups in all frequencies, and no statistically significant differences were found. Adjusted logistic regression models showed no increase in the odds for hearing thresholds >25 dB (HL) and DPOAE absence associated with blood lead levels, and no dose-response pattern was observed ( p > 0.05). CONCLUSIONS: Given the results from this cross-sectional study, no association was found between blood lead levels and hearing loss assessed with DPOAE. Future longitudinal work should consider chronic lead exposure estimates among underrepresented populations, which can potentially inform safer work practices to minimize the risk of ototoxicity.


Asunto(s)
Sordera , Pérdida Auditiva , Ototoxicidad , Adulto , Humanos , Plomo , Ototoxicidad/etiología , Estudios Transversales , Umbral Auditivo/fisiología , Emisiones Otoacústicas Espontáneas/fisiología , Pérdida Auditiva/inducido químicamente , Audiometría de Tonos Puros/métodos
2.
J Nephrol ; 36(5): 1383-1393, 2023 06.
Artículo en Inglés | MEDLINE | ID: mdl-37253904

RESUMEN

BACKGROUND: In recent years, chronic kidney disease has increased in the pediatric population and has been related to environmental factors. In the diagnosis of kidney damage, in addition to the traditional parameters, early kidney damage biomarkers, such as kidney injury molecule 1, cystatin C, and osteopontin, among others, have been implemented as predictors of early pathological processes. OBJECTIVE: This study aimed to evaluate the relationship between exposure to environmental pollutants and early kidney damage biomarkers. METHODS: A cross-sectional pilot study was conducted in February 2016 and involved 115 apparently healthy children aged 6-15 residing in Apizaco, Tlaxcala. Participant selection was carried out randomly from among 16,472 children from the municipality of Apizaco. A socio-demographic questionnaire included  age, sex, education, duration of residence in the area, occupation, water consumption and dietary habits, pathological history, and some non-specific symptoms. Physical examination included blood pressure, weight, and height. The urine concentrations of urinary aluminum, total arsenic, boron, calcium, chromium, copper, mercury, potassium, sodium, magnesium, manganese, molybdenum, lead, selenium, silicon, thallium, vanadium, uranium, and zinc, were measured. Four of the 115 participants selected for the study were excluded due to an incomplete questionnaire or lack of a medical examination, leaving a final sample population of 111 participants. RESULTS: The results showed a mean estimated glomerular filtration rate of 89.1 ± 9.98 mL/min/1.73m2 and a mean albumin/creatinine ratio of 12.9 ± 16.7 mg/g urinary creatinine. We observed a positive and significant correlation between estimated glomerular filtration rate with fluoride, total arsenic and lead, and a correlation of albumin/creatinine ratio with fluoride, vanadium, and total arsenic. There was also a significant correlation between the early kidney damage biomarkers and fluoride, vanadium, and total arsenic, except for cystatin C. CONCLUSION: In conclusion, our results show that four urinary biomarkers: α1-microglobulin, cystatin C, kidney injury molecule 1, and neutrophil gelatinase-associated lipocalin are related to environmental exposure to urinary fluoride, vanadium, and total arsenic in our pediatric population.


Asunto(s)
Arsénico , Insuficiencia Renal Crónica , Humanos , Niño , Arsénico/efectos adversos , Arsénico/análisis , Cistatina C , Fluoruros , Vanadio , México/epidemiología , Estudios Transversales , Creatinina , Proyectos Piloto , Riñón , Biomarcadores , Albúminas , Tasa de Filtración Glomerular , Lipocalina 2
3.
Biomed Res Int ; 2015: 175025, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26339590

RESUMEN

Inorganic arsenic (iAs) exposure induces a decrease in glucose type 4 transporter (GLUT4) expression on the adipocyte membrane, which may be related to premature births and low birth weight infants in women exposed to iAs at reproductive age. The aim of this study was to analyze the effect of sodium arsenite (NaAsO2) exposure on GLUT1, GLUT3, and GLUT4 protein expression and on placental morphology. Female Balb/c mice (n = 15) were exposed to 0, 12, and 20 ppm of NaAsO2 in drinking water from 8th to 18th day of gestation. Morphological changes and GLUT1, GLUT3, and GLUT4 expression were evaluated in placentas by immunohistochemical and image analysis and correlated with iAs and arsenical species concentration, which were quantified by atomic absorption spectroscopy. NaAsO2 exposure induced a significant decrease in fetal and placental weight (P < 0.01) and increases in infarctions and vascular congestion. Whereas GLUT1 expression was unchanged in placentas from exposed group, GLUT3 expression was found increased. In contrast, GLUT4 expression was significantly lower (P < 0.05) in placentas from females exposed to 12 ppm. The decrease in placental GLUT4 expression might affect the provision of adequate fetal nutrition and explain the low fetal weight observed in the exposed groups.


Asunto(s)
Arsenitos/toxicidad , Transportador de Glucosa de Tipo 1/biosíntesis , Transportador de Glucosa de Tipo 2/biosíntesis , Transportador de Glucosa de Tipo 4/biosíntesis , Compuestos de Sodio/toxicidad , Adipocitos/efectos de los fármacos , Adipocitos/patología , Animales , Femenino , Regulación del Desarrollo de la Expresión Génica/efectos de los fármacos , Glucosa/metabolismo , Transportador de Glucosa de Tipo 1/genética , Transportador de Glucosa de Tipo 2/genética , Transportador de Glucosa de Tipo 4/genética , Humanos , Recién Nacido de Bajo Peso/metabolismo , Ratones , Placenta/efectos de los fármacos , Placenta/metabolismo , Placenta/patología , Embarazo , Nacimiento Prematuro/inducido químicamente , Nacimiento Prematuro/genética , Nacimiento Prematuro/patología , Efectos Tardíos de la Exposición Prenatal/inducido químicamente , Efectos Tardíos de la Exposición Prenatal/genética , Efectos Tardíos de la Exposición Prenatal/patología , Espectrofotometría Atómica
4.
Pharmacol Ther ; 142(2): 206-30, 2014 May.
Artículo en Inglés | MEDLINE | ID: mdl-24333264

RESUMEN

Oxidative stress is a common hallmark of neuronal cell death associated with neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, as well as brain stroke/ischemia and traumatic brain injury. Increased accumulation of reactive species of both oxygen (ROS) and nitrogen (RNS) has been implicated in mitochondrial dysfunction, energy impairment, alterations in metal homeostasis and accumulation of aggregated proteins observed in neurodegenerative disorders, which lead to the activation/modulation of cell death mechanisms that include apoptotic, necrotic and autophagic pathways. Thus, the design of novel antioxidant strategies to selectively target oxidative stress and redox imbalance might represent important therapeutic approaches against neurological disorders. This work reviews the evidence demonstrating the ability of genetically encoded antioxidant systems to selectively counteract neuronal cell loss in neurodegenerative diseases and ischemic brain damage. Because gene therapy approaches to treat inherited and acquired disorders offer many unique advantages over conventional therapeutic approaches, we discussed basic research/clinical evidence and the potential of virus-mediated gene delivery techniques for antioxidant gene therapy.


Asunto(s)
Antioxidantes/metabolismo , Terapia Genética/métodos , Degeneración Nerviosa , Regeneración Nerviosa , Enfermedades Neurodegenerativas/terapia , Neuronas/metabolismo , Estrés Oxidativo , Animales , Muerte Celular , Técnicas de Transferencia de Gen , Vectores Genéticos , Humanos , Enfermedades Neurodegenerativas/genética , Enfermedades Neurodegenerativas/metabolismo , Enfermedades Neurodegenerativas/patología , Enfermedades Neurodegenerativas/fisiopatología , Neuronas/patología , Estrés Oxidativo/genética , Virus/genética
5.
Biol Trace Elem Res ; 156(1-3): 279-87, 2013 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-24218229

RESUMEN

Selenium (Se) is an essential component of several major metabolic pathways and controls immune function. Arsenic (As) is a human carcinogen with immunotoxic and genotoxic activities, functioning mainly by producing oxidative stress. Due to the ability of Se to interact with As and to possibly block its toxic effects, we investigated the impact of dietary Se-methionine (Se-Met) supplementation on the toxicity of As exposure in vivo in a mouse model. Sufficient and excess levels of Se-Met (0.2 and 2 ppm, respectively) were fed to C57BL/6N female mice exposed to sodium arsenite (3, 6 and 10 mg/kg) in tap water for 9 days. We observed that As exposure increased Se-Met excretion in the urine. Se-Met supplementation increased the relative liver weight and decreased the concentration of total liver proteins in animals exposed to 10 mg/kg of As. Se-Met supplementation maintained a normal pool of glutathione in the liver and increased glutathione peroxidase concentration, although the lipoperoxidation level was increased by Se-Met even without As exposure. Se-Met supplementation helped to maintain the CD4/CD8 ratio of lymphocytes in the spleen, although it increased the proportion of B cells. Se-Met supplementation prior to As exposure increased the secretion of interleukin-4, IL-12 and interferon-γ and the stimulation index of the spleen cells in in vitro assays. Se-Met intake improved the basal immunological parameters but did not reduce the damage caused by oxidative stress after low-dose As exposure.


Asunto(s)
Arsenitos/toxicidad , Carcinógenos/toxicidad , Suplementos Dietéticos , Selenometionina , Compuestos de Sodio/toxicidad , Animales , Arsénico/toxicidad , Inhibidores Enzimáticos/toxicidad , Femenino , Glutatión/metabolismo , Humanos , Interleucina-12/metabolismo , Interleucina-4/metabolismo , Hígado/metabolismo , Hígado/patología , Ratones , Estrés Oxidativo/efectos de los fármacos , Selenometionina/farmacología , Selenometionina/orina , Bazo/metabolismo , Bazo/patología
6.
Chem Res Toxicol ; 25(1): 216-24, 2012 Jan 13.
Artículo en Inglés | MEDLINE | ID: mdl-22136492

RESUMEN

Glutathione S-transferases, including GST-T1 and GST-M1, are known to be involved in the phase II detoxification pathways for xenobiotics as well as in the metabolism of endogenous compounds. Polymorphisms in these genes have been linked to an increased susceptibility to carcinogenesis and associated with risk factors that predispose to certain inflammatory diseases. In addition, GST-T1 and GST-M1 null genotypes have been shown to be responsible for interindividual variations in the metabolism of arsenic, a known human carcinogen. To assess the specific GST genotypes in the Mexican population chronically exposed to arsenic, we have developed a multiplex High Resolution Melting PCR (HRM-PCR) analysis using a LightCycler480 instrument. This method is based on analysis of the PCR product melting curve that discriminates PCR products according to their lengths and base sequences. Three pairs of primers that specifically recognize GST-T1, GST-M1, and ß-globin, an internal control, to produce amplicons of different length were designed and combined with LightCycler480 High Resolution Melting Master Mix containing ResoLight, a completely saturating DNA dye. Data collected from melting curve analysis were evaluated using LightCycler480 software to determine specific melting temperatures of individual melting curves representing target genes. Using this newly developed multiplex HRM-PCR analysis, we evaluated GST-T1 and GST-M1 genotypes in 504 DNA samples isolated from the blood of individuals residing in Zimapan, Lagunera, and Chihuahua regions in Mexico. We found that the Zimapan and Lagunera populations have similar GST-T1 and GST-M1 genotype frequencies which differ from those of the Chihuahua population. In addition, 14 individuals have been identified as carriers of the double null genotype, i.e., null genotypes in both GST-T1 and GST-M1 genes. Although this procedure does not distinguish between biallelic (+/+) and monoallelic (+/-) genotypes, it can be used in an automated workflow as a simple, sensitive, and time and money saving procedure for rapid identification of the GST-T1 and GST-M1 positive or null genotypes.


Asunto(s)
Genotipo , Glutatión Transferasa/genética , Reacción en Cadena de la Polimerasa Multiplex/métodos , Adulto , Anciano , ADN/genética , Femenino , Hepatocitos/enzimología , Humanos , Masculino , México , Persona de Mediana Edad , Polimorfismo Genético , Globinas beta/genética
7.
Chem Res Toxicol ; 24(2): 165-7, 2011 Feb 18.
Artículo en Inglés | MEDLINE | ID: mdl-21291286

RESUMEN

Inorganic arsenic (iAs) is an environmental toxicant currently poisoning millions of people worldwide, and chronically exposed individuals are susceptible to arsenicosis or arsenic poisoning. Using a state-of-the-art technique to map the methylomes of our study subjects, we identified a large interactome of hypermethylated genes that are enriched for their involvement in arsenic-associated diseases, such as cancer, heart disease, and diabetes. Notably, we have uncovered an arsenic-induced tumor suppressorome, a complex of 17 tumor suppressors known to be silenced in human cancers. This finding represents a pivotal clue in unraveling a possible epigenetic mode of arsenic-induced disease.


Asunto(s)
Intoxicación por Arsénico/genética , Arsénico/toxicidad , Epigénesis Genética , Contaminantes Químicos del Agua/toxicidad , Islas de CpG , Metilación de ADN , Exposición a Riesgos Ambientales/efectos adversos , Humanos , México , Abastecimiento de Agua
8.
J Appl Toxicol ; 31(6): 579-88, 2011 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-21089161

RESUMEN

Fluorosis, caused by drinking water contaminated with inorganic fluoride, is a public health problem in many areas around the world. The aim of this study was to evaluate oxidative stress in spermatozoa caused by fluoride and NADPH oxidase in relationship to fluoride. Four experimental groups of male Wistar rats were administered with deionized water, NaF, at a dose equivalent to 5 mg fluoride kg⁻¹ per 24 h, NaF plus 20 mg kg⁻¹ per 24 h α-tocopherol, or α-tocopherol alone for 60 days. We evaluated several spermatozoa parameters in the four groups: standard quality analysis, superoxide dismutase (SOD) activity, the generation of reactive oxygen species (ROS), NADPH oxidase activity, TBARS formation, ultrastructural analyses of spermatozoa using transmission electron microscopy and in vitro fertilization (IVF) capacity. After 60 days of treatment, urinary excretion of fluoride was not modified by α-tocopherol. Spermatozoa from fluoride-treated rats exhibited a significant increase in the generation of ROS, accompanied by a significant increase in NADPH oxidase activity. The increase in ROS generation was significantly diminished by diphenylene iodonium, an inhibitor of NADPH oxidase activity. In contrast, a decrease in the generation of ROS, an increase in SOD activity and the prevention of TBARS formation process were observed in spermatozoa of rats exposed to fluoride plus α-tocopherol. Finally, α-tocopherol treatment prevented the IVF incapacity observed in the spermatozoa from fluoride-treated rats. These results suggest that NADPH oxidase participates in the oxidative stress damage caused by subchronic exposure to fluoride.


Asunto(s)
Antioxidantes/farmacología , Fluoruros/toxicidad , NADPH Oxidasas/metabolismo , Estrés Oxidativo/efectos de los fármacos , Espermatozoides/efectos de los fármacos , alfa-Tocoferol/farmacología , Animales , Masculino , Microscopía Electrónica de Transmisión , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismo , Espermatozoides/patología , Sustancias Reactivas al Ácido Tiobarbitúrico/metabolismo , Pruebas de Toxicidad Subcrónica
9.
Chem Biol Interact ; 188(2): 319-33, 2010 Nov 05.
Artículo en Inglés | MEDLINE | ID: mdl-20650267

RESUMEN

Halfway through the twentieth century, fluoride piqued the interest of toxicologists due to its deleterious effects at high concentrations in human populations suffering from fluorosis and in in vivo experimental models. Until the 1990s, the toxicity of fluoride was largely ignored due to its "good reputation" for preventing caries via topical application and in dental toothpastes. However, in the last decade, interest in its undesirable effects has resurfaced due to the awareness that this element interacts with cellular systems even at low doses. In recent years, several investigations demonstrated that fluoride can induce oxidative stress and modulate intracellular redox homeostasis, lipid peroxidation and protein carbonyl content, as well as alter gene expression and cause apoptosis. Genes modulated by fluoride include those related to the stress response, metabolic enzymes, the cell cycle, cell-cell communications and signal transduction. The primary purpose of this review is to examine recent findings from our group and others that focus on the molecular mechanisms of the action of inorganic fluoride in several cellular processes with respect to potential physiological and toxicological implications. This review presents an overview of the current research on the molecular aspects of fluoride exposure with emphasis on biological targets and their possible mechanisms of involvement in fluoride cytotoxicity. The goal of this review is to enhance understanding of the mechanisms by which fluoride affects cells, with an emphasis on tissue-specific events in humans.


Asunto(s)
Cariostáticos/toxicidad , Fluoruros/toxicidad , Apoptosis , Cariostáticos/metabolismo , Fluoruros/metabolismo , Regulación de la Expresión Génica , Humanos , Estrés Oxidativo , Transducción de Señal
10.
J Hazard Mater ; 178(1-3): 450-4, 2010 Jun 15.
Artículo en Inglés | MEDLINE | ID: mdl-20189716

RESUMEN

This paper reports arsenic methylation in betaine-nontronite clay-water suspensions under environmental conditions. Two nontronites (<0.05 mm), NAu-1 (green color, Al-enriched) and NAu-2 (brown color, Al-poor, contains tetrahedral Fe) from Uley Mine - South Australia were selected for this study. Betaine (pK(a)=1.83) was selected as methyl donor. The reaction between 5 g L(-1) clay, 20 ppm As(III), and 0.4M betaine at 7< or =pH(0)< or =9 under anoxic conditions was studied. The presence of nontronite clays were found to favor As(III) conversion to monomethylarsenic (MMA). Arsenic conversion was found to be as high as 50.2 ng MMA/ng As(III)(0). Conversion of As was found to be more quantitative in the presence of NAu-2 ((Na(0.72)) [Si(7.55) Al(0.16)Fe(0.29)][Al(0.34) Fe(3.54) Mg(0.05)] O(20)(OH)(4)) than NAu-1 ((Na(1.05)) [Si(6.98) Al(0.95)Fe(0.07)][Al(0.36) Fe(3.61) Mg(0.04)] O(20)(OH)(4)). The inherent negative charge at the nontronite tetrahedral layer stabilizes positively charged organic intermediate-reaction species, thereby leading to decreases in the overall methylation activation energy. The outcome of this work shows that nontronite clays catalyze As methylation to MMA via non-enzymatic pathway(s) under environmental conditions.


Asunto(s)
Silicatos de Aluminio/química , Arsenicales/química , Betaína/química , Contaminantes del Suelo/química , Aluminio/química , Arcilla , Hierro/química , Metilación , Minerales/química , Tamaño de la Partícula , Suelo/análisis , Soluciones , Propiedades de Superficie , Suspensiones , Temperatura , Agua/química
11.
Toxicol Appl Pharmacol ; 230(3): 352-7, 2008 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-18455746

RESUMEN

Fluorosis, caused by drinking water contamination with inorganic fluoride, is a public health problem in many areas around the world. The aim of the study was to evaluate the effect of environmentally relevant doses of fluoride on in vitro fertilization (IVF) capacity of spermatozoa, and its relationship to spermatozoa mitochondrial transmembrane potential (DeltaPsi(m)). Male Wistar rats were administered at 5 mg fluoride/kg body mass/24 h, or deionized water orally for 8 weeks. We evaluated several spermatozoa parameters in treated and untreated rats: i) standard quality analysis, ii) superoxide dismutase (SOD) activity, iii) the generation of superoxide anion (O(2)(-)), iv) lipid peroxidation concentration, v) ultrastructural analyses of spermatozoa using transmission electron microscopy, vi) DeltaPsi(m), vii) acrosome reaction, and viii) IVF capability. Spermatozoa from fluoride-treated rats exhibited a significant decrease in SOD activity (~33%), accompanied with a significant increase in the generation of O(2)() (~40%), a significant decrease in DeltaPsi(m) (~33%), and a significant increase in lipid peroxidation concentration (~50%), relative to spermatozoa from the control group. Consistent with this finding, spermatozoa from fluoride-treated rats exhibited altered plasmatic membrane. In addition, the percentage of fluoride-treated spermatozoa capable of undergoing the acrosome reaction was decreased relative to control spermatozoa (34 vs. 55%), while the percentage fluoride-treated spermatozoa capable of oocyte fertilization was also significantly lower than the control group (13 vs. 71%). These observations suggest that subchronic exposure to fluoride causes oxidative stress damage and loss of mitochondrial transmembrane potential, resulting in reduced fertility.


Asunto(s)
Fertilidad/efectos de los fármacos , Fluoruros/toxicidad , Potencial de la Membrana Mitocondrial/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Espermatozoides/efectos de los fármacos , Reacción Acrosómica/efectos de los fármacos , Animales , Fertilización In Vitro , Masculino , Ratas , Ratas Wistar , Motilidad Espermática/efectos de los fármacos , Espermatozoides/ultraestructura
12.
Environ Res ; 104(3): 383-9, 2007 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-17475235

RESUMEN

Inorganic arsenic exposure in drinking water has been recently related to diabetes mellitus. To evaluate this relationship the authors conducted in 2003, a case-control study in an arseniasis-endemic region from Coahuila, a northern state of Mexico with a high incidence of diabetes. The present analysis includes 200 cases and 200 controls. Cases were obtained from a previous cross-sectional study conducted in that region. Diagnosis of diabetes was established following the American Diabetes Association criteria, with two fasting glucose values > or = 126 mg/100 ml (> or = 7.0 mmol/l) or a history of diabetes treated with insulin or oral hypoglycemic agents. The next subject studied, subsequent to the identification of a case in the cross-sectional study was taken as control. Inorganic arsenic exposure was measured through total arsenic concentrations in urine, measured by hydride-generation atomic absorption spectrophotometry. Subjects with intermediate total arsenic concentration in urine (63.5-104 microg/g creatinine) had two-fold higher risk of having diabetes (odds ratio=2.16; 95% confidence interval: 1.23, 3.79), but the risk was almost three times greater in subjects with higher concentrations of total arsenic in urine (odds ratio=2.84; 95% confidence interval: 1.64, 4.92). This data provides additional evidence that inorganic arsenic exposure may be diabetogenic.


Asunto(s)
Intoxicación por Arsénico , Arsenicales/orina , Diabetes Mellitus Tipo 2 , Exposición a Riesgos Ambientales , Contaminantes Químicos del Agua , Abastecimiento de Agua/normas , Adulto , Anciano , Anciano de 80 o más Años , Intoxicación por Arsénico/complicaciones , Intoxicación por Arsénico/orina , Estudios de Casos y Controles , Estudios Transversales , Diabetes Mellitus Tipo 2/epidemiología , Diabetes Mellitus Tipo 2/etiología , Diabetes Mellitus Tipo 2/orina , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Femenino , Humanos , Modelos Logísticos , Masculino , México/epidemiología , Persona de Mediana Edad , Análisis Multivariante , Contaminantes Químicos del Agua/toxicidad , Contaminantes Químicos del Agua/orina
13.
Food Chem Toxicol ; 45(7): 1147-53, 2007 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-17306430

RESUMEN

Many studies evaluating the effects of selenium (Se) status on immunity utilize inorganic Se, although selenomethionine (Se-Met) has been suggested to be more bioavailable and less toxic. In the current study, we investigated the effects of dietary Se-Met on immune system function and cellular redox status in C57BL/6N female mice fed with low (0.02 ppm), sufficient (0.2 ppm, control group), or excess Se-Met (2 ppm) in the diet for 50 days. Low Se-Met intake reduced glutathione peroxidase (GPx) activity and glutathione concentration without modifying lipoperoxidation. While low Se-Met intake also reduced the number of B cells in the spleen, it increased mitogen-induced proliferation, IL-4 and IL-12 secretion when compared to the sufficient Se-Met intake group. In comparison to controls, excess Se-Met intake increased splenocyte proliferation and reduced B cell numbers, IL-4, and IL-12 secretion without affecting oxidative stress markers. These data suggest that Se-Met supplementation should be carefully evaluated as it many influence immune function.


Asunto(s)
Antioxidantes/administración & dosificación , Sistema Inmunológico/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Selenometionina/administración & dosificación , Bazo/efectos de los fármacos , Animales , Antioxidantes/toxicidad , Linfocitos B/efectos de los fármacos , Linfocitos B/patología , Biomarcadores/metabolismo , Proliferación Celular/efectos de los fármacos , Dieta , Relación Dosis-Respuesta a Droga , Femenino , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Sistema Inmunológico/patología , Interleucina-12/metabolismo , Interleucina-4/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Hígado/efectos de los fármacos , Hígado/metabolismo , Ratones , Ratones Endogámicos C57BL , Selenometionina/toxicidad , Bazo/inmunología , Bazo/metabolismo , Bazo/patología , Aumento de Peso/efectos de los fármacos
14.
Biol Trace Elem Res ; 108(1-3): 115-26, 2005.
Artículo en Inglés | MEDLINE | ID: mdl-16327065

RESUMEN

The aim of this work is based in the premise that inorganic arsenic (AsIII) and trivalentmethylated metabolites monomethylarsonous (MMAIII) and dimethylarsinous (DMAIII) participate in DNA damage through the generation of reactive oxygen species (ROS). We have utilized two lymphoblastic lines, Raji (B cells) and Jurkat (T cells), which were treated with the trivalent arsenic species (dose: 0-100 microM) and analyzed by two assays (comet assay and flow cytometry) in the determination of DNA damage and ROS effects in vivo. The results showed that the damage to the DNA and the generation of ROS are different in both cellular lines with respect to the dose of organic arsenic, and the order of damage is MMAIII>DMAIII>AsIII. This fact suggests that the DMAIII is not always the more cytotoxic intermediary xenobiotic, as has already been reported in another study.


Asunto(s)
Arsénico/farmacología , Linfocitos B/efectos de los fármacos , Daño del ADN/efectos de los fármacos , Radicales Libres/farmacología , Compuestos Organometálicos/farmacología , Linfocitos T/efectos de los fármacos , Arsénico/química , Arsénico/metabolismo , Supervivencia Celular/efectos de los fármacos , Células Cultivadas , Ensayo Cometa/métodos , Relación Dosis-Respuesta a Droga , Citometría de Flujo , Radicales Libres/metabolismo , Humanos , Células Jurkat , Compuestos Organometálicos/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Rodaminas/metabolismo
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