Objective: To evaluate the expression of an activator of nuclear factor-kappa (RANK), osteoprotegerin (OPG), osteopontin (OPN), and transforming growth factor ß1 (TGF-ß1) in gingival crevicular fluid (GCF) of teeth subjected to orthodontic forces. Materials and Methods: A randomized, pilot clinical trial including 10 healthy volunteers was conducted using a split-mouth design. Orthodontic elastic separators were placed between the second premolar and first molar, with the contralateral quadrant serving as a control. The GCF samples were collected from the tension and compression sites at baseline, 24 hours, and 7 days after the placement of separators. The GCF sample volumes were measured using a Periotron 8000, and total protein concentrations were determined. Levels of RANK, OPG, OPN, and TGF-ß1 were also analyzed using a multiplex enzyme-linked immunosorbent assay. Results: The control sites remained unchanged throughout the study. In contrast, the concentration of OPG significantly decreased at the compression site by 24 hours, and the amount and concentration of RANK differed significantly between the control, compression, and tension sites after 7 days. A significant increase in absolute TGF-ß1 levels was also detected at the compression site versus the control and tension sites after 7 days. Conclusion: Bone metabolism is affected by application of force to the teeth by elastic separators. Both increased expression of bone resorptive mediators (eg, RANK and TGF-ß1) and decreased expression of a bone-forming mediator (eg, OPG) on the compression side were detected. (Angle
Chronic arsenic exposure during development is associated with alterations of chemical transmission and demyelination, which result in cognitive deficits and peripheral neuropathies. At the cellular level, arsenic toxicity involves increased generation of reactive species that induce severe cellular alterations such as DNA fragmentation, apoptosis, and lipid peroxidation. It has been proposed that arsenic-associated neurodegeneration could evolve to Alzheimer disease in later life.1,2 In this study, the effects of chronic exposure to inorganic arsenic (3 ppm by drinking water) in Wistar rats on the production and elimination of Amyloid-β (Aβ) were evaluated. Male Wistar rats were exposed to 3 ppm of arsenic in drinking water from fetal development until 4 months of age. After behavioral deficits induced by arsenic exposure through contextual fear conditioning were verified, the brains were collected for the determination of total arsenic by inductively coupled plasma-mass spectrometry, the levels of amyloid precursor protein and receptor for advanced glycation end products (RAGE) by Western blot analysis as well as their transcript levels by RT-qPCR, Aβ estimation by ELISA assay and the enzymatic activity of β-secretase (BACE1). Our results demonstrate that chronic arsenic exposure induces behavioral deficits accompanied of higher levels of soluble and membranal RAGE and the increase of Aβ cleaved. In addition, BACE1 enzymatic activity was increased, while immunoblot assays showed no differences in the low-density lipoprotein receptor-related protein 1 (LRP1) receptor among groups. These results provide evidence of the effects of arsenic exposure on the production of Aβ and cerebral amyloid clearance through RAGE in an in vivo model that displays behavioral alterations. This work supports the hypothesis that early exposure to metals may contribute to neurodegeneration associated with amyloid accumulation.
In Mexico, few studies have analyzed the associations between toxic elements and metabolic diseases. In the present study, we analyzed the associations between serum arsenic (As), cadmium (Cd), and mercury (Hg) levels and body mass index (BMI) and fasting plasma glucose (FPG) in a Mexican adult population. Anthropometric data corresponding to 86 Mexican healthy adults (59 females and 27 men) were analyzed. FPG was analyzed by an enzymatic colorimetric method, and serum As, Cd, and Hg levels were analyzed by inductively coupled plasma–mass spectrometry (ICP–MS). The data show that the median serum As, Cd, and Hg levels were relatively higher in females (As = 1.78 ng mL −1 , Cd = 1.00 ng mL −1 , Hg = 0.96 ng mL −1 ) than those in males (As = 1.22 ng mL −1 , Cd = 0.91 ng mL −1 , Hg = 0.95 ng mL −1 ). However, these differences were not statistically significant ( p ≥ 0.097). We also found that the median level of As significantly increased with an increase in the body weight categories (normal weight = 1.08; overweight = 1.50; obesity = 2.75; p < 0.001). In addition, a positive association between serum As levels and FPG before and after adjustment for BMI was demonstrated (Rho Unadjusted = 0.012; (RhoA djusted = 0.243, p = 0.032). Serum As levels are positively associated with BMI and FPG in the adult population of Mexico. Nevertheless, these results need to be replicated and confirmed with a larger sample size.
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