Relationships between alterations in the profile of urinary arsenic (As) species and the presence of cutaneous signs of arsenicism were studied in Region Lagunera, Mexico. The use of urinary concentrations of putative substrates and products of the As metabolism pathway, as indicators of metabolic efficiency is also discussed. Arsenic was determined by hydride generation atomic absorption spectrophotometry and separation of As species was performed by ion exchange chromatography. The exposed group had an average of 0.408 mg As/l of total As (TAs) in their drinking water, whereas "control' individuals had 0.031 mg/l. Urinary concentrations of arsenic species and TAs were 20 to 95 times higher in the exposed group. Significant increases in the relative proportions of inorganic arsenic (Asi) and monomethylarsonic acid (MMA), accompanied by decreases of dimethylarsinic acid (DMA) were also found in exposed individuals. Therefore, significant decreases in the value of the MMA/Asi, DMA/MMA and DMA/ Asi ratios were observed, suggesting a decreased As methylating ability. Exposed individuals bearing cutaneous signs had a significantly longer time of exposure, higher urinary concentrations and proportions of MMA and MMA/Asi values, and significantly lower DMA/ MMA than exposed individuals without cutaneous signs. Further research is needed to identify better parameters for assessing the efficiency of As metabolism in chronically exposed populations and to confirm the potential relationship between metabolic alterations and overt signs of As toxicity.
The effects of acute lead exposure on renal function, lipid peroxidation and the expression of haeme oxygenase (HO) in rat kidney were determined. A single injection of lead acetate (50 mg Pb/kg) was given to rats. Changes in renal function, characterized by a significant reduction in the Na excretion was observed six hours after Pb exposure; this effect persisted for 24 hours. TBARS levels increased in kidney cortex 24 hours after Pb administration. In kidney cortex, Pb exposure affected the expression of HO-1, a renal protein associated with oxidative stress. HO-1 mRNA increased 2.3-fold, three hours after Pb administration and remained increased for six, 12 and 24 hours. HO enzymatic activity and HO-1 protein increased six and three hours after Pb administration, respectively, and remained increased at 24 hours. HO inhibition by tin-protoporphyrin, potentiated Pb-induced increase in TBARS and prevented the Pb-induced reduction in Na excretion. Our data suggest that Pb may be acting through the generation of oxidant products and induction of HO.
In this article, we present a new CO2 analyzer which can be used for monitoring respiration rates in organic material. To demonstrate the potentiality of the analyzer, CO2 evolution of soil samples collected from three different edaphic environments were measured. The results obtained with this compact CO2 analyzer were compared with those carried out simultaneously using the chemical method, and the correlation between them has been established.
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It has been shown that losartan inhibits vasoconstriction through binding to the thromboxane A 2 receptors. We investigated whether Thromboxane A 2 -induced platelet aggregation can be inhibited by losartan and if this effect is present in losartantreated hypertensive patients. Platelet aggregation was measured in platelet rich plasma from healthy volunteers and hypertensive patients, with the use of an aggregometer. Losartan inhibited the effect of Thomboxane A 2 agonist (U46619)-induced platelet aggregation, with a pA 2 value of 48.9 M and inhibited both second and first phases of Adenosine diphosphate-induced aggregation, from 109 ± 9 to 65 ± 10 mm and from 62 ± 8 to 0 mm. U46619's and Adenosine diphosphate's concentration required to produce half-maximal Clinical Research and Regulatory Affairs Downloaded from informahealthcare.com by University of North Texas on 11/21/14 For personal use only. 130 K. Mauer et al. response were higher in normotensive volunteers (EC 50 2.01 ± .3 M and 2.6 ± .4 M) compared to the hypertensive patients without treatment (EC 50 0.6 ± .2 M and 2.0 ± .3 M). The concentration required to produce half-maximal response in losartan treated patients was similar to the healthy volunteers(EC 50 1.7 ± .2 M and 1.4 ± .3 M), whereas in the lisinopril hypertension treated patients the concentrations used, were lower (EC 50 1.4 ± .3 M and 2.11 ± .5 M).Losartan plasma concentration of hypertensive patients was 60.3 ± 18.7 ng/ml. Computer analysis showed that losartan, Thromboxane A 2 and the Thromboxane A 2 receptor antagonist, SQ29548 have equivalent functional groups and spatial distribution. Conclusion. We suggest that losartan inhibits platelet aggregation through Thromboxane A 2 dependent and independent mechanisms.
A stable intestinal epithelium is the basis for healthy intestines. Its dysfunction causes increased intestinal permeability and bacterial translocation that may eventually cause an aberrant immune response leading to chronic inflammatory diseases of the intestines such as inflammatory bowel disease (IBD). The actin cytoskeleton regulates epithelial barrier integrity but the role of actin regulators such as cortactin (CTTN) is not well understood. Analyzing CTTN‐KO mice, we found increased basal intestinal permeability similar to what has been shown in the vasculature. Using a CTTN‐depleted Caco‐2 cell line, we confirmed epithelial dysfunction by reduced transepithelial resistance (TER), a weaker cortical actin ring, internalization of occludin and ZO‐1 and accelerated transmigration of neutrophils. Calcium‐switch assays revealed a strong delay in barrier formation without CTTN. While CTTN depletion did not cause increased apoptosis, we observed increased proliferation. Importantly, CTTN localized at cell contacts in colon biopsies of healthy individuals, whereas in IBD patients we observed strong translocation of CTTN into the cytosol and loss of colocalization with actin and ZO‐1. Our data imply that CTTN controls intestinal barrier integrity under basal conditions and that loss of CTTN triggers epithelial dysfunction as seen in IBD.
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