Wistar rats were divided into 8 groups:control, 300 ppm F, 130 ppm F, 300 ppm Al, 1200 ppm Al, 130 ppm Al + 130 ppm F. 300 ppm Al + 300 ppm F and 1200 ppm Al + 300 ppm F. The chemicals were mixed into the standard diet. The animals were fed on the diets for 12 weeks. Contents of F, Al, Ca and P in the blood (or serum) and humerus were determined at the end of 12 weeks. The results showed that the level of F in the blood and bone in the unadulterated F group was increased, especially F in the bone reached a level more than 10 times that of the control. In the 3 mixture groups, blood F and bone F were lowered, while blood F was restored to normal level, but bone F was not nevertheless, the results showed that Al was in antagonism to the absorption of F. In the unadulterated Al groups, blood and bone Al did not parallel with the amount of Al administered. The level of Al in the median Al group was higher than that of the high Al group. Taking the level of blood and bone Al as a measure, when different doses of Al were administered with F, in the low and median dosage of Al, F was in antagonism to Al absorption, but in case of high dosage of Al, F was in potentiation to Al absorption. In all the experimental groups serum P was elevated, but serum Ca was not disturbed. Bone Ca and P were decreased only in the 3 groups with unadulterated F as well as unadulterated and adulterated high dosage of Al. Mechanism of the nonlinearity of Al absorption vs Al dosage, as well as the dual effect of F on the absorption of Al was proposed. 相似文献
Background: Isoflurane preconditions neurons to improve tolerance of subsequent ischemia in both intact animal models and in in vitro preparations. The mechanisms for this protection remain largely undefined. Because isoflurane increases intracellular Ca2+ concentrations and Ca2+ is involved in many processes related to preconditioning, the authors hypothesized that isoflurane preconditions neurons via Ca2+-dependent processes involving the Ca2+- binding protein calmodulin and the mitogen-activated protein kinase-ERK pathway.
Methods: The authors used a preconditioning model in which organotypic cultures of rat hippocampus were exposed to 0.5-1.5% isoflurane for a 2-h period 24 h before an ischemia-like injury of oxygen-glucose deprivation. Survival of CA1, CA3, and dentate neurons was assessed 48 later, along with interval measurements of intracellular Ca2+ concentration (fura-2 fluorescence microscopy in CA1 neurons), mitogen-activated protein kinase p42/44, and the survival associated proteins Akt and GSK-3[beta] (in situ immunostaining and Western blots).
Results: Preconditioning with 0.5-1.5% isoflurane decreased neuron death in CA1 and CA3 regions of hippocampal slice cultures after oxygen-glucose deprivation. The preconditioning period was associated with an increase in basal intracellular Ca2+ concentration of 7-15%, which involved Ca2+ release from inositol triphosphate-sensitive stores in the endoplasmic reticulum, and transient phosphorylation of mitogen-activated protein kinase p42/44 and the survival-associated proteins Akt and GSK-3[beta]. Preconditioning protection was eliminated by the mitogen-activated extracellular kinase inhibitor U0126, which prevented phosphorylation of p44 during preconditioning, and by calmidazolium, which antagonizes the effects of Ca2+-bound calmodulin. 相似文献