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Calcium metabolism rats, effect

In attempting to reconcile these findings, it should be pointed out that rats may not be appropriate models for the study of calcium metabolism in humans. Unlike humans, the rat does not undergo epiphyseal plate closure and does not have a significant haversian remodeling sequence (21) Furthermore, rats excrete only l-270 of their calcium intake in their urine whereas humans excrete approximately 20-30% or more. This fact is especially significant, since most of the known effects of phosphates on calcium retention in humans are effected by alterations in urinary calcium. [Pg.35]

Several comprehensive reviews on oxalic acid have been published in which effects on calcium metabolism were discussed (7-11). A review of studies on the effect of oxalic acid on calcium bioavailability in rats and humans is presented in this paper. [Pg.106]

It has been further reported that not only the calcium metabolism but also other minerals and other aspects of mineral status may be influenced by CPPs. Ait-Oukhatar et al. (1997) found that in young iron-deficient rats, CPP-bound iron had a positive effect on some parameters of iron status and metabolism, such as mean cell volume, haemoglobulin and haematocrit, and a negative effect on some parameters, such as urine iron. Other parameters,... [Pg.236]

Melamed, B. and O Neill, J.J. 1979 Effects of anticholinergic compounds on calcium metabolism In rat brain. The Pharmacologist 21 18. [Pg.286]

Roe, F.J.C. Relevance for man of the effects of lactose, polyols and other carbohydrates on calcium metabolism seen in rats a review. Hum. Toxicol. 1989, 8, 87-98. [Pg.2781]

Morohashi T, Sano T, Yamada S. 1994. Effects of strontium on calcium metabolism in rats I. A distinction between the pharmacological and toxic doses. Jpn J Pharmacol 64 155-162. [Pg.369]

WiNDiscH W and Kiechgessnee M (1994a) Distribution of calcium and zinc, and zinc exchange in tissues at deficient and moderately high calcium supply. 2. Effect of differing calcium supplies on the quantitative calcium and zinc in the metabolism of adult rats. J Anim Physiol Anim Nutr 72 195-206. [Pg.1238]

On the other hand, microsomes may also directly oxidize or reduce various substrates. As already mentioned, microsomal oxidation of carbon tetrachloride results in the formation of trichloromethyl free radical and the initiation of lipid peroxidation. The effect of carbon tetrachloride on microsomes has been widely studied in connection with its cytotoxic activity in humans and animals. It has been shown that CCI4 is reduced by cytochrome P-450. For example, by the use of spin-trapping technique, Albani et al. [38] demonstrated the formation of the CCI3 radical in rat liver microsomal fractions and in vivo in rats. McCay et al. [39] found that carbon tetrachloride metabolism to CC13 by rat liver accompanied by the formation of lipid dienyl and lipid peroxydienyl radicals. The incubation of carbon tetrachloride with liver cells resulted in the formation of the C02 free radical (identified as the PBN-CO2 radical spin adduct) in addition to trichoromethyl radical [40]. It was found that glutathione rather than dioxygen is needed for the formation of this additional free radical. The formation of trichloromethyl radical caused the inactivation of hepatic microsomal calcium pump [41]. [Pg.768]

The ability of SP to stimulate histamine release from isolated rat peritoneal mast cells is now well demonstrated [31, 97-101], The release is rapid (< 1 min), non-cytotoxic, dependent on a supply of Ca and metabolic energy, and independent of cell-bound IgE [99]. Moreover, as with other peptides, its secretory effect on the mast cell is affected by moderate levels of extracellular cations. For example, the addition of Ca to the bathing medium after the addition of SP increased the secretory response of the cells, while adding calcium (0.1-1 mM), magnesium (1-10 mM) or cobalt (0.01-1 mM) to the cell suspension before SP inhibited histamine release, suggesting the possibility of cation competition for SP binding [99]. [Pg.156]

Mehorta and coworkers (1989) observed that isolated fractions of brain and heart cells from rats orally administered 0.5-10 mg endrin/kg showed significant inhibition of Ca+2 pump activity and decreased levels of calmodulin, indicating disruption of membrane Ca+2 transport mechanisms exogenous addition of calmodulin restored Ca+2-ATPase activity. In vitro exposure of rat brain synaptosomes and heart sarcoplasmic reticuli decreased total and calmodulin-stimulated calcium ATPase activity with greater inhibition in brain preparations (Mehorta et al. 1989). However, endrin showed no inhibitory effects on the calmodulin-sensitive calcium ATPase activity when incubated with human erythrocyte membranes (Janik and Wolf 1992). In vitro exposure of rat brain synaptosomes to endrin had no effect on the activities of adenylate cyclase or 3, 5 -cyclic phosphodiesterase, two enzymes associated with synaptic cyclic AMP metabolism (Kodavanti et al. 1988). [Pg.74]

Results of in vitro studies suggest an interaction between calcium ions and cyanide in cardiovascular effects (Allen and Smith 1985 Robinson et al. 1985a). It has been demonstrated that exposure to cyanide in metabolically depleted ferret papillary muscle eventually results in elevated intracellular calcium levels, but only after a substantial contracture develops (Allen and Smith 1985). The authors proposed that intracellular calcium may precipitate cell damage and arrhythmias. The mechanism by which calcium levels are raised was not determined. Franchini and Krieger (1993) produced selective denervation of the aortic and carotid bifurcation areas, and confirmed the carotid body chemoreceptor origin of cardiovascular, respiratory and certain behavioral responses to cyanide in rats. Bradycardia and hyperventilation induced by cyanide are typical responses evoked by carotid body chemoreceptor stimulation (Franchini and Krieger 1993). [Pg.90]

Nagata, N., Sasaki, M., Kinuira, N., Nakane, K. Effects of porcine calcitonin on the metabolism of calcium and cyclic AMP in rat skeletal tissue in vivo. Endocrinology 97, 527 (1975)... [Pg.125]

Stewaitm, A.K. and A.C. Magee Effect of Zinc Toxicity on Calcium. Phosphorus and Magnesium Metabolism of Young Rats, J. Nutrition, 82, 287 (1964). Underwood, E.J. and W. Mertz Trace Elements in Human and Animal Nutrition, 5th Edition, Academic Press. Inc, San Diego, CA, 1990. [Pg.1778]

Levy, J., Zhu, Z., and Dunbar, J. C., 1998, The effect of glucose and calcium on Ca2+-adenosine triphosphatase in pancreatic islets isolated from a normal and a non-insulin-dependent diabetes mellitus rat model. Metabolism, 47 185-9. [Pg.360]


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