Effect of Depleted Uranium on Bones,Kidneys, and Vitamin D

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Depleted Uranium Induces Renal Damage and Inhibits Synthesis of Vitamin D

From China of all places we have research on depleted uranium effects.  This research is using rats but is it not possible to get these measurements from some of the gulf war veterans, especially those followed with shrapnel left in purposefully for research or those that were in tank battles that are famous from the Gulf War 1990-91.  The information on vitamin D is critical!  There is blood measurements available Vitamin D that the VA hospitals could be testing for right now.  Vitamin D lately has been a hot topic in research and health effects of low levels.  This would not be hard or expensive to test in clinical setting and to start treatment since one can get Vitamin D supplements over the counter!

Another shout out to the VA Headquarters, researchers, and health care professionals.  It is time for Action!  Do something clinically to help the ill gulf war veterans of 90-91!

Hum Exp Toxicol. 2010 Jul 29. [Epub ahead of print]

The effects of depleted uranium on 1{alpha}-hydroxylase in kidney of rats.

Yan M, Zhong G, Gao L, Xia X, Wang L, Hu H, Weng S.

Department of Environmental epidemiology and Bone toxicology, Institute of Radiation Medicine, Fudan University, Shanghai, People’s Republic of China.

Abstract

This study was designed to evaluate the effects of depleted uranium (DU) on 1alpha-hydroxylase in the kidney of rats and to delinerate the mechanism of damage to kidneys and bones by DU. Male Sprague-Dawley rats were surgically implanted with DU fragments at three dose levels (0.1 g, 0.2 g and 0.3 g). After 3, 6 or 12 months, the concentration of 1alpha,25(OH)2D3 in the kidney was measured by radioimmunoassay. The activity of 1alpha-hydroxylase was shown by the production of 1alpha,25(OH)2D3 after incubation. The results showed that the 1alpha-hydroxylase activity in the kidney was decreased after 3 months (27.2% at the medium dose DU group, p < 0.05; 33.4% at the high dose DU group, p < 0.01). In contrast, at 6 months and 12 months after implantation of DU, the activity of renal 1alpha-hydroxylase in DU-treated animals was not decreased significantly in comparison with the controls (p > 0.05). On the other hand, the activity of renal 1alpha-hydroxylase was decreased by 33.1% (p < 0.05) and 34.4% (p < 0.01) in blank control groups at 6 and 12 months, respectively, when compared with the blank control group at 3 months. In conclusion, this study showed that chronic DU exposure could induce renal damages and inhibit the synthesis of biologically active form of vitamin D, which may be the underlying mechanism of bone metabolic disorder caused by renal injury after DU exposure.

PMID: 20670993 [PubMed – as supplied by publisher]

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