Effects of uranium depletion on 1α-hydroxylase in kidney of rats

Abstract

<jats:p> This study was designed to evaluate the effects of depleted uranium (DU) on 1α-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 1α,25(OH)<jats:sub>2</jats:sub>D<jats:sub>3</jats:sub> in the kidney was measured by radioimmunoassay. The activity of 1α-hydroxylase was shown by the production of 1α,25(OH)<jats:sub>2</jats:sub>D<jats:sub>3</jats:sub> after incubation. The results showed that the 1α-hydroxylase activity in the kidney was decreased after 3 months (27.2% at the medium dose DU group, p &lt; 0.05; 33.4% at the high dose DU group, p &lt; 0.01). In contrast, at 6 months and 12 months after implantation of DU, the activity of renal 1α-hydroxylase in DU-treated animals was not decreased significantly in comparison with the controls (p &gt; 0.05). On the other hand, the activity of renal 1α-hydroxylase was decreased by 33.1% (p &lt; 0.05) and 34.4% (p &lt; 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. </jats:p>