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Am J Physiol Renal Physiol 282: F795-F801, 2002. First published January 2, 2002; doi:10.1152/ajprenal.00203.2001
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Vol. 282, Issue 5, F795-F801, May 2002

alpha -Melanocyte-simulating hormone and interleukin-10 do not protect the kidney against mercuric chloride-induced injury

Takehiko Miyaji, Xuzhen Hu, and Robert A. Star

Renal Diagnostics and Therapeutics Unit, National Institutes of Health, Bethesda, Maryland 20892-1268

The anti-inflammatory cytokines alpha -melanocyte-stimulating hormone (MSH) and interleukin (IL)-10 inhibit acute renal failure (ARF) after ischemia or cisplatin administration; however, these agents have not been tested in a pure nephrotoxic model of ARF. Therefore, we examined the effects of alpha -MSH and IL-10 in HgCl2-induced ARF. Mice were injected subcutaneously with HgCl2 and then given vehicle, alpha -MSH, or IL-10 by intravenous injection. Animals were killed to study serum creatinine, histology, and myeloperoxidase activity. Treatment with either alpha -MSH or IL-10 did not alter the increase in serum creatinine, tubular damage, or leukocyte accumulation at 48 h after HgCl2 injection. Because alpha -MSH and IL-10 are active in other injury models that involve leukocytes, we studied the time course of tubular damage and leukocyte accumulation to investigate whether leukocytes caused the tubular damage or accumulated in response to the tubular damage. Tubular damage was present in the outer stripe 12 h after HgCl2 injection. In contrast, the number of leukocytes and renal myleoperoxidase activity were normal at 12 h but were significantly increased at 24 and 48 h after injection. We conclude that neither alpha -MSH nor IL-10 altered the course of HgCl2-induced renal injury. Because the tubular damage preceded leukocyte infiltration, the delayed leukocyte accumulation may play a role in the removal of necrotic tissue and/or tissue repair in HgCl2-induced ARF.

mercury; acute renal failure; leukocytes


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