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Am J Physiol Renal Physiol (January 2, 2002). doi:10.1152/ajprenal.00203.2001
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Articles in PresS, published online ahead of print January 2, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00203.2001
Submitted on July 2, 2001
Accepted on November 29, 2001

{alpha}-Melanocyte Simulating Hormone and Interleukin-10 do not protect the kidney against mercuric chloride-induced injury

Takehiko Miyaji1, Xuxhen Hu1, and Robert A Star1*

1 Renal Diagnostics and Therapeutics Unit, National Institutes of Health, Bethesda, MD, USA

* To whom correspondence should be addressed. E-mail: Robert_Star{at}nih.gov.

The anti-inflammatory cytokines {alpha}-MSH and IL-10 inhibit acute renal failure (ARF) following 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 sacrificed 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 hr after HgCl2 injection. Since {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 at 12 hr after HgCl2 injection. In contrast, the number of leukocytes and renal myleoperoxidase activity was normal at 12 hrs, but was significantly increased at 24 and 48 hr after injection. We conclude that neither {alpha}-MSH nor IL-10 altered the course of HgCl2-induced renal injury. Since the tubular damage proceeds leukocyte infiltration, the delayed leukocyte accumulation may play a role in the removal of necrotic tissue and/or tissue repair in HgCl2-induced ARF.




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