Chitosan Increases the Release of Renal Dipeptidase from Porcine Renal Proximal Tubule Cells

  • Hyun Joong, Yoon (College of Pharmacy, and Research Institute of Drug Development, Chonnam National University) ;
  • Kim, Young-Ho (Department of Biology, College of Natural Sciences, Chosun University) ;
  • Park, Sung-Wook (College of Pharmacy, and Research Institute of Drug Development, Chonnam National University) ;
  • Lee, Hwanghee-Blaise (Department of Biology, College of Natural Sciences, Chonnam National University) ;
  • Park, Haeng-Soon (College of Pharmacy, and Research Institute of Drug Development, Chonnam National University)
  • Published : 2003.12.01

Abstract

Renal dipeptidase (RDPase, membrane dipeptidase, dehydropeptidase 1, EC 3.4.13.19) has been widely studied since it was first purified from porcine kidney brush border membrane. It was reported that RDPase activity in urine samples of acute and chronic renal failure patients decreases. Nitric oxide (NO) is a highly reactive free radical involved in a number of physiological and pathological processes. NO is able to act in a dual mode, leading either to induction of apoptosis or to blunted execution of programmed cell death. NO inhibited the RDPase release from porcine renal proximal tubules, which could be blocked by L-NAME. Chitosan, the linear polymer of D-glucosamine in $\beta$(1\longrightarrow4) linkage, not only reversed the decreased RDPase release by NO but also increased NO production in the proximal tubule cells. The stimulatory effect of NO on RDPase release from proximal tubules in the presence of chitosan must be different from the previously proposed mechanism of RDPase release via NO signaling pathway. Chitosan stimulated the RDPase release in the proximal tubules and increased RDPase activity to 220% and 250% at 0.1% and 1%, respectively. RDPase release was decreased to about 40% in the injured proximal tubules and was recovered in proportion to the increase of chitosan. Chitosan may be useful in recovery of renal function from $HgCl_2$injury.

Keywords

References

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