Abstract

The research: Of critical importance in understanding the intracellular mechanisms of aminoglycoside nephrotoxicity and the potentiating effects of mild renal ischemia is whether aminoglycosides remain sequestered within the endosomal-lysosomal compartment of renal epithelial cells or are released into the cytoplasm. This question will be examined using several complementary approaches designed to evaluate the intracellular processing of gentamicin including: 1.) immunocytochemical localization of gentamicin internalized across the apical and basolateral membranes of LLC-PK1 cells, and 2.) direct video-microscopy of the dynamic handling of internalized and microinjected FITC labeled gentamicin during normal control conditions and following """"""""chemical ischemia"""""""" in LLC-PKl cells.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08DK002144-02
Application #
3081076
Study Section
Diabetes, Endocrinology and Metabolic Diseases B Subcommittee (DDK)
Project Start
1992-09-01
Project End
1996-08-31
Budget Start
1993-09-01
Budget End
1994-08-31
Support Year
2
Fiscal Year
1993
Total Cost
Indirect Cost

  Institution

Name
University of Colorado Denver
Department
Type
Schools of Medicine
DUNS #
065391526
City
Aurora
State
CO
Country
United States
Zip Code
80045

  Publications

Ford, D M; Thieme, R E; Lamp, C A et al. (1995) HWA-448 reduces gentamicin toxicity in LLC-PK1 cells. J Pharmacol Exp Ther 274:29-33
Ford, D M; Dahl, R H; Lamp, C A et al. (1994) Apically and basolaterally internalized aminoglycosides colocalize in LLC-PK1 lysosomes and alter cell function. Am J Physiol 266:C52-7