|
KMID : 0857020050200010006
|
|
Kosin Medical Journal
2005 Volume.20 No. 1 p.6 ~ p.15
|
|
|
Mechanism of Reduced Bicarbonate Reabsorption in Cadmium-Intoxicated Rat Kidneys
|
|
Gil Young-Gi
Ahn Do-Whan
Rim Hark
|
|
|
Abstract
|
|
|
Background: We and others have demonstrated that cadmium (Cd) intoxication used bicarbonaturia, reduced maxium transport of HCO^(-)₃, low plasma HCO^(-)₃level, and finally renal tubular acidosis. These findings imply that the transporters and/or enzymes that mediate HCO^(-)₃reabsoption may be inhibited. Therefore, we examined the changes in sodium-hydorgen exchanger type 3 (NHE3) and carbonic anhydrase Ⅳ(CA Ⅳ) enzyme in Cd-intoxicated rats.
Methods: Brush border membrane vesicles (BBMV) from renal cortex were prepared by Mg precipitation method. NHE3 activity in BBMV was measured by spectrofluorometery using acridine orange dye. The expression of NHE3 antigen was determined by immunoblot and immunohistochemistry. CA Ⅳ activity was measured by a end-point colorimetric method.
Results: Proton (H^(+)) permeability of BBMV prepared from Cd-treated rats was not different from that of control BBMV. Hofstee plot indicated that Vmax of NHE3 activity was decreased in the cadmium group but Kna was not change. Hill coefficient was also not altered by cadmium. Western blot showed that NHE3 antigen was reduced in Cd-treated rats compared to the control, which was confirmed by immunohistochemistry. Ca IV activity was not changed.
Conclusion: The results demonstrate that the decreased expression of NHE3 in Cd-treated rats reduces bicarbonate reabsoption in the proximal tubule, which is likely to cause bicarbonaturia and renal tubular acidosis in Cd intoxication.
|
|
|
KEYWORD
|
|
|
brush-border membrance, NHE3, bicarbonaturia
|
|
|
FullTexts / Linksout information
|
|
|
|
|
Listed journal information
|
|
|