[Toxicity of cadmium and its mechanism on renal tubular epithelial cells in vitro].
The direct effects of cadmium on the functions and metabolism of renal tubular epithelial cells were observed with radio-immune assay, cytochemical and biochemical methods to study further the mechanism of nephrotoxicity of cadmium. Results revealed uptake of alpha-methyl-D-glucoside (alpha-MG) in renal tubular epithelial cells obviously reduced, outflow of potassium ions increased, c-AMP content reduced and activity of Na+-K+-ATPase was inhibited significantly after exposure to cadmium. Electrochemical gradient of tubular cells maintained by Na+-K+-ATPase played an important role in transference of sodium and glucose, and damage in energy resource system within tubular epithelial cells may be one of the pathogenic mechanisms of kidney injury caused by cadmium. In addition, changes in a group of biological markers and functional enzymes (alkaline phosphatase, AKP; gamma-glutamyltransferase, gamma-GT; lactate dehydrogenase, LDH; glucose-6-phosphate dehydrogenase, G-6-PD; N-acetylglucoside, NAG) were determined in the study, and it was found that they all could reflect better the degree of injury in tubular epithelial cells and their metabolic status and could be used in clinical practice.
Jiang
T
T
Institute of Nephrology, Sun Yat-sen University of Medical Sciences, Guangzhou.
Fan
J
J
Tan
B
B
D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D005260:Female; D007684:Kidney Tubules / Q000187:drug effects* / Q000201:enzymology / Q000648:ultrastructure; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008757:Methylglucosides / Q000378:metabolism*; D011817:Rabbits; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D008757:Methylglucosides; D002104:Cadmium; C027020:methylglucoside; D007770:L-Lactate Dehydrogenase; D000254:Sodium-Potassium-Exchanging ATPase