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Abstract
To explore the me chanism of Cd nephrotoxicity, CdCl2 was subcu taneou sly injected to rats, at 3 mg Cd/kg body weight onc e a day, for 8 d. In the liver, Cd bound to metallothioneins (MTs-Cd) rose from d 7 after the initiation of CdCl2 administration, and reached a plateau after the administration ceased. In the plasma, MTs-Cd rose from d 4, peaked on d 8, and gradually fell thereafter. In the kidneys, leucine aminopeptidase (LAP) and N-acetyl β D-glu cosaminida se (NAG) fell during d 6–20, and Cd bound to cellular membranes (Mem-Cd) rose from d 7 and reached a plateau during d 6–20. The Mem -Cd levels were significantly correlated with the redu ction in the LAP and NAG activity; the values o f MTs-Cd plus Mem-Cd were almos t equivalent to those of total Cd. These findings showed that the hepatic synth esis of MTs-Cd oc curred followed by its release into plasma; the extent of renal injury was aggravated as the plasma level of MTs-Cd rose; and a greater part of the renal Cd distributed intracellularly as the MTsbinding form, while the residual Cd distributed as the cellular membrane-bindin g form. Also, it was suggested that Cd that occurred as the cellular membrane-binding form in the kidneys was involved in manifestation of renal injury.
