EFFECTS OF A HEPATO-PROTECTIVE AGENT AND A HEPATO-SECRETING CHELATOR ON CADMIUM-INDUCED NEPHROTOXICITY IN SYRIAN-HAMSTERS

Cadmium (Cd)-induced nephropathy in male Syrian hamsters was treated w ith D/L-penicillamine (D/L-p) or neomynophagen C (NMC). The subcutaneo us injection of CdCl2, 3 mg/kg, three times a week led to marked renal damage, ie., increased proteinuria and the excretion of urinary N-ace tyl-beta-D-glucosaminidase (NAG) as compared with the saline-injected controls. Cd-treated hamsters that were injected intraperitoneally wit h D/L-p, 0.1 mg/kg, five times a week, showed less renal damage, inclu ding a reduction in urinary protein from 3.60 +/- 0.42 to 1.77 +/- 0.7 mg/d. NMC-treated hamsters showed a reduced excretion of NAG (from 1. 47 +/- 0.34 to 0.91 +/- 0.68 u/d). The concentration of Cd in renal co rtical tissue was reduced slightly (from 2.78 +/- 0.08 to 2.34 +/- 0.3 mg/g.prot) by NMC treatment, but not by D/L-p. The elevated malondial dehyde (MDA) in renal cortical tissue was unaffected by administering D/L-p or NMC. The concentration of glutathione (GSH) in the renal cort ex was not elevated after administering Cd, but the ratio of the reduc ed to the oxidized GSH was elevated. The Cd induced liver dysfunction, as compared with untreated controls. The dysfunction was improved sli ghtly by NMC administration, but not by that of D/L-p. Changes in rena l morphology induced by Cd involving marked degeneration and necrosis of tubules as shown by light microscopy, were unaffected by treatment with D/L-p or NMC.