Key word\ c i y h t i n , ATP-MgCI?. rend toxicity
The purpose of this 5tudy was to examine if ATP-MgCI,, an agent that protects against acute cisplatin toxicity in vitro, protected against cisplatin toxicity in viva Baseline renal function measurements were obtained on dogs ( n = 12) and rats ( n = 20) on day -1. Dogs were given 90 mg m-' cisplatin ( n = 5), 90 mg m-' cisplatin and 50 pmol kg-' ATP-MgCI' (n = 5), or 90 mg m-' cisplatin and 150 pmol kg-' ATP-MgCI, ( n = 2), in a slow bolus i.v. injection on day 0. Rats were given 4 mg kg-' cisplatin i.p. ( n = 6) and 25 pmol kg ATP-MgCI, ( n = 8) i.v. or 4 mg kg-' cisplatin i.p. and 25 pmol kg ATP-MgCI2 ( n = 6) i.v. on day 0. Renal function was assessed on a routine basis for 14 days. All dogs had significantly decreased creatinine clearance following cisplatin administration. There were no significant differences in renal function tests between groups of dogs. One dog given 50 pmol kg-' ATP-MgCI' and both dogs given 150 pmol kg-' ATP-MgCI, in addition to cisplatin developed acute anuric renal failure and were euthanatized prior to completion of the study. Rats given 4 mg kg-' cisplatin and 25 pmol kg-' ATP-MgCI, had significantly increased blood urea nitrogen and serum creatinine after drug administration, compared to rats given cisplatin alone. The results indicated that ATP-MgCI, worsened in vivo cisplatin renal toxicity in the dog and rat.