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Acta Medica Medianae
Vol. 43
Number 2, April, 2004
UDK 61
YU ISSN 0365-4478

 


Contact:
Jelenka Nikolic
Department of Biochemistry, Faculty of Medicine
81 Dr Zoran Djindjic street,
18000 Nis, Serbia and Montenegro
Phone: 018/326-712,
e-mail: nikdan@bankerinter.net

 

EFFECT OF ACUTE RENAL FAILURE ON KIDNEY AMIDINOTRANSFERASE ACTIVITY

 

Jelenka Nikolic*, Dusan Sokolovic* and Boris Djindjic**


Department of Biochemistry, Faculty of Medicine, Nis*
Department of Pathological Physiology, Faculty of Medicine, Nis* *

 

    L-Arginine-:glycine amidinotransferase (EC 2.1.4.1) catalyzes the transfer of an amidino group from arginine to glycine to form guanidinoacetate, precursor in creatine synthesis. The kidneys are major site of the creatine synthesis and primary target organs for mercury toxicity. In evaluation of molecular mechanisms of mercury chloride intoxication relating to creatine metabolism we have investigated the enzyme activity in kidney tissue after mercury chloride administration. Acute renal failure was induced by i.p administration of mercury chloride in a dose of 3 mg/kg to male Spraque Dawley rats weighing about 200 g. The results of our study indicate an acute renal failure 24 hours after mercury chloride administration. Urea and creatinine levels in blood plasma were significantly elevated compared to control group (p<0.001). Amidinotransferase activity in kidney tissue was depressed, while, in plasma of intoxicated rats activity of enzyme was increased (p<0.001). The obtained results indicate that mercury chloride has strong nephrotoxic effect. Depressed amidinotransferase activity and decreased production of guanidinoacetate, initial product in creatine synthesis, may be implicated in neurotoxicity, cardiotoxicity and muscle damage in mercury intoxication, because creatine and its phosphorylated form creatine phosphate play an important role in the energy metabolism. Acta Medica Medianae 2004; 43(2):5-8.

    Key words: mercury chloride, kidney, amidinotransferase, urea, creatinine, creatine