Abstract
INTRODUCTION AND OBJECTIVES: An experimental study in rats was performed to evaluate the potential protective effects of a calcium channel blocking agent (Verapamil) on the ischemia induced oxidative stress related changes during hyperoxaluric phase. METHODS: A total of 32 rats have been included into the study program. Hyperoxaluria was induced by continuous administration of ethyleneglycol (EG) (0.75%). In addition to hyperoxaluria induction applied in Group1 animals in Groups 2 did receive a calcium channel blocking agent (verapamil) and animals in Group 3 consituted the control group. Histologic alterations of the kidneys including crystal formation were evaluated on days 1,7 and 28, respectively. In addition to the scavenger enzymes (catalase (CAT), superoxide dismutase (SOD), total glutathione (GSH)),malonil dialdehid (MDA) levels, (nitric oxide)NO levelsand the total antioxidant capacity (TAOC) of the kidney were also assessed both in the serum as well as the kidney tissue specimens of the animals in all groups. RESULTS: While the evlautaion of the antioxidant enzyme levels did reveal a significant reduction in animals receiving EG only; application of verapamil was found to be protective with limited reduction with a statistical significance when compared with the control group animals (Sidak-Bonferroni method, alpha1⁄41.000%). Moreover, comparison of kidney tissue T-AOC as well as NO levels in a comparative manner between the groups agan showed a statistically significant difefrence between Group 1 and the other group animals where the antioxidant capacity of the kidney seemed to be protected by verapamil application (Sidak-Bonferroni method, alpha1⁄4 1.000%). Lastly, both serum as well as tissue MDA levels were also statistically significant high in animals receiving EG only when compared with Group 2 and control animals during day7 as well as day 28 evaluation. CONCLUSIONS: Our current results indicate that as a potent calcium channel blocking agent Verapamil may limit the extent of oxidative stress related changes in renal tubules following hyperoxaluria induction and preservation of antioxidant capacity of the kidney along with the limitation of crystallization by this agent may allow us to understand the pathophysiology of stone formation as well as the possible use of this agent to limit both stone formation and recurrence.
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