Dosing-time dependent effects of sodium nitroprusside on cerebral, renal, and hepatic catalase activity in mice.

Mamane Sani,Mossadok Ben-Attia,Mohan Mondal,Roberto Refinetti,Hichem Sebai,Néziha Ghanem-Boughanmi,Naceur A Boughattas

doi:10.1155/2015/790480

Abstract

To investigate the time dependence of sodium nitroprusside- (NPS-) induced oxidative effects, the authors study the variation of the antioxidant enzyme CAT activity in various tissues after the administration of a single 2.5 mg/kg dose of SNP or sodium chloride (NaCl 0.9%). For each of the two dosing times (1 and 13 hours after light onset, HALO, which correspond to the beginning of diurnal rest span and of nocturnal activity span of mice, resp.), brain, kidney, and liver tissues were excised from animals at 0, 1, 3, 6, 9, 12, 24, and 36 h following the drug administration and CAT activity was assayed. The results suggest that SNP-induced stimulation of CAT activity is greater in all three tissues when the drug is administered at 1 HALO than at 13 HALO. Two-way ANOVA revealed that CAT activity significantly (P < 0.004) varied as a function of the sampling time but not of the treatment in all three tissues. Moreover, a statistically significant (P < 0.004) interaction between the organ sampling-time and the SNP treatment was revealed in kidney regardless of the dosing time, whereas a highly significant (P < 0.0002) interaction was validated in liver only in animals injected at 13 HALO.

Highlights

The use of SNP as an antihypertensive agent [1,2,3,4] in a growing list of clinical conditions has been associated with cyanide- (CN−-) induced toxicity [5, 6]
The redox status is controlled by a wide spectrum of intracellular antioxidant systems, with CAT strongly contributing to reduce reactive oxygen species (ROS) levels by scavenging H2O2 that is considered as the main ROS
The present study showed the importance of SNP administration time on the activity of the antioxidant enzyme CAT

Summary

Introduction

The use of SNP as an antihypertensive agent [1,2,3,4] in a growing list of clinical conditions has been associated with cyanide- (CN−-) induced toxicity [5, 6]. As for many other drugs, side toxic effects of SNP have been reported both in experimental [10,11,12,13] and in clinical [14, 15] designs. There have been few reported cases of CN− toxicity following the therapeutic administration of SNP [18,19,20]. SNP-induced oxidative damage has been reported [13, 29]. This phenomenon occurs when there is an impairment of the balance between pro- and antioxidant systems. It is well known that SNP-induced oxidative effects are related to the release of NO that might be potentially toxic

Methods

Results

Conclusion