Research Article Dosing-Time Dependent Effects of Sodium Nitroprusside on Cerebral, Renal, and Hepatic Catalase Activity in Mice Mamane Sani, 1,2 Hichem Sebai, 3 Roberto Refinetti, 2 Mohan Mondal, 4 Néziha Ghanem-Boughanmi, 3 Naceur A. Boughattas, 5 and Mossadok Ben-Attia 6 1 UMR Biosurveillance et Toxicologie Environnementale, D´ epartement de Biologie, Facult´ e des Sciences et Techniques de Maradi, 465 Maradi, Niger 2 Circadian Rhythm Laboratory, Boise State University, 1910 University Drive, Boise, ID 83725, USA 3 UR Ethnobotanie et Stress Oxydant, D´ epartement des Sciences de la Vie, Facult´ e des Sciences de Bizerte, 7021 Zarzouna, Tunisia 4 National Dairy Research Institute, Eastern Regional Station, A-12, Kalyani,West Bengal 741235, India 5 Laboratoire de Pharmacologie, Facult´ e de M´ edecine, 5019 Monastir, Tunisia 6 Laboratoire de Biosurveillance de l’Environnement, Facult´ e des Sciences de Bizerte, 7021 Zarzouna, Tunisia Correspondence should be addressed to Mamane Sani; sanimamane@yahoo.fr Received 2 December 2014; Revised 9 February 2015; Accepted 19 February 2015 Academic Editor: A. Fadda Copyright © 2015 Mamane Sani et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. To investigate the time dependence of sodium nitroprusside- (NPS-) induced oxidative efects, the authors study the variation of the antioxidant enzyme CAT activity in various tissues ater 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 ater 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. he 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 signiicantly ( < 0.004) varied as a function of the sampling time but not of the treatment in all three tissues. Moreover, a statistically signiicant ( < 0.004) interaction between the organ sampling-time and the SNP treatment was revealed in kidney regardless of the dosing time, whereas a highly signiicant ( < 0.0002) interaction was validated in liver only in animals injected at 13 HALO. 1. Introduction he use of SNP as an antihypertensive agent [1–4] in a growing list of clinical conditions has been associated with cyanide- (CN − -) induced toxicity [5, 6]. Moreover, previous reports revealed that besides these released CN − ions, other metabolites as nitric monoxide (NO) [7, 8] may also con- tribute to the toxicity of this drug trough generation of reac- tive oxygen species (ROS) such as superoxide ion (O 2 ∙− )[5] and hydrogen peroxide (H 2 O 2 )[9]. As for many other drugs, side toxic efects of SNP have been reported both in experi- mental [10–13] and in clinical [14, 15] designs. Indeed, it has been reported that, within minutes of infusion, SNP decom- poses into metabolites that are pharmacologically inactive but toxicologically important [16]. hus, one molecule of SNP is metabolized by combination with haemoglobin to produce one molecule of cyanmethaemoglobin and four CN ions [17]. Despite this, there have been few reported cases of CN − toxicity following the therapeutic administration of SNP [18–20]. It is well established that the toxic free CN − can be converted in vivo into the much less toxic thiocyanate (SCN) by a ubiquitous enzyme rhodanese [21] that is present in various tissues [22–25] of all living organisms, from bacteria to humans [26–28]. SNP-induced oxidative damage has also been reported [13, 29]. his phenomenon occurs when there is an impairment of the balance between pro- and antioxidant systems. It is well known that SNP-induced oxidative efects are related to the release of NO that might be potentially toxic Hindawi Publishing Corporation Journal of Drug Delivery Volume 2015, Article ID 790480, 8 pages http://dx.doi.org/10.1155/2015/790480