Dosing-time dependent oxidative effects of sodium nitroprusside in brain, kidney, and liver of mice

Manniophyton fulvum extract attenuates sodium nitroprusside induced oxidative stress in wistar rats

“…The primary biological function of rhodanese is to catalyze the detoxification of cyanide via transfer of the sulfane sulfur from thiosulfate to cyanide and to generate thiocyanate and sulfite which are less toxic. 27 Recently, the enzyme has been described as a multifunctional enzyme owing to its ubiquitous nature and variety of functional domain. 28 It has been involved in many cellular functions such as supply of sulfur for iron-sulphur centers, biosynthesis of thiamine/ molybdenum cofactors, selenium metabolism, thioredoxin oxidation (as thioredoxin oxidase).…”

Dosing-Time Dependent Effects of Sodium Nitroprusside on Cerebral, Renal, and Hepatic Catalase Activity in Mice

“…Moreover, previous reports revealed that besides these released CN − ions, other metabolites as nitric monoxide (NO) [ 7 , 8 ] may also contribute to the toxicity of this drug trough generation of reactive 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 effects of SNP have been reported both in experimental [ 10 – 13 ] and in clinical [ 14 , 15 ] designs. Indeed, it has been reported that, within minutes of infusion, SNP decomposes into metabolites that are pharmacologically inactive but toxicologically important [ 16 ].…”

“…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 ]. This phenomenon occurs when there is an impairment of the balance between pro- and antioxidant systems.…”

“…Other authors revealed that low concentrations of SNP had a prominent effect in producing oxidative damage in platelets in comparison to rat brain tissue [ 44 ]. Similarly, we recently revealed that a neurotoxic 2.5 mg/kg dose of SNP induced LPO in brain, kidney, and liver tissues [ 13 ], but not in erythrocytes [ 45 ]. Therefore, any variation of oxidative damage among organs might be related to their respective sensitivity and/or antioxidant system efficiency.…”

“…Therefore, any variation of oxidative damage among organs might be related to their respective sensitivity and/or antioxidant system efficiency. For that and since we previously found that these three tissues showed different sensitivity to SNP-induced LPO [ 13 ], the potentiality and efficiency of their antioxidant systems deserve to be investigated. Hence, we were interested in examining the effects of SNP, a well-known NO donor, on an antioxidant enzyme CAT activity.…”