An<i>in Vitro</i>. Comparative Study on the Antioxidant Activity and Determination of Antibacterial Potential of Atorvastatin and Simvastatin

Ajith, Thekkuttuparambil Ananthanarayanan; Divya, K.

doi:10.1080/13880200701574992

Cited by 7 publications

(3 citation statements)

References 25 publications

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“…The ferric reducing anti‐oxidant power (FRAP) assay was performed by incubating ferric ion with TPTZ in the presence and absence of rosuvastatin (0.01–1 mg/mL) in a total volume of 1 mL 17 . After incubation, the OD of the reaction mixture was measured at 540 nm.…”

Section: Methodsmentioning

confidence: 99%

IN VITRO ANTI‐OXIDANT AND DNA PROTECTIVE EFFECTS OF THE NOVEL 3‐HYDROXY‐3‐METHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR ROSUVASTATIN

Ajith

Riji

Anu

2007

Clin Exp Pharma Physio

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1. Free radical-induced lipid peroxidation and changes in protein and nucleic acid structures can result in various human ailments, including ageing, neurodegenerative disorders and cancer. High body fat or dietary fat further enhances the free radical-mediated pathogenesis of various diseases. 2. In the present study, the in vitro anti-oxidant and DNA protective effects of the novel cardiovascular drug rosuvastatin were evaluated. Anti-oxidant activity was evaluated on the basis of inhibition of lipid peroxidation, scavenging of superoxide radical and the reduction of ferric ions (Fe(3+)). Inhibition of lipid peroxidation was determined using Fenton's reaction-induced lipid peroxidation in rat liver and brain homogenates and liver mitochondria. Superoxide radical-scavenging activity was evaluated by scavenging of the superoxide anion generated by photo illumination of riboflavin and Fe(3+)-reducing activity was determined by the ferric-reducing anti-oxidant power (FRAP) assay. DNA protection was evaluated according to changes in H(2)O(2)-induced pBR322 plasmid DNA and Fenton's reaction-induced-fragmentation of rat liver DNA. 3. The results indicate that rosuvastatin (1.5 or 2 mg/mL) is able to protect against lipid peroxidation. Furthermore, H(2)O(2)-induced changes in pBR322 plasmid DNA and fragmentation of hepatic DNA were alleviated by rosuvastatin. However, rosuvastatin did not show any superoxide anion-scavenging activity. The protective mechanism of rosuvastatin can be correlated with the reducing equivalent donating property or direct hydroxyl radical-scavenging activity of the drug. 4. The pleiotropic activities of rosuvastatin exhibited suggest its clinical advantages against oxidative stress-induced human ailments in addition to its widely using hypolipidaemic effect.

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Section: Methodsmentioning

confidence: 99%

IN VITRO ANTI‐OXIDANT AND DNA PROTECTIVE EFFECTS OF THE NOVEL 3‐HYDROXY‐3‐METHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR ROSUVASTATIN

Ajith

Riji

Anu

2007

Clin Exp Pharma Physio

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“…3,4 Studies of the statins showed that they delay the progression of coronary artery disease, 5 reduce mortality from cardiovascular diseases 6 and have anti-inflammatory 7 and anti-oxidant activity. 8 There are some reports on testing HMG-CoA reductase inhibitors against cancer, 9 Alzheimer's disease, and osteoporosis. 10 a Quantum Chemistry Group, Faculty of Chemistry, A. Mickiewicz University, Grunwaldzka 6,Poznan,Poland b BioInfoBank Institute, Limanowskiego 24A, 60-744, Poznan, Poland.…”

Section: Introductionmentioning

confidence: 99%

DFT study on hydroxy acid–lactone interconversion of statins: the case of atorvastatin

Hoffmann

Nowosielski

2008

Org. Biomol. Chem.

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Atorvastatin (ATV), the best known HMG-CoA reductase inhibitor family member, undergoes pH-dependent hydroxy acid-lactone interconversion similar to other statins. Although the only active form is a linear one, it was shown that drug interactions should also be considered for the lactone. The ATV lactonisation-hydrolysis mechanism was investigated theoretically using the density functional theory (DFT) method. Under both mildly acidic and basic conditions, the ATV lactone form is less stable than its hydroxy acid form. However, in the presence of a carboxylic acid, the equilibrium was only slightly shifted towards the lactone side (4 kcal mol(-1) difference between the substrate and the product), while energy gain for the hydrolysis under basic conditions amounts to 18 kcal mol(-1). Hydrolysis activation energy barriers were 19 and 6 kcal mol(-1), in acidic and basic conditions, respectively. We determined one-step interconversion as unfavourable under physiological conditions due to a 35 kcal mol(-1) activation energy barrier. All data were compared with analogue ones for fluvastatin (FLV) reported earlier and indicated that ATV is more flexible than FLV, not only due to the fact that it has more rotatable carbon-carbon single bonds, but also because ATV lactonistation-hydrolysis energy barriers are lower.

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“…Besides the application of CoQ10 in CVD, its use against the adverse effect of drugs, mainly statins, in the intervention of CVD has recently attracted attention. Nevertheless, the antioxidant property of statins [32,33] can block the endogenous biosynthesis of CoQ10 required for the ETC, resulting in cardiomyopathy and muscle pain [34] . CoQ10 supplementation (100 mg/d) for 30 d has been found to decrease the muscle pain associated with statin treatment [35] .…”

Section: Of Mitochondria In the Cardiomyocytesmentioning

confidence: 99%

Mitochondria-targeted agents: Future perspectives of mitochondrial pharmaceutics in cardiovascular diseases

Ajith

Jayakumar

2014

WJC

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Mitochondria are one of the major sites for the generation of reactive oxygen species (ROS) as an undesirable side product of oxidative energy metabolism. Damaged mitochondria can augment the generation of ROS. Dysfunction of mitochondria increase the risk for a large number of human diseases, including cardiovascular diseases (CVDs). Heart failure (HF) following ischemic heart disease, infantile cardiomyopathy and cardiac hypertrophy associated with left ventricular dilations are some of the CVDs in which the role of mitochondrial oxidative stress has been reported. Advances in mitochondrial research during the last decade focused on the preservation of its function in the myocardium, which is vital for the cellular energy production. Experimental and clinical trials have been conducted using mitochondria-targeted molecules like: MnSOD mimetics, such as EUK-8, EUK-134 and MitoSOD; choline esters of glutathione and N -acetyl-L-cysteine; triphenylphosphonium ligated vitamin E, lipoic acid, plastoquinone and mitoCoQ10; and Szeto-Schiller (SS)-peptides (SS-02 and SS-31). Although many results are inconclusive, some of the findings, especially on CoQ10, are worthwhile. This review summarizes the role of mitochondria-targeted delivery of agents and their consequences in the control of HF.

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Anin Vitro. Comparative Study on the Antioxidant Activity and Determination of Antibacterial Potential of Atorvastatin and Simvastatin

Cited by 7 publications

References 25 publications

IN VITRO ANTI‐OXIDANT AND DNA PROTECTIVE EFFECTS OF THE NOVEL 3‐HYDROXY‐3‐METHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR ROSUVASTATIN

IN VITRO ANTI‐OXIDANT AND DNA PROTECTIVE EFFECTS OF THE NOVEL 3‐HYDROXY‐3‐METHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR ROSUVASTATIN

DFT study on hydroxy acid–lactone interconversion of statins: the case of atorvastatin

Mitochondria-targeted agents: Future perspectives of mitochondrial pharmaceutics in cardiovascular diseases

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