Potential markers of oxidative stress in stroke

Cherubini, Antonio; Ruggiero, Carmelinda; Polidori, Maria Cristina; Mecocci, Patrizia

doi:10.1016/j.freeradbiomed.2005.06.025

Cited by 367 publications

(240 citation statements)

References 89 publications

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“…Malondialdehyde, Testes ischemia a stable end-product of lipid peroxidation generated by ROS, is usually used as a good indicator of the degree of lipid peroxidation. 27 In our study, we demonstrated that the levels of tissue MDA were significantly increased in the I-R/untreated group. The increase of MDA levels indicated the presence of oxidative damage I-R injury induced on ipsilateral testes.…”

Section: Discussionsupporting

confidence: 53%

Montelukast protects against testes ischemia/reperfusion injury in rats

Öztürk

Gideroğlu

et al. 2013

CUAJ

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Introduction: In this study, we investigate the effect of montelukast on histologic damage induced by testicular torsion-detorsion in rats. Methods: Twenty-one male Sprague-Dawley rats were separated into 3 groups, each containing 7 rats. A sham operation was performed in group 1 (control). In group 2 (ischemia-reperfusion [I-R]/untreated), 1-hour detorsion of the testis was performed after 6 hours of unilateral testicular torsion. In group 3 (I-R/dextroamphetamine), after performing the same surgical procedures as in group 2, montelukast was given intraperitoneally. In all experimental rats, ipsilateral orchiectomies were performed for histological examination and tissue malondialdehyde (MDA), glutathione and myeloperoxidase assays. Results: Montelukast treatment significantly decreased the I-Rinduced elevation in testes tissue MDA and glutathione levels were found to be preserved. The level of myeloperoxidase (MPO) activity was significantly increased in the testes tissue of the I-R/untreated group. However, in I-R/montelukast treatment group significantly decreased testes tissue MPO level. Histopathologically, the in the group 2 rats, edema, congestion, hemorrhage between seminiferous tubules and necrosis of the germinal cells were predominant features in sections. However, most of the specimens in the montelukast treated group 3 showed grades-I and II injury. Additionally, the testicular injury score was lower in group 3 rats compared with group 2. Conclusion: The current findings demonstrate that the montelukast decreased the severity of testicular injury by reversing the oxidative effects of testes I-R. RésuméIntroduction : Dans cette étude, nous examinons l'effet du montélukast sur les lésions tissulaires provoquées par torsion-détorsion testiculaire chez le rat. Méthodologie : Vingt-et-un rats Sprague-Dawley mâles ont été répartis en trois groupes de 7 rats. Une opération fictive a été réalisée dans le groupe 1 (groupe témoin). Dans le groupe 2 (ischémie-reperfusion / non traité), une détorsion testiculaire d'une heure a été réalisée après 6 heures de torsion testiculaire unilatérale. Dans le groupe 3 (ischémie-reperfusion / dextroamphét-amine), on a administré du montélukast par voie intrapéritonéale après les mêmes interventions chirurgicales que pour le groupe 2. Chez tous les rats, une orchidectomie homolatérale a été effectuée en vue d'un examen histologique et de mesures du malonaldéhyde, du glutathion et de la myéloperoxidase dans les tissus. Résultats :Le traitement par montélukast a significativement réduit l'élévation dans les tissus testiculaires provoquée par l'ischémie-reperfusion, mais les taux de malonaldéhyde et de glutathion sont demeurés les mêmes. Le niveau d'activité de la myéloperoxidase (MPO) a significativement augmenté dans les tissus testiculaires du groupe ayant subi l'ischémie-reperfusion sans traitement subséquent. Cependant, dans le groupe ayant subi l'ischémie-reperfusion avec traitement par montélukast, le taux de MPO dans les tissus testiculaires avait significativ...

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Section: Discussionsupporting

confidence: 53%

Montelukast protects against testes ischemia/reperfusion injury in rats

Öztürk

Gideroğlu

et al. 2013

CUAJ

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“…IsoPs are prostanoids produced independently of cyclooxygenase by free radicalcatalysed peroxidation of arachidonic acid-containing lipids (Marin et al, 2000). Quantification of IsoPs has therefore been proposed as an accurate marker of oxidative stress in experimental models of free radical-induced injury and human diseases being deemed more reliable and specific than the more commonly measured thiobarbituric acid reactive substances (TBARS) and malondialdehyde (MDA) (Cherubini et al, 2005). An increased production of isoprostanes has been observed in human stroke (van Kooten et al, 1997).…”

Section: Antioxidant Activity and Tamoxifen-induced Neuroprotectionmentioning

confidence: 99%

Neuroprotection by tamoxifen in focal cerebral ischemia is not mediated by an agonist action at estrogen receptors but is associated with antioxidant activity

Zhang

Milatović²,

Aschner³

et al. 2007

Experimental Neurology

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We have previously shown that tamoxifen can induce marked neuroprotection after middle cerebral artery occlusion (MCAo) in rats and have described two possible mechanisms of action: namely inhibition of EAA release and inhibition of nNOS activity. In this study we tested other potential mechanisms. Namely, agonist action at estrogen receptors and an antioxidative action. Tamoxifentreated rats had significantly improved neurobehavioral deficit scores after 24 hours and showed ∼75% reduced infarct volumes. These were unaffected by ICI 182,780 (a high affinity and pure receptor antagonist) administered intravenously, or intracisternally to avoid possible lack of brain penetration, 15 minutes before intravenous administration of tamoxifen. In rats subjected to 2 hours MCAo followed by 22 hours reperfusion, a 1.8-fold and 2.9-fold increase of F 2 -IsoPs and F 4 neuroprostanes, respectively, as relatively stable markers of oxidative damage, were measured in the ischemic hemisphere compared with the corresponding contralateral hemisphere or sham controls. Tamoxifen given at 3 hours after the start of ischemia reduced the IsoPs and NeuroPs to sham control levels, and also inhibited their production by chemically induced lipid peroxidation in brain homogenates. These data are consistent with at least part of tamoxifen's marked neuroprotection in focal cerebral ischemic injury being due to its antioxidant activity but not by an acute action on estrogen receptors (212 words).

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“…Lipid peroxidation is one of the major consequences of free-radical-mediated injury to the brain (Cherubini et al, 2005). The brain tissue MDA levels reflect the oxidative damage to brain lipids in this study.…”

Section: Discussionmentioning

confidence: 83%