Low dose (−)deprenyl is cytoprotective: It maintains mitochondrial membrane potential and eliminates oxygen radicals

Szabó, László; Szilágyi, G.; Bori, Zoltán; Telek, Géza; Magyar, K.; Nagy, Zoltán

doi:10.1016/j.lfs.2005.04.078

Cited by 28 publications

(14 citation statements)

References 34 publications

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“…ROS are known as key regulators of normal cell proliferation and differentiation, however, high levels of ROS have also been associated with damage of DNA and proteins and thus with the occurrence of apoptosis [59,60] . Moreover, an overdone oxidative stress has been shown capable of inducing a reduction of the normal mitochondrial membrane potential, which in turn leads to apoptosis [21,[61][62][63] . It has been shown that ROS generation, is crucial for the apoptosis induced by sanguinarine in human breast cancer [52] , SK-Mel-2 human melanoma [37] , human prostate cancer [25] and in both HCT-116 [21] and HT-29…”

Section: Sanguinarine-induced Apoptosis Through the Generation Of Reamentioning

confidence: 99%

Antitumor effects of the benzophenanthridine alkaloid sanguinarine: Evidence and perspectives

Gaziano

Moroni

Buè

et al. 2016

WJGO

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Historically, natural products have represented a significant source of anticancer agents, with plant-derived drugs becoming increasingly explored. In particular, sanguinarine is a benzophenanthridine alkaloid obtained from the root of Sanguinaria canadensis , and from other poppy Fumaria species, with recognized anti-microbial, anti-oxidant and anti-inflammatory properties. Recently, increasing evidence that sanguinarine exibits anticancer potential through its capability of inducing apoptosis and/or antiproliferative effects on tumor cells, has been proved. Moreover, its antitumor seems to be due not only to its pro-apoptotic and inhibitory effects on tumor growth, but also to its antiangiogenic and anti-invasive properties. Although the precise mechanisms underlying the antitumor activity of this compound remain not fully understood, in this review we will focus on the most recent findings about the cellular and molecular pathways affected by sanguinarine, together with the rationale of its potential application in clinic. The complex of data currently available suggest the potential application of sanguinarine as an adjuvant in the therapy of cancer, but further pre-clinical studies are needed before such an antitumor strategy can be effectively translated in the clinical practice.

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Section: Sanguinarine-induced Apoptosis Through the Generation Of Reamentioning

confidence: 99%

Antitumor effects of the benzophenanthridine alkaloid sanguinarine: Evidence and perspectives

Gaziano

Moroni

Buè

et al. 2016

WJGO

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“…Semi-quantitative analysis of Western blot products was performed by measuring the OD of the bands corresponding to Bax and Bcl-2 with respect to the OD of the band corresponding to the respective b-actin. [34,35], cells were then washed in HBSS/Hepes and loaded for 10 min at 37°C, 5% CO 2 with the permeant cationic fluorescent indicator JC1 (2.5 lg/ml), the most reliable dye for detecting the collapse of Dw m [28]. Under normal circumstances (hyperpolarized Dw m ), JC1 accumulates in the inner mitochondrial membrane in which it oligomerizes and fluoresces red.…”

Section: Western Blottingmentioning

confidence: 99%

Molecular mechanisms of euplotin C-induced apoptosis: involvement of mitochondrial dysfunction, oxidative stress and proteases

et al. 2007

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The metabolite euplotin C (EC), isolated from the marine ciliate Euplotes crassus, is a powerful cytotoxic and pro-apoptotic agent in tumour cell lines. For instance, EC induces the rapid depletion of ryanodine Ca(2+) stores, the release of cytochrome c from the mitochondria, and the activation of caspase-3, leading to apoptosis. The purpose of this study was to gain further insight into the mechanisms of EC-induced apoptosis in rat pheochromocytoma PC12 cells. We found that EC increases Bax/Bcl-2 ratio and that Bax is responsible of the EC-induced dissipation of the mitochondrial membrane potential (Deltapsi(m)). In addition, EC induces the generation of reactive oxygene species (ROS) without involvement of p53. The inhibition of ROS generation prevents, at least in part, the pro-apoptotic effects of EC as well as the effects of EC on Bax, Deltapsi(m) and intracellular free Ca(2+), indicating a cross-talk between different pathways. However, definition of the effector cascade turns out to be more complex than expected and caspase-independent mechanisms, acting in parallel with caspases, should also be considered. Among them, EC increases the expression/activity of calpains downstream of ROS generation, although calpains seem to exert protective effects.

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“…Its neuroprotective effect was documented in the permanent MCA occlusion model in rats [2,3]. (−)Deprenyl maintains mitochondrial membrane integrity ΔY m , and reduces the level of ROS, as we reported previously [4,5]. It was proposed furthermore that (−)deprenyl increases cell plasticity after hypoxia [6].…”

Section: Introductionmentioning

confidence: 81%

(−)Deprenyl-N-oxide, a (−)deprenyl metabolite, is cytoprotective after hypoxic injury in PC12 cells, or after transient brain ischemia in gerbils

Szilágyi

Szabó

Wappler

et al. 2009

Journal of the Neurological Sciences

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Low dose (−)deprenyl is cytoprotective: It maintains mitochondrial membrane potential and eliminates oxygen radicals

Cited by 28 publications

References 34 publications

Antitumor effects of the benzophenanthridine alkaloid sanguinarine: Evidence and perspectives

Antitumor effects of the benzophenanthridine alkaloid sanguinarine: Evidence and perspectives

Molecular mechanisms of euplotin C-induced apoptosis: involvement of mitochondrial dysfunction, oxidative stress and proteases

(−)Deprenyl-N-oxide, a (−)deprenyl metabolite, is cytoprotective after hypoxic injury in PC12 cells, or after transient brain ischemia in gerbils

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