dc.creatorMori Sequeiros, María de Las Mercedes
dc.creatorAcquier, Andrea Beatriz
dc.creatorSuárez, Guadalupe Verónica
dc.creatorGómez, Natalia
dc.creatorGorostizaga, Alejandra Beatriz
dc.creatorMendez, Carlos Fernando
dc.creatorPaz, Cristina del Valle
dc.date.accessioned2017-04-12T22:00:04Z
dc.date.accessioned2018-11-06T12:06:19Z
dc.date.available2017-04-12T22:00:04Z
dc.date.available2018-11-06T12:06:19Z
dc.date.created2017-04-12T22:00:04Z
dc.date.issued2012-09
dc.identifierMori Sequeiros, María de Las Mercedes; Acquier, Andrea Beatriz; Suárez, Guadalupe Verónica; Gómez, Natalia; Gorostizaga, Alejandra Beatriz; et al.; Cisplatin inhibits testosterone synthesis by a mechanism that includes the action of reactive oxygen species (ROS) at the level of P450scc; Elsevier Ireland; Chemico-biological Interactions; 199; 3; 9-2012; 185-191
dc.identifier0009-2797
dc.identifierhttp://hdl.handle.net/11336/15277
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1863128
dc.description.abstractCisplatin (Cs) is a chemotherapeutic agent able to generate reactive oxygen species (ROS) which are linked to several side effects of the drug. Even when it is known that Cs produces Leydig cell dysfunction, it is unknown whether this particular side effect is mediated by ROS. The aim of this study was to evaluate the in vitro effects of Cs on testosterone production and the participation of ROS in this effect. We demonstrate that Cs promotes the generation of ROS in a time-, and concentration-dependent fashion, not only in mouse testicular interstitial cells but also in MA-10 Leydig cells. Also, Cs inhibits testosterone synthesis in a concentration-dependent fashion (5–50 μM for 4 h) and to a similar extent, in cells exposed to human chorionic gondadotropin hormone (hCG), to an analog of the second messenger cAMP (8Br-cAMP) or to a freely diffusible cholesterol analog (22R-hydroxycholesterol). However, this treatment does not inhibit the conversion of pregnenolone to testosterone. These data suggest that Cs exerts its inhibitory action on testosterone synthesis by an action at the level of P450scc. We also demonstrated that an antioxidant impairs the inhibitory effect of Cs on the conversion of the cholesterol analog into pregnenolone and that Cs does not change the expression level of P450scc mRNA. Therefore, it is concluded that Cs inhibits testosterone synthesis by a mechanism that includes the inhibition of P450scc by ROS.
dc.languageeng
dc.publisherElsevier Ireland
dc.relationinfo:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0009279712001500
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.cbi.2012.08.012
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectLEYDIG CELLS
dc.subjectSTEROIDOGENESIS
dc.subjectROS
dc.subjectCISPLATIN
dc.subjectP450 SCC ENZYME
dc.titleCisplatin inhibits testosterone synthesis by a mechanism that includes the action of reactive oxygen species (ROS) at the level of P450scc
dc.typeArtículos de revistas
dc.typeArtículos de revistas
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución