Novel N,N'-disubstituted selenoureas as potential antioxidant and cytotoxic agents

A series of 30 novel N,N disubstituted selenoureas were synthesized, characterized, and their antioxidant ability was tested using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,20-azinobis( 3-ethylbenzthiazoline-6-sulfonic acid (ABTS) assays. Additionally, their cytotoxic activity was tested in vitro in a panel of three different cancer (breast, lung and colon) and two normal cell lines. Each selenourea entity contains a para-substituted phenyl ring with different electron-withdrawing and electron-donating groups, and different aliphatic and aromatic nuclei. All of the synthesized selenoureas present antioxidant capacity at high concentrations in the DPPH assay, and three of them (2b, 2c and 2d) showed greater radical scavenging capacity than ascorbic acid at lower concentrations. These results were confirmed by the ABTS assay, where these novel selenoureas present even higher antioxidant capacity than the reference compound Trolox. On the other hand, 10 selenoureas present IC50 values below 10 M in at least one cancer cell line, resulting in the adamantyl nucleus (6a¿ 6e), the most interesting in terms of activity and selectivity. Outstanding results were found for selenourea 6c, tested in the NCI60 cell line panel and showing an average GI50 of 1.49 M for the 60 cell lines, and LC50 values ranging from 9.33 M to 4.27 M against 10 of these cancer cell lines. To gain insight into its anticancer activity mechanism, we investigated the cell cycle progression of the promising

Moléculas pequeñas conteniendo selenio como agentes antitumorales: Síntesis y Desarrollo preclínico

El cáncer es una enfermedad causada por el crecimiento anormal y descontrolado de células, que destruyen células sanas y causan frecuentemente la muerte [1]. Esta proliferación incontrolada de células puede conducir al crecimiento de tumores. Además, algunas de estas células anormales pueden viajar por el cuerpo a través del torrente sanguíneo o del sistema linfático, expandiendo el tumor a otras partes del cuerpo y generando nuevos tumores. Este proceso se conoce como metástasis y es la principal causa de muerte relacionada con el cáncer [2]. Las células normales se convierten en células cancerosas debido principalmente a mutaciones en sus genes. Habitualmente son necesarias muchas mutaciones antes de que una célula sana se convierta en tumoral, y a este proceso se le conoce como tumorgénesis. Las mutaciones pueden afectar a diferentes genes encargados del control del crecimiento y división celular. Algunos de estos genes son los llamados genes supresores de tumores. Las mutaciones también pueden causar que genes normales se conviertan en oncogenes, o genes causantes de tumores. Las células cancerosas acumulan defectos en múltiples oncogenes y genes supresores de tumores; la inactivación de un único oncogén crítico puede inducir a las células cancerosas a diferenciarse en células con un fenotipo normal o sufrir apoptosis [3]

Moléculas pequeñas conteniendo selenio como agentes antitumorales: Síntesis y Desarrollo preclínico

El cáncer es una enfermedad causada por el crecimiento anormal y descontrolado de células, que destruyen células sanas y causan frecuentemente la muerte [1]. Esta proliferación incontrolada de células puede conducir al crecimiento de tumores. Además, algunas de estas células anormales pueden viajar por el cuerpo a través del torrente sanguíneo o del sistema linfático, expandiendo el tumor a otras partes del cuerpo y generando nuevos tumores. Este proceso se conoce como metástasis y es la principal causa de muerte relacionada con el cáncer [2]. Las células normales se convierten en células cancerosas debido principalmente a mutaciones en sus genes. Habitualmente son necesarias muchas mutaciones antes de que una célula sana se convierta en tumoral, y a este proceso se le conoce como tumorgénesis. Las mutaciones pueden afectar a diferentes genes encargados del control del crecimiento y división celular. Algunos de estos genes son los llamados genes supresores de tumores. Las mutaciones también pueden causar que genes normales se conviertan en oncogenes, o genes causantes de tumores. Las células cancerosas acumulan defectos en múltiples oncogenes y genes supresores de tumores; la inactivación de un único oncogén crítico puede inducir a las células cancerosas a diferenciarse en células con un fenotipo normal o sufrir apoptosis [3]

Novel N,N'-disubstituted selenoureas as potential antioxidant and cytotoxic agents

A series of 30 novel N,N disubstituted selenoureas were synthesized, characterized, and their antioxidant ability was tested using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,20-azinobis( 3-ethylbenzthiazoline-6-sulfonic acid (ABTS) assays. Additionally, their cytotoxic activity was tested in vitro in a panel of three different cancer (breast, lung and colon) and two normal cell lines. Each selenourea entity contains a para-substituted phenyl ring with different electron-withdrawing and electron-donating groups, and different aliphatic and aromatic nuclei. All of the synthesized selenoureas present antioxidant capacity at high concentrations in the DPPH assay, and three of them (2b, 2c and 2d) showed greater radical scavenging capacity than ascorbic acid at lower concentrations. These results were confirmed by the ABTS assay, where these novel selenoureas present even higher antioxidant capacity than the reference compound Trolox. On the other hand, 10 selenoureas present IC50 values below 10 M in at least one cancer cell line, resulting in the adamantyl nucleus (6a¿ 6e), the most interesting in terms of activity and selectivity. Outstanding results were found for selenourea 6c, tested in the NCI60 cell line panel and showing an average GI50 of 1.49 M for the 60 cell lines, and LC50 values ranging from 9.33 M to 4.27 M against 10 of these cancer cell lines. To gain insight into its anticancer activity mechanism, we investigated the cell cycle progression of the promising

Clinical applications of exercise in Parkinson’s disease: what we need to know?

Introduction: Exploring the potential of exercise in the rehabilitation process of patients with Parkinson’s (PD) may be an interesting treatment perspective. Exercise-induced responses derived from neurotrophic elements appear to ameliorate the decline in neurodegeneration. Despite this understanding, the literature needs to be updated. Areas covered: Our review focuses on: a) the key mechanisms of exercise on PD, highlighting mainly the responses related to neuroplasticity; b) the effects induced by different traditional types of exercise, also highlighting the effects of complementary therapies related to movement; c) the volume of exercise required to support efficient results are explored in the context of PD. Additionally, the proposition of new clinical application strategies in the context of PD will also be determined. Expert opinion: It is suggested that different intensities of aerobic exercise be explored for the treatment of PD. The results associated with high intensity seem promising for performance, physiological and clinical parameters, such as BDNF production and cognition. On the other hand, the diversification of tasks and repetition of motor gestures appear as consistent arguments to exercise prescription. Finally, for future investigations, the neuromodulation strategy in association with aerobic exercise appears as a potential inducer of benefits on gait and cognitive function