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      Synthesis of silver nanoparticles using a Mentha spicata extract and evaluation of its anticancer and cytotoxic activity

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          Abstract

          In this study, silver nanoparticles (NP) were synthesized by two methods: using an aqueous extract of Mentha spicata leaves and using citrate ions as stabilizing agent, and the cytotoxicity and anticancer activity of both NP were evaluated in vitro. The particles synthesized with the aqueous extract were spherical with a size ranging from 15 to 45 nm. These NP decreased cell viability in all of the cells studied; however, the IC 50 could only be estimated in the Chang liver cells (IC 50 = 21.37 µg/mL). These particles also decreased the generation of reactive oxygen species in Chang and SiHa cells. Additionally, the dispersions decreased the activity of caspase-3. There was no significant difference between the biological activities of the NP obtained with the aqueous extract and the NP synthesized using citrate ions. This study showed that an aqueous extract of M. spicata is an excellent alternative for the synthesis of silver NP. These NP showed cytotoxicity and anticancer activity in vitro. Although more experiments are required, the cell death occurs probably through a mechanism different from apoptosis.

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          JNK signaling in apoptosis.

          Jun N-terminal kinases or JNKs play a critical role in death receptor-initiated extrinsic as well as mitochondrial intrinsic apoptotic pathways. JNKs activate apoptotic signaling by the upregulation of pro-apoptotic genes through the transactivation of specific transcription factors or by directly modulating the activities of mitochondrial pro- and antiapoptotic proteins through distinct phosphorylation events. This review analyses our present understanding of the role of JNK in apoptotic signaling and the various mechanisms by which JNK promotes apoptosis.
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            Detection of necrosis by release of lactate dehydrogenase activity.

            Apoptosis and necrosis are two major forms of cell death observed in normal and disease pathologies. Although there are many assays for detection of apoptosis, relatively few assays are available for measuring necrosis. A key signature for necrotic cells is the permeabilization of the plasma membrane. This event can be quantified in tissue culture settings by measuring the release of the intracellular enzyme lactate dehydrogenase (LDH). When combined with other methods, measuring LDH release is a useful method for the detection of necrosis. In this chapter, we describe the step-by-step procedure for detection of LDH release from necrotic cells using a microtiter plate-based colorimetric absorbance assay.
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              Silica nanoparticles induce autophagy dysfunction via lysosomal impairment and inhibition of autophagosome degradation in hepatocytes

              Autophagy dysfunction is considered as a potential toxic mechanism of nanomaterials. Silica nanoparticles (SiNPs) can induce autophagy, but the specific mechanism involved remains unclear. Therefore, the aim of this study was to confirm the effects of SiNPs on autophagy dysfunction and explore the possible underlying mechanism. In this article, we reported that cell-internalized SiNPs exhibited dose- and time-dependent cytotoxicity in both L-02 and HepG2 cells. Multiple methods verified that SiNPs induced autophagy even at the noncytotoxic level and blocked the autophagic flux at the high-dose level. Notably, SiNPs impaired the lysosomal function through damaging lysosomal ultrastructures, increasing membrane permeability, and downregulating the expression of lysosomal proteases, cathepsin B, as evidenced by transmission electron microscopy, acridine orange staining, quantitative reverse transcription-polymerase chain reaction, and Western blot assays. Collectively, these data concluded that SiNPs inhibited autophagosome degradation via lysosomal impairment in hepatocytes, resulting in autophagy dysfunction. The current study not only discloses a potential mechanism of autophagy dysfunction induced by SiNPs but also provides novel evidence for the study of toxic effect and safety evaluation of SiNPs.
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                Author and article information

                Contributors
                Journal
                PeerJ
                PeerJ
                PeerJ
                PeerJ
                PeerJ
                PeerJ Inc. (San Diego, USA )
                2167-8359
                9 December 2019
                2019
                : 7
                : e8142
                Affiliations
                [1 ]Universidad Autónoma de Nuevo León, UANL, Facultad de Ciencias Químicas, Laboratorio de Farmacología Molecular y Modelos Biológicos , Monterrey, Nuevo León, Mexico
                [2 ]Universidad Autónoma de Nuevo León, UANL, Facultad de Ciencias Químicas, Laboratorio de Materiales I, San Nicolás de los Garza , Nuevo León, Mexico
                [3 ]Universidad Autónoma de Nuevo León, UANL, Centro de Investigación en Biotecnología y Nanotecnología (CIBYN), Laboratorio de Nanociencias y Nanotecnología, Apodaca , Nuevo León, Mexico
                [4 ]Centro de Investigación en Materiales Avanzados, S.C. (CIMAV), Unidad Monterrey, Apodaca , Nuevo León, Mexico
                Author information
                http://orcid.org/0000-0003-3092-0222
                http://orcid.org/0000-0003-1841-1783
                http://orcid.org/0000-0002-3894-597X
                http://orcid.org/0000-0002-0957-3062
                Article
                8142
                10.7717/peerj.8142
                6907090
                31844570
                4f8193e1-bd8b-473c-b468-7ecccf4768d1
                © 2019 Torres-Martínez et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.

                History
                : 27 May 2019
                : 1 November 2019
                Funding
                Funded by: Consejo Nacional de Ciencia y Tecnología (CONACyT)
                Award ID: 236456 (CB 201401)
                This work was supported by the Consejo Nacional de Ciencia y Tecnología (CONACyT), grant 236456 (CB 201401). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Cell Biology
                Toxicology
                Translational Medicine

                silver nanoparticles,anticancer,citotoxicity,mentha spicata

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