Apoptosis control by death and decoy receptors Curr Opin Cell Biol 11 : — Death and decoy receptors and pmediated apoptosis Leukemia 14 : — Hierarchical control of lymphocyte survival Science : 67— The TNF receptor superfamily of cellular and viral proteins: activation, costimulation, and death Cell 76 : — Nagata S. Apoptosis by death factor Cell 88 : — FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis Cell 81 : — Tumor necrosis factor induces phosphorylation and translocation of BAD through a phosphatidylinositideOH kinase-dependent pathway J Biol Chem : — Induction of apoptosis by Apo-2 ligand, a new member of the tumor necrosis factor receptor family J Biol Chem : — Identification and characterization of a new member of the TNF family that induces apoptosis Immunity 3 : — X-linked IAP is a direct inhibitor of cell-death proteases Nature : — An apoptosis-inhibiting baculovirus gene with a zinc finger-like motif J Virol 67 : — Miller LK.
Regulation of apoptosis by viral gene products J Virol 71 : — Conservation of baculovirus inhibitor of apoptosis repeat proteins BIRPs in viruses, nematodes, vertebrates and yeasts Trends Biochem Sci 23 : — The inhibitors of apoptosis IAPs and their emerging role in cancer Oncogene 17 : — A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma Nat Med 3 : — Control of apoptosis and mitotic spindle checkpoint by survivin Nature : — Freemont PS.
RING for destruction? Curr Biol 10 : R84—R Ubiquitin protein ligase activity of IAPs and their degradation in proteasomes in response to apoptotic stimuli Science : — Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition Cell : 33— Schlessinger J. New roles for src kinases in control of cell survival and angiogenesis Cell : — Phosphoinositide 3-kinase: the key switch mechanism in insulin signalling Biochem J : — Courtneidge SA, Heber A.
PDGF-dependent tyrosine phosphorylation stimulates production of novel polyphosphoinositides in intact cells Cell 57 : — Structure of the insulin receptor substrate IRS-1 defines a unique signal transduction protein Nature : 73— Pawson T, Gish GD. SH2 and SH3 domains: from structure to function Cell 71 : — Protein kinase B c-Akt : a multifunctional mediator of phospatidylinositol 3-kinase activation Biochem J : 1— Protein kinase B kinases that mediate phosphatidylinositol 3,4,5-triphosphate-dependent activation of protein kinase B Science : — Interleukininduced phosphorylation of BAD through the protein kinase Akt Science : — Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery Cell 91 : — Toker A.
Protein kinases as mediators of phosphoinositide 3-kinase signaling Mol Pharm 57 : — Regulation of cell death protease caspase-9 by phosphorylation Science : — Caspase phosphorylation, cell death, and species variability Science : a. Caspase phosphorylation, cell death, and species variability.
Response Science : a. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor Cell 96 : — Pap M, Cooper GM. Pten is essential for embryonic development and tumour suppression Nat Genet 19 : — PTEN gene alterations in lymphoid neoplasms Blood 92 : — Loss of heterozygosity on 10q and microsatellite instability in advanced stages of primary cutaneous T-cell lymphoma and possible association with homozygous deletion of PTEN Blood 95 : — Barkett M, Gilmore TD.
Whiteside ST, Israel A. I kappa B proteins: structure, function and regulation Semin Cancer Biol 8 : 75— Rayet B, Gelinas C. Gilmore TD. Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel Oncogene 18 : — Structure and expression of c-rel, the cellular homolog to the oncogene of reticuloendotheliosis virus strain T J Virol 45 : — The v-Rel oncoprotein blocks apoptosis and proteolysis of I kappa B-alpha in transformed chicken spleen cells Oncogene 10 : — Sen R, Baltimore D.
Inducibility of kappa immunoglobulin enhancer-binding protein Nf-kappa B by a posttranslational mechanism Cell 47 : — Sonenshein G. NF-kappa B signaling promotes both cell survival and neurite process formation in nerve growth factor-stimulated PC12 cells J Neurosci 20 : — Requirement of NF-kappaB activation to suppress pindependent apoptosis induced by oncogenic Ras Science : — NF-kappaB activation by tumor necrosis factor requires the Akt serine-threonine kinase Nature : 82— A role for nuclear factor kappaB in the antiapoptotic function of insulin J Biol Chem : — Insulin-like growth factormediated neuroprotection against oxidative stress is associated with activation of nuclear factor kappaB J Biol Chem : — DNA damage-induced cell cycle checkpoints and DNA strand break repair in development and tumorigenesis Oncogene 18 : — Kaelin WG.
The p53 gene family Oncogene 18 : — Drexler HG. Review of alterations of the cyclin-dependent kinase inhibitor INK4 family p15, p16, p18 and p19 in human leukemia—lymphoma cells Leukemia 12 : — The p53 network J Biol Chem : 1—4.
Regulation of p53 in response to DNA damage Oncogene 18 : — Sionov RV, Haupt Y. The cellular response to p the decision between life and death Oncogene 18 : — Download references.
You can also search for this author in PubMed Google Scholar. Reprints and Permissions. White, M. Suppression of apoptosis: role in cell growth and neoplasia. Leukemia 15, — Download citation. Received : 19 January Accepted : 23 February Published : 19 July Issue Date : 01 July Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative.
Archives of Virology Leukemia Apoptosis Advanced search. Skip to main content Thank you for visiting nature. Download PDF. Abstract A cell is a potentially dangerous thing.
Introduction Metazoan cells are able to initiate a series of events that causes the activation of intracellular proteases and ultimately results in the destruction of the cell. There are two reasons for a cell to undergo apoptosis. How apoptosis transpires: caspase activation Activation of the family of proteins known as caspases cysteinyl, aspartate-specific proteases constitutes the means of execution of apoptosis.
Lamins Lamins are the major structural component proteins of the nuclear envelope. Translation initiation factors When apoptosis is induced, the rate of cellular protein synthesis is rapidly diminished and this occurs at the level of translation initiation. Cell signaling proteins Certain cell signaling proteins are cleaved by caspases and this may contribute to apoptosis. How apoptosis is initiated; mechanisms of induction of apoptosis What makes a cell decide to kill itself? Figure 1. Full size image.
Protection from apoptosis: the other side of the coin The life or death decision-making process responsible for apoptosis hangs in the balance of positive and negative influences.
Help from the outside: how extracellular cytokines protect cells from apoptosis As discussed above, the survival of a cell depends on a balance between positive and negative signals.
Figure 2. Conclusions Apoptosis is a very tightly regulated cellular program with many levels of checks and balances. Signal transduction, cell cycle regulatory, and anti-apoptotic pathways regulated by IL-3 in hematopoietic cells: possible sites for intervention with anti-neoplastic drugs Leukemia 13 : — Article CAS Google Scholar 28 Green DR.
Bcl-2 expression in chronic lymphocytic leukemia and its correlation with the induction of apoptosis and clinical outcome Leukemia 10 : — CAS Google Scholar 83 Meijerink JP. View author publications. Rights and permissions Reprints and Permissions. About this article Cite this article White, M. Several observations revealed that oxidative stress induces damage in both nuclear and mtDNA and cells lacking mtDNA exhibit a marked resistance to cell death Yoneda et al.
Attempts to determine whether loss of mtDNA and disturbance in respiratory chain function result in apoptosis in vivo were also undertaken Wang et al. Using embryos with homozygous disruption of the gene encoding the mitochondrial transcription factor Tfam, as well as tissue-specific Tfam knockout animals with severe respiratory chain deficiency in the heart, the authors showed massive apoptosis in both experimental systems.
These data provide in vivo evidence that respiratory chain deficiency predisposes cells to apoptosis. Interestingly, Tfam is essential not only for mitochondrial gene expression, but also for maintenance and repair of mtDNA. More detailed investigation revealed that binding of Tfam to cisplatin-modified DNA was significantly enhanced by p53, with which Tfam was found to interact physically Yoshida et al.
Thus, although the role of mtDNA in cell death is contentious, it is clear that its absence or impaired function can profoundly influence the rate of apoptosis. Mutations in the mtDNA leading to mitochondrial dysfunction have been reported in a variety of cancers. Might these mutations influence cellular responses to cancer therapy? Importantly, resistance to adriamycin, which induces ROS formation as well as acting as a topoisomerase II inhibitor, was not due to the lack of drug uptake, or to altered cell cycle responses.
Thus, mitochondrial function is a determinant of cellular sensitivity to important cancer therapeutic agents. The data reviewed above concerning the involvement of histones H1. Compared with native chromatin, apoptotic oligonucleosomal fragments contained less histone H1 Borisova et al. This histone modification increases the accessibility of chromatin to nucleases and probably promotes DNA fragmentation during apoptosis.
On the other hand, histone H1. Moreover, no modifications in H1. In certain experimental systems, induction of apoptosis was accompanied by histone H1 phosphorylation Lee et al. These data suggest that apoptotic cells could be entering premature, and therefore catastrophic, mitosis in response to DNA damage. Broadly speaking, similar data have been obtained for histone H3, which is phosphorylated during mitosis and premature chromosome condensation, but not during apoptosis.
Histone H2AX phosphorylation, as noted above, plays a role in DNA damage signalling, but has no known direct connection with the chromatin changes that accompany apoptosis. Perhaps the most clearcut case for direct involvement of histone phosphorylation in DDIA concerns mammalian histone H2B, which is phosphorylated at Ser14 in response to UV irradiation or treatment with the topoisomerase II inhibitor etoposide, which induces DNA strand breaks.
This phosphorylation is mediated by mammalian sterile twenty Mst1 kinase Cheung et al. This comprises elements of the DNA damage detection machinery, including proteins that also signal cell cycle checkpoint arrest, signal transducers including CHK2, p53 and E2F-1, as well as the downstream caspases and their regulators Figure 2. The setting of the rheostat is determined in part by the abundance and basal activities of these various components, in part by their upregulation during cell proliferation and in part by the in-built amplification loops that operate via Fas and the release of mitochondrial regulators of apoptosis.
Multiple independent routes have now been traced by which nuclear DNA damage can be signalled to the mitochondria. These encompass pdependent transcriptional activation, less well-characterized direct mitochondrial roles for p53, histone H1. A degree of coordination between DNA repair and cellular commitment to apoptosis may be achieved through the release of Ku70, conventionally considered to be a nuclear DNA repair protein, into the cytoplasm.
It is also apparent that damage to the mitochondrial genome, as well as nuclear DNA damage, has the capacity to influence the extent of subsequent apoptosis. Each of these events is potentially of crucial importance both in tumour development and in the response of cancer cells to therapies based on the induction of DNA damage. EMBO J. Cancer Res. USA , 91 , — Cell , , — Genes Dev. Radiobiologiya , 24 , — in Russian. Cell Biol. Nature , , — Caspari T.
Science , , — Cory S and Adams JM. Cancer , 2 , — Cell , , 51— Durocher D and Jackson SP. Cell , 44 , — Cell Sci. Cell , 5 , — Cell Death Differ. Cancer , 26 , — USA , 96 , — Nucleic Acids Res. Oncogene , 21 , — FEBS Lett. Cell , 86 , — Cell , 74 , — Lu X and Lane DP. Cell , 75 , — Biochemistry , 32 , — USA , 99 , — Michaelson JS and Leder P. Cell , 11 , — Miyashita T and Reed JC. Cell , 80 , — Nakano K and Vousden KH. Cell , 7 , — Nature , , 90— Reinke V and Lozano G.
Oncogene , 15 , — USA , , — Sheikh SM and Huang Y. Cell Cycle , 2 , — Shen Y and White E. Shiloh Y. Oncogene , 18 , — Anticancer Res. Cell Biochem. Thornberry NA. Apoptosis , 7 , — Vousden KH and Lu X. USA , 98 , — Biochimie , 84 , — Neoplasia , 4 , — Wyllie AH. USA , 97 , — Cell , 89 , — Zhou L and Steller H. Cell , 4 , — Download references.
We apologize to those authors whose work could not be cited directly due to space limitations. You can also search for this author in PubMed Google Scholar. Correspondence to Boris Zhivotovsky.
Reprints and Permissions. Norbury, C. DNA damage-induced apoptosis. Oncogene 23, — Download citation. Published : 12 April Issue Date : 12 April Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Laboratory Investigation Cancer Gene Therapy Environmental Science and Pollution Research It is well known that tumor cells can be resistant to chemotherapeutics.
With the assistance of nanoparticles, medical treatment can advance more smoothly. Polysaccharides, as major bioactive compounds, are reported to have anti-cancer properties. They have been able to induce cell death in a hepatoma cell lines Hep G2 [ 94 ]. Here, Nano-encapsulated in chitosan-silica or just silica, the nano-conjunction caused a more significant decrease in Hep G2 cell viability than mere polysaccharides alone and induced apoptosis like ROS generation, DNA fragmentation, caspase activation and cell sub-G1 phase arrest.
In the study of Li et al. There it significantly inhibited the growth of tumors as compared to free Dox treatment. It may be that the released Dox induced cancer cell apoptosis through interference with DNA repair and replication by DNA intercalation in highly proliferating cells.
In such a process normal cells may be spared [ 97 ]. ENPs are also explored as small interfering RNA siRNA carriers in the treatment of breast cancer [ 98 ], ovarian cancer [ 99 ], hepatocellular carcinoma [ ], and B-cell malignancies [ ] etc. The above examples show that ENP-dependent drug delivery systems prove to be a promising therapeutic system for the treatment of cancer.
Despite the promising drug delivery system provided by ENPs in cancer therapy, one has to consider the safety and efficiency of the delivery and targeting. To achieve selective treatment and to reduce toxicity, ENPs are usually endowed with tumor targeting abilities by binding to antibodies directed against highly expressed cancer cell surface receptors.
In the newly published literature of Palanca-Wessels et al. Plus, the effective targeting can be realized by designing smart nano-carriers that respond to certain changes in the bio-environment and release the encapsulated contents on demanded sites.
Gurka et al. It was found that the tumor specificity of MSN was improved with the addition of chitosan targeting acid PH and urokinase plasminogen activator UPA, targeting UPAR , ensuring drug release and accumulation preferentially at the pancreatic tumors compared to liver or kidney. Targeted as well as controlled drug delivery and release can also be realized with magnetoelectric nanoparticles MEN , which, with its load, can be controlled and placed at the intended site via application of an external magnetic field [ ].
ENPs, having great potential for application in cancer treatment, also arouse concerns about potential risks for human exposure. How to use ENPs wisely at minimum side effects is becoming an increasingly important focal area. Here we introduce several examples concerning ENP type, size and shape as well as surface modification.
Before application, the comparable cytotoxicities between many differing particles must be established by comparing their effects in different cell lines.
In one case six different fine- or nano- particles were investigated on the macrophage-like murine cell line RAW In another report, silver particles of nano- 20 nm and submicron- nm were compared with TiO 2 -NPs 21 nm in the human testicular embryonic carcinoma cell line Ntera2 and primary testicular cells from C57BL6 mice. The results showed that the silver particles exerted more of a cytotoxic effect than did the TiO 2 -NPs, causing apoptosis, necrosis and decreased proliferation in dose and time dependent manner [ ].
TiO 2 NPs seemed to be less toxic than other particles, though case by case analyses remain necessary. In general, the smaller the ENPs size, the more concerns there is for human exposure. This may be due to the effect of mass-specific surface area, leading to the smaller sized ENPs exerting a more toxic effect.
In this, CuO NPs were seen to exert the strongest effects. However, small particles do not necessarily lead to better uptake or enhanced toxicity. In a NT2 study, for example, primary testicular cells were treated with nano- 20 nm and submicron- nm Ag particles. Another study by Park reconfirmed that by investigating different cell fates induced by different sizes of TiO 2 nanotubes, in which cellular activities were enhanced by particles less than 30 nm while reduced by particles larger than 50 nm with a high extent of apoptosis [ ].
In addition to size, the shapes of ENPs are also directly correlated to their induced cytotoxicity. Two graphitic nanomaterials, graphene layers G and single-wall carbon nanotubes SWCNT , having similar chemical composition and crystalline structures, were presented with different shapes.
Here, G occurs in flat atomic sheets and nanotubes are tubular. In the concentration-dependent toxicity testing of these two ENPs on PC12 cells, results were dissimilar. G had a higher toxic effect at lower concentrations and SWCNT a more intense toxic effect at higher concentrations.
This indicates different toxic mechanisms related to shape [ ]. These different effects were assumed to be that the needle-like CNTs were more mobile and more easily able to penetrate the cell membrane and thereby caused strong interactions with various protein systems. The indication is that these two ENPs have different cellular target sites. In another case four types of hydroxyapatite nanoparticles nano-HAP with different nanocrystal morphologies short rod-like, long rod like, spherical and needle-shaped crystals and sizes , , and nm were compared for their effects upon primary cultured rat osteoblasts [ ].
These nano-HAPs induced mitochondrial and caspase dependent apoptosis in the osteoblasts, with needle-shaped and the spherical particles inducing the greater cellular injury than short rod-like and long rod-like particles.
It has been recognized that the specific surface area of ENPs can determine the activities of the materials. Particles with higher specific surface area tend to have greater activity and more easily attach to the cells and lead to toxicity.
This is in accordance with the above study in which the needle-shaped ENPs of different surface modifications have numerous technological and biomedical applications. They interact with biological structures and display distinct and specific impacts to the cell systems.
It was found that exposure to GOs led to mitochondrial dysfunction and increased the amount of HLF apoptotic cells, while values of the cell viability rates and DNA damage differed among the various modifications. This may be a result of different electronic charges on the surface of GOs after modification The electronic charge on the surface of the ENPs may play important roles in determining their toxicity to targeted cells. Similarly, Arvizo et al. Some modifications might be able to lighten the cytotoxic effects of ENPs.
These modifications were supposed to improve their solubility and biocompatibility and alter their cellular interaction pathways, resulting in an enhanced ability to penetrate biological membranes with relatively low cytotoxicity [ 89 ].
Carbon-based substances were considered to be less bio-reactive in biological systems and thus be critical for reducing the inherent reactivity of ENPs with biomolecules. In another case, nano-TiO 2 was coated with polyacrylate and the cytotoxicity on Chinese hamster lung fibroblast V79 cells was compared with nano-TiO 2 and micro-TiO 2.
Here, the cell viability decreased and induction of apoptosis was observed for the administration of all types of TiO 2 particles, but for polyacrylate-coated nano-TiO 2 , it was only detected in higher concentrations with no DNA damage detected [ ].
Nanoparticles offer a numerous application possibilities in the industrial sector. These include their use as fuel additives for catalysis, as sunscreen additives for UV protection, various applications in the textile industry and their use in biomedicine as drug targeting agents or drug carriers [ ].
In recent years directs ENP applications towards cancer therapy for inducing cancer cell apoptosis has been an increasing focus. Unfortunately such widely usage may also pose unwanted threat to human health. In addition, some aspects of surface modification may be able to reduce the bio-reactivity of ENPs, thus alleviating their toxicities in certain circumstances. This may provide a way to design even more effective particles of minimum undesired toxicity.
The authors are grateful to all members of the Sperm Laboratory in Zhejiang University for their valuable perspectives as to this topic and suggestion in the writing. The authors thank Chris Wood for his effort in linguistic polishing of this manuscript. The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of this review. Nowack B, Bucheli TD. Occurrence, behavior and effects of nanoparticles in the environment.
Environ Pollut. Toxic potential of materials at the nanolevel. Evaluating engineered nanoparticles in natural waters. Trend Anal Chem. Nanotoxicology: an emerging discipline evolving from studies of ultrafine particles.
Environ Health Persp. Principles for characterizing the potential human health effects from exposure to nanomaterials: elements of a screening strategy. Part Fibre Toxicol. Ultrafine particle-ling interactions: Does size matter? J Aerosol Med. The effect of formulation on the penetration of coated and uncoated zinc oxide nanoparticles into the viable epidermis of human skin in vivo. Eur J Pharm Biopharm.
Nano-sized cosmetic formulations or solid nanoparticles in sunscreens: a risk to human health? Arch Toxicol. Srikanth M, Kessler JA. Nanotechnology-novel therapeutics for CNS disorders. Nat Rev Neurol. Particulate matter in polluted air may increase biomarkers of inflammation in mouse brain. Lan Z, Yang WX. Nanoparticles and spermatogenesis: how do nanoparticles affect spermatogenesis and penetrate the blood-testis barrier.
Differential nanoreprotoxicity of silver nanoparticles in male somatic cells and spermatogonial stem cells. Int J Nanomed. Long-term toxicity of reduced graphene oxide nanosheets: Effects on female mouse reproductive ability and offspring development. In vitro evaluation of cellular response induced by manufactured nanoparticles.
Chem Res Toxicol. Gold nanoparticles interfere with sperm functionality by membrane adsorption without penetration. Multi-walled carbon nanotubes injure the plasma membrane of macrophages. Toxicol Appl Pharm. Nano-hydroxyapatite and nano-titanium dioxide exhibit different subcellular distribution and apoptotic profile in human oral epithelium. Acs Appl Mater Interfaces. Silver nanoparticles-allies or adversaries? Ann Agr Env. Med ; Electrochemical modeling of the silica nanoparticle-biomembrane interaction.
Cell penetrating peptides: intracellular pathways and pharmaceutical perspectives. Pharma Res. Anti-proliferative activity of silver nanoparticles. BMC Cell biology.
Silver nanoparticles and mitochondrial interaction. Int J Dentistry. Gerium dioxide nanoparticles induce apoptosis and autophagy in human peripheral blood monocytes.
Acs Nano. Molecular mechanisms of nanosized titanium dioxide-induced pulmonary injury in mice. PloS ONE. Endoplasmic reticulum stress and oxidative stress are involved in ZnO nanoparticles-induced hepatotoxicity.
Toxicol Lett. Endoplasmic reticulum stress induced by zinc oxide nanoparticles is an earlier biomarker for nanotoxicological evaluation. Nano-SiO2 induces apoptosis via activation of p53 and Bax mediated by oxidative stress in human hepatic cell line. Toxicol in Vitro. Nano-TiO2-induced apoptosis by oxidative stress-mediated DNA damage and activation of p53 in human embryonic kidney cells. Appl Biochem Biotechnol. Genotoxicity and carcinogenicity of cobalt-, nickel- and copper-based nanoparticles Review.
Exp Ther Med ; 4: Controllable synthesis of monodispersed silver nanoparticles as standards for quantitative assessment of their cytotoxicity. Molecular characterization of the cytotoxic mechanism of multiwall carbon nanotubes and nano-onions on human skin fibroblast.
Nano lett. SiO2 nanoparticles induce cytotoxicity and protein expression alteration in HaCaT cells. Biosci Biotech Bioch. Chromium III oxide nanoparticles induced remarkable oxidative stress and apoptosis on culture cells. Environ Toxicol. Nickel carcinogenesis. Mutat Res. J Nanobiotecg. Drug delivery to the central nervous system: a review.
J Pharm Sci. Neurotoxicity of silica nanoparticles: brain localization and dopaminergic neurons damage pathways. Ishima T, NishimuraT. Iyo M, Hashimoto K. Potentiation of nerve growth factor-induced neurite outgrowth in PC12 Cells by donepezil: Role of sigma-1 receptors and IP3 receptors. Prog Neuro-Psychoph. Role of oxidative stress in neurodegeneration: recent developments in assay methods for oxidative stress and nutraceutical Antioxidants.
Oxidative mechanisms contribute to nanosized silican dioxide-induced development neurotoxicity in PC12 cells. Toxicol In Vitro. Oxidative stress and apoptosis induced by nanosized titanium dioxide in PC12 cells. The similar neurotoxic effects of nanoparticulate and ionic silver in vivo and in vitro. Ehringer H, Hornykiewicz O. Distribution of noradrenaline and dopamine 3-hydroxytyramine in the human brain and their behavior in diseases of the extrapyramidal system. Klin Wochenschr.
Maternal exposure to nanoparticulate titanium dioxide during the prenatal period alters gene expression related to brain development in the mouse. Hussain S, Garantziotis S. Interplay between apoptotic and autophagy pathways after exposure to cerium dioxide nanoparticles in human monocytes.
Autophagy ; Wluka A, Olszewski WL. Innate and adaptive processes in the spleen. Ann Transplant. Nano-sized titanium dioxide-induced splenic toxicity: A biological pathway explored using microarray technology. J Hazard Mater. Biochem Bioph Res Co. Toxicity of cobalt oxide nanoparticles to normal cells: an in vitro and in vivo study. Chem-Biol Interact. Thubagere A, Reinhard BM. Nanoparticle-induced apoptosis propagates through hydrogen-peroxide-mediated bystander killing: insights from a human intestinal epithelium in vitro model.
Characterization of translocation of silver nanoparticles and effects on whole-genome gene expression using an in vitro intestinal epithelium coculture model. Endoplasmic reticulum stress and oxidative stress are involved in ZnO nanoparticle-induced hepatotoxicity. Cell biology of the glomerular podocyte.
Physiol Rev. Nanosized copper oxide induces apoptosis through oxidative stress in podocytes. Nano-copper induces oxidative stress and apoptosis in kidney via both extrinsic and intrinsic pathways. Particulate air pollution induces progression of atherosclerosis. Am Coil Cardiol. Multiwall carbon nano-onions induce DNA damage and apoptosis in human umbilical vein endothelial cells.
Single-walled carbon nanotube induction of rat aortic endothelial cell apoptosis: reactive oxygen species are involved in the mitochondrial pathway. Int J Biochem Cell B. Protective effect of beta-carotene against titanium dioxide nanoparticles induced apoptosis in mouse testicular tissue. Oxidative damages and ultrastructral changes in the sperm of freshwater crab Sinopotamon henanense exposed to cadmium.
Ecotox Environ Safe. Observing real-time molecular event dynamics of apoptosis in living cancer cells using nuclear-targeted plasmonically enhanced raman nanoprobes. Cytotoxicity of nanoparticles is independent from oxidative stress. J Toxicol Sci. Dysfunction of methionine sulfoxide reductases to repair damaged proteins by nickel nanoparticles. Wong RSY.
Apoptosis in cancer: from pathogenesis to treatment. J Exp Clin Canc Res. Nat Cell Biol. Molecular components of a cell death pathway activated by endoplasmic reticulum stress.
J Biol Chem. Biogenic silver nanoparticles for cancer treatment: An experimental report. Colloid Surface B. Silver nanoparticles of Albizia adianthifolia: the induction of apoptosis in human lung carcinoma cell line.
Synthesis and characterization of silver nanoparticles using crystal compound of sodium para-hydroxybenzoate tetrahydrate isolated from Vitex negundo. L leaves and its apoptotic effect on human colon cancer cell lines.
0コメント