In vivo DNA damaging and apoptotic potential of&amp;nbsp;silver nanoparticles in Swiss albino mice

Gurabi, Mohammed A Al; Ali, Daoud; Alakahtani, Saad; Alarifi, Saud

doi:10.2147/ott.s77572

Cited by 22 publications

(11 citation statements)

References 19 publications

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“…According to Asharani et al ( 2009 ), AgNPs enter the organelles, particularly the mitochondria. Cristolysis induced by AgNPs may affect oxidative phosphorylation and ATP production due to hampering of electron transport (Al Gurabi et al 2015 ). Mitochondria play the key role in hepatic metabolism, and obviously, most chronic hepatic diseases are related to mitochondrial disorders.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity of silver and copper nanoparticles on rainbow trout (Oncorhynchus mykiss) hepatocytes

Ostaszewska

Śliwiński

Kamaszewski

et al. 2017

Environ Sci Pollut Res

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Nanoparticles are commonly used in the industry and are present in consumer goods; therefore, evaluation of their potential toxicity is necessary. The aim of the present study was to assess the cytotoxic effects of the nanoparticles of silver (AgNPs) at the concentration of 1.5 mg L−1 and copper (CuNPs) at 0.15 mg L−1 on rainbow trout (Oncorhynchus mykiss) hepatocytes after 28 days of exposure. Histological analysis revealed dilated sinusoids, shrunken hepatocytes, nuclear necrosis, and increased number of Kupffer cells in the liver of fish exposed to nanoparticles. The lowest hepatocyte proliferation index was observed in fish treated with AgNPs. Ultrastructural studies revealed mitochondrial edema and cristolysis, dilated and loosened endoplasmic reticulum, cytoplasm vacuolation, accumulation of lipid droplets, glycogen depletion, and formation of myelin-like bodies. The results also revealed that the liver of fish exposed to copper nanoparticles showed higher regenerative potential indicated by higher proliferation index, more abundant glycogen, and more numerous Kupffer cells compared to the fish treated with silver nanoparticles.

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Section: Discussionmentioning

confidence: 99%

Cytotoxicity of silver and copper nanoparticles on rainbow trout (Oncorhynchus mykiss) hepatocytes

Ostaszewska

Śliwiński

Kamaszewski

et al. 2017

Environ Sci Pollut Res

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“…In one study, Swiss albino mice were analyzed 24 h and 72 h after intraperitoneal administration of varying doses of AgNPs (26 mg kg −1 , 52 mg kg −1 , and 78 mg kg −1 ). 188 A dose- and time-dependent increase in DNA damage was observed in liver cells and lymphocytes. Further, staining of liver tissue samples revealed dose- and time-dependent apoptosis of liver cells and necrosis in some regions.…”

Section: Silver Nanoparticlesmentioning

confidence: 96%

Redox-active nanomaterials for nanomedicine applications

et al. 2017

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Nanomedicine utilizes the remarkable properties of nanomaterials for the diagnosis, treatment, and prevention of disease. Many of these nanomaterials have been shown to have robust antioxidative properties, potentially functioning as strong scavengers of reactive oxygen species. Conversely, several nanomaterials have also been shown to promote the generation of reactive oxygen species, which may precipitate the onset of oxidative stress, a state that is thought to contribute to the development of a variety of adverse conditions. As such, the impacts of NMs on biological entities are often associated with and influenced by their specific redox properties. In this review, we overview several classes of nanomaterials that have been or projected to be used across a wide range of biomedical applications, with discussion focusing on their unique redox properties. Amongst the nanomaterials examined include iron, cerium, and titanium metal oxide nanoparticles, gold, silver, and selenium nanoparticles, and various nanoscale carbon allotropes such as graphene, carbon nanotubes, fullerenes, and their derivatives/variations. Principal topics of discussion include the chemical mechanisms by which the nanomaterials directly interact with biological entities and the biological cascades that are thus indirectly impacted. Selected case studies highlighting the redox properties of nanomaterials and how they affect biological responses are used to exemplify the biologically-relevant redox mechanisms for each of the described nanomaterials.

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“…Toxicity of nanoparticles is attributed to oxidative stress, followed by DNA damage and apoptosis. Nanoparticles can cause a wide variety of DNA damage, ranging from chromosomal fragmentation, DNA strand breakages and the induction of gene mutations [ 69 , 70 , 71 , 72 ]. AuNPs (20 nm size) at 1 nM concentration have been shown to exhibit DNA damage in the form of 8-hydroxydoxyguanosine (8OHdG) adducts formation in embryonic lung fibroblasts with a decreased expression of DNA repair and the cell cycle checkpoint genes MAD2 , cyclin B1 and cyclin B2 [ 73 ].…”

Section: Molecular Mechanisms Underlying Nanotoxicitymentioning

confidence: 99%

Nanotoxicity: An Interplay of Oxidative Stress, Inflammation and Cell Death

et al. 2015

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Nanoparticles are emerging as a useful tool for a wide variety of biomedical, consumer and instrumental applications that include drug delivery systems, biosensors and environmental sensors. In particular, nanoparticles have been shown to offer greater specificity with enhanced bioavailability and less detrimental side effects as compared to the existing conventional therapies in nanomedicine. Hence, bionanotechnology has been receiving immense attention in recent years. However, despite the extensive use of nanoparticles today, there is still a limited understanding of nanoparticle-mediated toxicity. Both in vivo and in vitro studies have shown that nanoparticles are closely associated with toxicity by increasing intracellular reactive oxygen species (ROS) levels and/or the levels of pro-inflammatory mediators. The homeostatic redox state of the host becomes disrupted upon ROS induction by nanoparticles. Nanoparticles are also known to up-regulate the transcription of various pro-inflammatory genes, including tumor necrosis factor-α and IL (interleukins)-1, IL-6 and IL-8, by activating nuclear factor-kappa B (NF-κB) signaling. These sequential molecular and cellular events are known to cause oxidative stress, followed by severe cellular genotoxicity and then programmed cell death. However, the exact molecular mechanisms underlying nanotoxicity are not fully understood. This lack of knowledge is a significant impediment in the use of nanoparticles in vivo. In this review, we will provide an assessment of signaling pathways that are involved in the nanoparticle-induced oxidative stress and propose possible strategies to circumvent nanotoxicity.

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In vivo DNA damaging and apoptotic potential of silver nanoparticles in Swiss albino mice

Cited by 22 publications

References 19 publications

Cytotoxicity of silver and copper nanoparticles on rainbow trout (Oncorhynchus mykiss) hepatocytes

Cytotoxicity of silver and copper nanoparticles on rainbow trout (Oncorhynchus mykiss) hepatocytes

Redox-active nanomaterials for nanomedicine applications

Nanotoxicity: An Interplay of Oxidative Stress, Inflammation and Cell Death

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