Selenium and silver nanoparticles: A new approach for treatment of bacterial and viral hepatic infections via modulating oxidative stress and DNA fragmentation

Green nanoparticles represent a revolution in bionanotechnology, providing opportunities to fight life-threatening diseases, such as cancer, with less risk to the environment and to human health. Here, for the first time, we systematically investigated the anticancer activity and possible mechanism of novel silver nanoparticles (N-SNPs) synthesized by Nostoc Bahar M against the MCF-7 breast cancer cells, HCT-116 colorectal adenocarcinoma cells, and HepG2 liver cancer cells, using cell viability assays, morphological characterization with inverted light and transmission electron microscopy, antioxidants and enzymes (glutathione peroxidase (GPx), glutathione (GSH), adenosine triphosphatase (ATPase), and lactate dehydrogenase (LDH)), and western blotting (protein kinase B (Akt), phosphorylated-Akt (p-Akt), mammalian target of rapamycin (mTOR), B-cell lymphoma 2 (Bcl-2), tumor suppressor (p53), and caspase 3). N-SNPs decreased the viability of MCF-7, HCT-116, and HepG2 cells, with half-maximal inhibitory concentrations of 54, 56, and 80 µg/mL, respectively. They also significantly increased LDH leakage, enhanced oxidative stress via effects on antioxidative markers, and caused metabolic stress by significantly decreasing ATPase levels. N-SNPs caused extensive ultrastructural alterations in cell and nuclear structures, as well as in various organelles. Furthermore, N-SNPs triggered apoptosis via the activation of caspase 3 and p53, and suppressed the mTOR signaling pathway via downregulating apoptosis-evading proteins in MCF-7, HCT-116, and HepG2 cells. Ultrastructural analysis, together with biochemical and molecular analyses, revealed that N-SNPs enhanced apoptosis via the induction of oxidative stress and/or through direct interactions with cellular structures in all tested cells. The cytotoxicity of Nostoc-mediated SNPs represents a new strategy for cancer treatment via targeting various cell death pathways. However, the potential of N-SNPs to be usable and biocompatible anticancer drug will depend on their toxicity against normal cells.

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Oxidation of Sperm DNA and Male Infertility

Antioxidants ◽

10.3390/antiox10010097 ◽

2021 ◽

Vol 10 (1) ◽

pp. 97

Author(s):

Leila Rashki Ghaleno ◽

AliReza Alizadeh ◽

Joël R. Drevet ◽

Abdolhossein Shahverdi ◽

Mojtaba Rezazadeh Valojerdi

Keyword(s):

Oxidative Stress ◽

Male Infertility ◽

Oxidative Damage ◽

Dna Fragmentation ◽

Dna Bases ◽

De Novo Mutation ◽

Easy Access ◽

Sperm Dna Fragmentation ◽

Dna Base ◽

Sperm Dna

One important reason for male infertility is oxidative stress and its destructive effects on sperm structures and functions. The particular composition of the sperm membrane, rich in polyunsaturated fatty acids, and the easy access of sperm DNA to oxidative damage due to sperm cell specific cytologic and metabolic features (no cytoplasm left and cells unable to mount stress responses) make it the cell type in metazoans most susceptible to oxidative damage. In particular, oxidative damage to the spermatozoa genome is an important issue and a cause of male infertility, usually associated with single- or double-strand paternal DNA breaks. Various methods of detecting sperm DNA fragmentation have become important diagnostic tools in the prognosis of male infertility and such assays are available in research laboratories and andrology clinics. However, to date, there is not a clear consensus in the community as to their respective prognostic value. Nevertheless, it is important to understand that the effects of oxidative stress on the sperm genome go well beyond DNA fragmentation alone. Oxidation of paternal DNA bases, particularly guanine and adenosine residues, the most sensitive residues to oxidative alteration, is the starting point for DNA damage in spermatozoa but is also a danger for the integrity of the embryo genetic material independently of sperm DNA fragmentation. Due to the lack of a spermatozoa DNA repair system and, if the egg is unable to correct the sperm oxidized bases, the risk of de novo mutation transmission to the embryo exists. These will be carried on to every cell of the future individual and its progeny. Thus, in addition to affecting the viability of the pregnancy itself, oxidation of the DNA bases in sperm could be associated with the development of conditions in young and future adults. Despite these important issues, sperm DNA base oxidation has not attracted much interest among clinicians due to the lack of simple, reliable, rapid and consensual methods of assessing this type of damage to the paternal genome. In addition to these technical issues, another reason explaining why the measurement of sperm DNA oxidation is not included in male fertility is likely to be due to the lack of strong evidence for its role in pregnancy outcome. It is, however, becoming clear that the assessment of DNA base oxidation could improve the efficiency of assisted reproductive technologies and provide important information on embryonic developmental failures and pathologies encountered in the offspring. The objective of this work is to review relevant research that has been carried out in the field of sperm DNA base oxidation and its associated genetic and epigenetic consequences.

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Silver nanoparticles mitigate Aeromonas hydrophila-induced immune suppression, oxidative stress, and apoptotic and genotoxic effects in Oreochromis niloticus

Aquaculture ◽

10.1016/j.aquaculture.2021.736430 ◽

2021 ◽

Vol 535 ◽

pp. 736430

Author(s):

Walaa El-Houseiny ◽

Mohamed Fouad Mansour ◽

Wafaa A.M. Mohamed ◽

Naif A. Al-Gabri ◽

Ahmed A. El-Sayed ◽

...

Keyword(s):

Oxidative Stress ◽

Silver Nanoparticles ◽

Immune Suppression ◽

Aeromonas Hydrophila ◽

Oreochromis Niloticus ◽

Genotoxic Effects

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Cellular repair mechanisms triggered by exposure to silver nanoparticles and ionic silver in embryonic zebrafish cells

Environmental Science Nano ◽

10.1039/d1en00422k ◽

2021 ◽

Author(s):

Ana C. Quevedo ◽

Iseult Lynch ◽

Eugenia Valsami-Jones

Keyword(s):

Oxidative Stress ◽

Silver Nanoparticles ◽

Cell Death ◽

Zebrafish Embryo ◽

Genetic Damage ◽

Cellular Repair ◽

Embryo Cells ◽

Repair Mechanisms ◽

Toxicity Pathways ◽

Dynamic Interplay

The dynamic interplay between toxicity pathways (oxidative stress, calcium disturbances, genetic damage) caused by nanoparticles and the repair mechanisms of inhibition of cell division and induction of cell death is explored in zebrafish embryo cells.

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The oral administration of silver nanoparticles activates the kynurenine pathway in rat brain independently of oxidative stress

Chemico-Biological Interactions ◽

10.1016/j.cbi.2019.01.034 ◽

2019 ◽

Vol 302 ◽

pp. 22-27 ◽

Cited By ~ 4

Author(s):

Oluyomi Stephen Adeyemi ◽

Rhoda Ananu Uloko ◽

Oluwakemi Josephine Awakan ◽

Anne Adebukola Adeyanju ◽

David Adeiza Otohinoyi

Keyword(s):

Oxidative Stress ◽

Silver Nanoparticles ◽

Oral Administration ◽

Rat Brain ◽

Kynurenine Pathway

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Impact of silver nanoparticles exposure on neuro-behavior, hematology, and oxidative stress biomarkers of African catfish (Clarias gariepinus)

Aquaculture ◽

10.1016/j.aquaculture.2021.737082 ◽

2021 ◽

pp. 737082

Author(s):

Heba H. Mahboub ◽

Mariam H.E. Khedr ◽

Gehad E. Elshopakey ◽

Medhat S. Shakweer ◽

Dalia Ibrahim Mohamed ◽

...

Keyword(s):

Oxidative Stress ◽

Silver Nanoparticles ◽

Clarias Gariepinus ◽

African Catfish ◽

Oxidative Stress Biomarkers ◽

Stress Biomarkers ◽

And Oxidative Stress

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Role of Oxidative and Nitro-Oxidative Damage in Silver Nanoparticles Cytotoxic Effect against Human Pancreatic Ductal Adenocarcinoma Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/8251961 ◽

2018 ◽

Vol 2018 ◽

pp. 1-15 ◽

Cited By ~ 17

Author(s):

Ewelina Barcińska ◽

Justyna Wierzbicka ◽

Agata Zauszkiewicz-Pawlak ◽

Dagmara Jacewicz ◽

Aleksandra Dabrowska ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Pancreatic Cancer ◽

Silver Nanoparticles ◽

Oxidative Damage ◽

Pancreatic Ductal Adenocarcinoma ◽

Cytotoxic Effect ◽

Mrna Level ◽

Ductal Adenocarcinoma ◽

Adenocarcinoma Cells

Pancreatic ductal adenocarcinoma is one of the most aggressive human malignancies, where the 5-year survival rate is less than 4% worldwide. Successful treatment of pancreatic cancer is a challenge for today’s oncology. Several studies showed that increased levels of oxidative stress may cause cancer cells damage and death. Therefore, we hypothesized that oxidative as well as nitro-oxidative stress is one of the mechanisms inducing pancreatic cancer programmed cell death. We decided to use silver nanoparticles (AgNPs) (2.6 and 18 nm) as a key factor triggering the reactive oxygen species (ROS) and reactive nitrogen species (RNS) in pancreatic ductal adenocarcinoma cells (PANC-1). Previously, we have found that AgNPs induced PANC-1 cells death. Furthermore, it is known that AgNPs may induce an accumulation of ROS and alteration of antioxidant systems in different type of tumors, and they are indicated as promising agents for cancer therapy. Then, the aim of our study was to evaluate the implication of oxidative and nitro-oxidative stress in this cytotoxic effect of AgNPs against PANC-1 cells. We determined AgNP-induced increase of ROS level in PANC-1 cells and pancreatic noncancer cell (hTERT-HPNE) for comparison purposes. We found that the increase was lower in noncancer cells. Reduction of mitochondrial membrane potential and changes in the cell cycle were also observed. Additionally, we determined the increase in RNS level: nitric oxide (NO) and nitric dioxide (NO2) in PANC-1 cells, together with increase in family of nitric oxide synthases (iNOS, eNOS, and nNOS) at protein and mRNA level. Disturbance of antioxidant enzymes: superoxide dismutase (SOD1, SOD2, and SOD3), glutathione peroxidase (GPX-4) and catalase (CAT) were proved at protein and mRNA level. Moreover, we showed cells ultrastructural changes, characteristic for oxidative damage. Summarizing, oxidative and nitro-oxidative stress and mitochondrial disruption are implicated in AgNPs-mediated death in human pancreatic ductal adenocarcinoma cells.

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