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Copyright of Turkish Journal of Pharmaceutical Sciences is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Turkish Journal of Pharmaceutical Sciences is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose: The wide application of cupric oxide nanoparticles (copper (II) oxide, CuO-NPs) in various fields has increased exposure to the kind of active nanomaterials, which can cause negative effects on human and environment health. Although CuO-NPs were reported to be harmful to human, there is still a lack information related to their toxic potentials. In the present study, the toxic potentials of CuO-NPs were evaluated in the liver (HepG2 hepatocarcinoma) and intestine (Caco-2 colorectal adenocarcinoma) cells. Methods: After the characterization of particles, cellular uptake and morphological changes were determined. The potential of cytotoxic, genotoxic, oxidative and apoptotic damage was investigated with several in vitro assays. Results: The average size of the nanoparticles was 34.9 nm, about 2%-5% of the exposure dose was detected in the cells and mainly accumulated in different organelles, causing oxidative stress, cell damages, and death. The IC50 values were 10.90 and 10.04 µg/mL by MTT assay, and 12.19 and 12.06 µg/mL by neutral red uptake (NRU) assay, in HepG2 and Caco-2 cells respectively. Apoptosis assumes to the main cell death pathway; the apoptosis percentages were 52.9% in HepG2 and 45.5% in Caco-2 cells. Comet assay result shows that the highest exposure concentration (20 µg/mL) causes tail intensities about 9.6 and 41.8%, in HepG2 and Caco-2 cells, respectively. Conclusion: CuO-NPs were found to cause significant cytotoxicity, genotoxicity, and oxidative and apoptotic effects in both cell lines. Indeed, CuO-NPs could be dangerous to human health even if their toxic mechanisms should be elucidated with further studies. [ABSTRACT FROM AUTHOR]

Nickel oxide nanoparticles (NiO-NPs) are used in many industrial sectors including printing inks, ceramics and catalysts, and electrical and electronics industry because of their magnetic and optical properties. However, there has been still a serious lack of information about their toxicity at the cellular and molecular levels on nervous system. For that, we aimed to investigate the in vitro toxic potentials of NiO-NPs in neuronal (SH-SY5Y) cells. The particle characterisation, cellular uptake and morphological changes were determined using Transmission Electron Microscopy, dynamic light scattering and Inductively Coupled Plasma-Mass Spectrometry. Then, the cytotoxicity was evaluated by MTT and neutral red uptake assays, the genotoxicity by comet assay, the oxidative potentials by the determination of malondialdehyde, 8-hydroxy deoxyguanosine, protein carbonyl, and glutathione levels with Enzyme-Linked Immune Sorbent Assays, and the apoptotic potentials by Annexin V-FITC apoptosis detection assay with propidium iodide. According to the results, it was observed that NiO-NPs (15.0 nm ± 4.2–38.1 nm); (i) were taken up by the cells in concentration dependent manner, (ii) caused 50% inhibition in cell viability at ≥229.34 μg/mL, (iii) induced some morphological changes, (iv) induced dose-dependent DNA damage (3.2–11.0 fold) and apoptosis (80–99%), (v) significantly induced oxidative damage. In conclusion, our results support the hypothesis that NiO-NPs affect human health especially neuronal system negatively and should raise the concern about the safety associated with their applications in consumer products. [ABSTRACT FROM AUTHOR]

Worldwide researchers have rising concerns about magnesium-based materials, especially magnesium oxide (MgO) nanaoparticles, due to increasing usage as promising structural materials in various fields including cancer treatment. However, there is a serious lack of information about their toxicity at the cellular and molecular levels. In this study, the toxic potentials of MgO nanoparticles were investigated on liver (HepG2), kidney (NRK-52E), intestine (Caco-2), and lung (A549) cell lines. For the toxicological assessment, the following assays were used: the particle characterization by transmission electron microscopy, the determination of cellular uptake by inductively coupled plasma-mass spectrometry, MTT and neutral red uptake assays for cytotoxicity, comet assay for genotoxicity, and the determination of malondialdehyde (MDA), 8-hydroxydeoxyguanosine, protein carbonyl, and glutathione levels by enzyme-linked immune sorbent assays for the potential of oxidative damage and annexin V-fluorescein isothiocyanate (FITC) apoptosis detection assay with propidium iodide (PI) for apoptosis. Magnesium oxide nanoparticles were taken up by the cells depending on their concentration and agglomeration/aggregation potentials. Magnesium oxide nanoparticles induced DNA (≤14.27 fold) and oxidative damage. At a concentration of ≥323.39 µg/mL, MgO nanoparticles caused 50% inhibition in cell viability by 2 different cytotoxicity assays. The cell sensitivity to cytotoxic and genotoxic damage induced by MgO nanoparticles was ranked as HepG2 < A549 < Caco-2 < NRK-52E. Although it was observed that MgO nanoparticles induced apoptotic effects on the cells, apoptosis was not the main cell death. DNA damage, cell death, and oxidative damage effects of MgO nanoparticles should raise concern about the safety associated with their applications in consumer products. [ABSTRACT FROM AUTHOR]

The wide uses of zinc oxide nanoparticles (nano-ZnO) in industrial, cosmetics, medicine, food production and electronics associate with increase in occupational and public exposure. Although, toxicity of nano-ZnO has been extensively studied on many different cell types and animal systems, there is a significant lack of toxicological data focus on nephrotoxic potential of nano-ZnO. In this study, the cyto- and genotoxic effects of nano-ZnO on rat kidney epithelial cells (NRK-52E) were investigated by using different assays. Nano-ZnO (10–50 nm of sizes) were synthesized by sol–gel method. For the cytotoxic effect of nano-ZnO, mean of inhibition concentration (IC50) values in cell line was evaluated by MTT, Trypan Blue (TB) and Neutral Red Uptake (NRU) assays at 25.0–100.0 μg/mL exposure concentrations. Nano-ZnO showed cytotoxic activity by acting on different targets in renal cells, with IC50 ≥ 73.05 μg/mL. Comet assay was used to evaluate the genotoxicity of nano-ZnO (12.5–50.0 μg/mL). Nano-ZnO caused statistically significant DNA damage. Our results highlight the important risk of cyto- and genotoxic effects of nano-ZnO over the kidney. [ABSTRACT FROM PUBLISHER]

At first 28 orally administered drugs, considered to be potentially nitrosatable on the basis of their chemical structure, have been nitrosated with nitrite under simulated stomach conditions. A maximum daily dose of each drug was incubated with a nitrite concentration that can be found after a normal meal in the stomach at 37°C over 1 h. Reaction was started at pH 6.8–7.0 and stopped at pH 2.0, so we had the same pH change that occurs in the stomach. Secondly the genotoxic activities of drug-nitrite interaction products were tested by the umu-test with Salmonella typhimurium TA 1535/pSK1002 as tester strain in the presence and absence of metabolic activation. By the umu-test, among the nitrosation products of drugs examined 22 products showed genotoxicity at different levels. Other six products showed negative results by the umu-test. [ABSTRACT FROM AUTHOR]

Nanoparticles have been drawn attention in various fields ranging from medicine to industry because of their physicochemical properties and functions, which lead to extensive human exposure to nanoparticles. Bismuth (Bi)-based compounds have been commonly used in the industrial, cosmetic and medical applications. Although the toxicity of Bi-based compounds was studied for years, there is a serious lack of information concerning their toxicity and effects in the nanoscale on human health and environment. Therefore, we aimed to investigate the toxic effects of Bi (III) oxide (Bi 2 O 3 ) nanoparticles in liver (HepG2 hepatocarcinoma cell), kidney (NRK-52E kidney epithelial cell), intestine (Caco-2 colorectal adenocarcinoma cell), and lung (A549 lung carcinoma cell) cell cultures. Bi 2 O 3 nanoparticles (∼149.1 nm) were easily taken by all cells and showed cyto- and genotoxic effects. It was observed that the main cell death pathways were apoptosis in HepG2 and NRK-52E cells and necrosis in A549 and Caco-2 cells exposed to Bi 2 O 3 nanoparticles. Also, the glutathione (GSH), malondialdehyde (MDA), and 8-hydroxy deoxyguanine (8-OHdG) levels were significantly changed in HepG2, NRK-52E, and Caco-2 cells, except A549 cell. The present study is the first to evaluate the toxicity of Bi 2 O 3 nanoparticles in mammalian cells. Bi 2 O 3 nanoparticles should be thoroughly assessed for their potential hazardous effects to human health and the results should be supported with in vivo studies to fully understand the mechanism of their toxicity. [ABSTRACT FROM AUTHOR]