Comparative Study of Antidiabetic Activity and Oxidative Stress Induced by Zinc Oxide Nanoparticles and Zinc Sulfate in Diabetic Rats

In the current study, antidiabetic activity and toxic effects of zinc oxide nanoparticles (ZnO) were investigated in diabetic rats compared to zinc sulfate (ZnSO₄) with particular emphasis on oxidative stress parameters. One hundred and twenty male Wistar rats were divided into two healthy and diabetic groups, randomly. Each major group was further subdivided into five subgroups and then orally supplemented with various doses of ZnO (1, 3, and 10 mg/kg) and ZnSO₄ (30 mg/kg) for 56 consecutive days. ZnO showed greater antidiabetic activity compared to ZnSO₄ evidenced by improved glucose disposal, insulin levels, and zinc status. The altered activities of erythrocyte antioxidant enzymes as well as raised levels of lipid peroxidation and a marked reduction of total antioxidant capacity were observed in rats receiving ZnO. ZnO nanoparticles acted as a potent antidiabetic agent, however, severely elicited oxidative stress particularly at higher doses.     

Effect of Maternal Exposure to Zinc Oxide Nanoparticles on Reflexive Motor Behaviors in Mice Offspring

International Journal of Peptide Research and Therapeutics - Zinc oxide may influence central nervous system development in offspring but there is no information on role of the zinc oxide...     

Long-Term Toxicity of 213Bi-Labelled BSA in Mice

Background

Short-term toxicological evaluations of alpha-radioimmunotherapy have been reported in preclinical assays, particularly using bismuth-213 (²¹³Bi). Toxicity is greatly influenced not only by the pharmacokinetics and binding specificity of the vector but also by non-specific irradiation due to the circulating radiopharmaceutical in the blood. To assess this, an acute and chronic toxicity study was carried out in mice injected with ²¹³Bi-labelled Bovine Serum Albumin (²¹³Bi-BSA) as an example of a long-term circulating vector.

Method

Biodistribution of ²¹³Bi-BSA and ¹²⁵I-BSA were compared in order to evaluate ²¹³Bi uptake by healthy organs. The doses to organs for injected ²¹³Bi-BSA were calculated. Groups of nude mice were injected with 3.7, 7.4 and 11.1 MBq of ²¹³Bi-BSA and monitored for 385 days. Plasma parameters, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN) and creatinine, were measured and blood cell counts (white blood cells, platelets and red blood cells) were performed. Mouse organs were examined histologically at different time points.

Results

Haematological toxicity was transient and non-limiting for all evaluated injected activities. At the highest injected activity (11.1 MBq), mice died from liver and kidney failure (median survival of 189 days). This liver toxicity was identified by an increase in both ALT and AST and by histological examination. Mice injected with 7.4 MBq of ²¹³Bi-BSA (median survival of 324 days) had an increase in plasma BUN and creatinine due to impaired kidney function, confirmed by histological examination. Injection of 3.7 MBq of ²¹³Bi-BSA was safe, with no plasma enzyme modifications or histological abnormalities.

Conclusion

Haematological toxicity was not limiting in this study. Liver failure was observed at the highest injected activity (11.1 MBq), consistent with liver damage observed in human clinical trials. Intermediate injected activity (7.4 MBq) should be used with caution because of the risk of long-term toxicity to kidneys.     

Iron Oxide Nanoparticles Affects Behaviour and Monoamine Levels in Mice

Iron oxide (Fe₂O₃) nanoparticles (NPs) attract the attention of clinicians for its unique magnetic and paramagnetic properties, which are exclusively used in neurodiagnostics and therapeutics among the other biomedical applications. Despite numerous research findings has already proved neurotoxicity of Fe₂O₃-NPs, factors affecting neurobehaviour has not been elucidated. In this study, mice were exposed to Fe₂O₃-NPs (25 and 50 mg/kg body weight) by oral intubation daily for 30 days. It was observed that Fe₂O₃-NPs remarkably impair motor coordination and memory. In the treated brain regions, mitochondrial damage, depleted energy level and decreased ATPase (Mg²⁺, Ca²⁺ and Na⁺/K⁺) activities were observed. Disturbed ion homeostasis and axonal demyelination in the treated brain regions contributes to poor motor coordination. Increased intracellular calcium ([Ca²⁺]_i) and decreased expression of growth associated protein 43 (GAP43) impairs vesicular exocytosis could result in insufficient signal between neurons. In addition, levels of dopamine (DA), norepinephrine (NE) and epinephrine (EP) were found to be altered in the subjected brain regions in correspondence to the expression of monoamine oxidases (MAO). Along with all these factors, over expression of glial fibrillary acidic protein (GFAP) confirms the neuronal damage, suggesting the evidences for behavioural changes.

     

Zinc Oxide Nanoparticles Promote the Aggregation of Concanavalin A

The ability of nanoparticles to influence protein folding and aggregation is interesting, not only because of the potential beneficial applications, but also the potential risks to human health and the environment. The interactions of concanavalin A (Con A) with zinc oxide nanoparticles (ZnO-NPs) were investigated by using fluorescence, fourier transform infrared spectroscopy, circular dichroism (CD) and dynamic light scattering techniques. ANS fluorescence and CD spectroscopy authenticated the formation of molten globule state of Con A after its incubation with ZnO-NPs for 36 h. Further incubation of 48 h resulted in the aggregation of unadsorbed Con A, proved by decrease in ANS fluorescence while an increase in thioflavin T fluorescence, characteristic of an aggregates. Moreover, Fourier transform-infrared spectroscopy confirmed the aggregation of unadsorbed Con A. The aggregated products were negligible genotoxic as analyzed by pUC19 plasmid degradation and comet assay. It is clear that ZnO-NPs morphology affect unadsorbed proteins structure. A better understanding of these differences will be essential to engineer fully functional nanobioconjugates and NPs which do not damage the proteins present in the biological system.     

Acute Toxicity of Intravenously Administered Titanium Dioxide Nanoparticles in Mice

Background

With a wide range of applications, titanium dioxide (TiO₂) nanoparticles (NPs) are manufactured worldwide in large quantities. Recently, in the field of nanomedicine, intravenous injection of TiO₂ nanoparticulate carriers directly into the bloodstream has raised public concerns on their toxicity to humans.

Methods

In this study, mice were injected intravenously with a single dose of TiO₂ NPs at varying dose levels (0, 140, 300, 645, or 1387 mg/kg). Animal mortality, blood biochemistry, hematology, genotoxicity and histopathology were investigated 14 days after treatment.

Results

Death of mice in the highest dose (1387 mg/kg) group was observed at day two after TiO₂ NPs injection. At day 7, acute toxicity symptoms, such as decreased physical activity and decreased intake of food and water, were observed in the highest dose group. Hematological analysis and the micronucleus test showed no significant acute hematological or genetic toxicity except an increase in the white blood cell (WBC) count among mice 645 mg/kg dose group. However, the spleen of the mice showed significantly higher tissue weight/body weight (BW) coefficients, and lower liver and kidney coefficients in the TiO₂ NPs treated mice compared to control. The biochemical parameters and histological tissue sections indicated that TiO₂ NPs treatment could induce different degrees of damage in the brain, lung, spleen, liver and kidneys. However, no pathological effects were observed in the heart in TiO₂ NPs treated mice.

Conclusions

Intravenous injection of TiO₂ NPs at high doses in mice could cause acute toxicity effects in the brain, lung, spleen, liver, and kidney. No significant hematological or genetic toxicity was observed.     

Uptake and Toxicity of Copper Oxide Nanoparticles in C6 Glioma Cells

Copper oxide nanoparticles (CuO-NPs) are frequently used for many technical applications, but are also known for their cell toxic potential. In order to investigate a potential use of CuO-NPs as a therapeutic drug for glioma treatment, we have investigated the consequences of an application of CuO-NPs on the cellular copper content and cell viability of C6 glioma cells. CuO-NPs were synthesized by a wet-chemical method and were coated with dimercaptosuccinic acid and bovine serum albumin to improve colloidal stability in physiological media. Application of these protein-coated nanoparticles (pCuO-NPs) to C6 cells caused a strong time-, concentration- and temperature-dependent copper accumulation and severe cell death. The observed loss in cellular MTT-reduction capacity, the loss in cellular LDH activity and the increase in the number of propidium iodide-positive cells correlated well with the specific cellular copper content. C6 glioma cells were less vulnerable to pCuO-NPs compared to primary astrocytes and toxicity of pCuO-NPs to C6 cells was only observed for incubation conditions that increased specific cellular copper contents above 20 nmol copper per mg protein. Both cellular copper accumulation as well as the pCuO-NP-induced toxicity in C6 cells were prevented by application of copper chelators, but not by endocytosis inhibitors, suggesting that liberation of copper ions from the pCuO-NPs is the first step leading to the observed toxicity of pCuO-NP-treated glioma cells.     

Nitric Oxide Is Associated with Long-Term Zinc Tolerance in Solanum nigrum

Nitric oxide (NO) has been identified as a signal molecule that interplays with reactive oxygen species in response to heavy metal stresses. Roles of NO in regulating cadmium toxicity and iron deficiency have been proposed; however, the function of NO in zinc (Zn) tolerance in plants remains unclear. Here, we investigated NO accumulation and its role in plant Zn tolerance. Zn-induced NO production promoted an increase in reactive oxygen species accumulation in Solanum nigrum roots by modulating the expression and activity of antioxidative enzymes. Subsequently, programmed cell death (PCD) was observed in primary root tips. Inhibiting NO accumulation by 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (a specific NO scavenger) or N^G-nitro-l-arginine-methyl ester (a NO synthase inhibitor) prevented the increase of superoxide radical and hydrogen peroxide as well as the subsequent cell death in the root tips, supporting the role of NO in Zn-induced PCD in the root tips. Zn-induced NO production affected the length of primary roots, the number of lateral roots, and root hair growth and thereby modulated root system architecture and activity. Investigation of metal contents in Zn-treated roots suggests that NO is required for metal (especially iron) uptake and homeostasis in plants exposed to excess Zn. Taken together, our results indicate that NO production and the subsequent PCD in root tips exposed to excess Zn are favorable for the S. nigrum seedling response to long-term Zn toxicity by modulating root system architecture and subsequent adaptation to Zn stress.Heavy metal contamination is a serious problem for the environment. Some metallic elements, such as zinc (Zn), are essential micronutrients and play a role as enzyme cofactors in many metabolic reactions. However, uptake of high concentrations of Zn is found to be toxic to plant growth and development. High concentrations of Zn (260–16,000 mg kg⁻¹) have been found in the soil near smelting sites (Bi et al., 2006), and Zn contamination has been of increasing concern in these regions due to its threat to agriculture and human health (Bi et al., 2006).Zn homeostasis is a tightly regulated process because Zn can be both essential and deleterious to plants depending on its concentration. The effects of Zn on plants have been widely reported (Broadley et al., 2007; Wang et al., 2009), including tolerance to Zn accumulation and Zn deficiency as well as the protective effects of Zn in plants. Zn is closely involved in protein synthesis and nitrogen metabolism; the growth of Zn-deficient plants is markedly inhibited. Zn is also a constituent of copper/zinc superoxide dismutase (Cu/Zn SOD). Zn deficiency reduces antioxidative enzyme activity and thereby results in reactive oxygen species (ROS) accumulation and oxidative damage (Sharma et al., 2004). Tolerance to Zn accumulation in plants is a complex phenomenon. Aside from Zn deficiency, excess Zn can also inhibit plant growth and development by disequilibrating the uptake and redistribution of mineral nutrition and by disturbing the antioxidant defense system and metabolic processes such as photosynthesis, transpiration, and antioxidative enzyme activity. Recent studies have shown that Zn toxicity affects the activity of antioxidative enzymes, such as SOD, catalase (CAT), and ascorbate peroxidase (APX), in plants (Wójcik et al., 2006; Tewari et al., 2008). The mechanisms of Zn toxicity are not fully understood; however, they may involve competition for catalytic sites or for transporter proteins (González-Guerrero et al., 2005). Zn toxicity also inhibits the uptake of other nutrient elements, such as iron (Fe). Deficiency of these elements can lead to ROS accumulation and oxidative stress (Bonnet et al., 2000). Excess Zn may bind to proteins and lead to the displacement of other ions, such as Fe²⁺, from protein-binding sites. Plants exposed to excess Zn become Fe deficient (Wintz et al., 2003). However, the effects of Zn stress on root system development have not been elucidated.Nitric oxide (NO) is a free radical gas that has emerged as an important signaling molecule in plants (Neill et al., 2002). NO accumulation in roots mediates auxin-induced lateral root formation (Correa-Aragunde et al., 2004), adventitious root growth (Tewari et al., 2008), and root hair development (Lombardo et al., 2006). Graziano and Lamattina (2007) have reported that root hair proliferation induced by Fe deficiency is involved in NO accumulation in tobacco (Nicotiana tabacum). It has also been indicated that NO protects plant cells against oxidative stress by reducing ROS accumulation (Wink and Mitchell, 1998; Xu et al., 2010). NO enhances the tolerance of plants to heavy metal stresses (Yang et al., 2006; Sun et al., 2007; Zhang et al., 2008; Xu et al., 2009). However, very little is known about the level of Zn-mediated NO accumulation in plants and the physiological and molecular mechanisms of the effects of NO on tolerance to Zn toxicity.Programmed cell death (PCD) is an active process of cellular suicide that is essential for development and stress responses in plants. Diverse abiotic stresses, such as salt, drought, nutrient deficiency, and cadmium (Cd) toxicity, can induce PCD in plants. Salt stress has been reported to induce PCD in root apical meristem cells (Huh et al., 2002). Subbaiah and Sachs (2003) have demonstrated that flooding stress induces PCD-like root tip death in maize (Zea mays) and pea (Pisum sativum) plants. Duan et al. (2010) have shown that drought induces PCD in Arabidopsis (Arabidopsis thaliana) root tips. De Michele et al. (2009) have reported that Arabidopsis cell suspension cultures undergo PCD when exposed to Cd stress and that NO is involved in this process. Many studies have indicated that PCD plays a role in the developmental plasticity of plant architecture (Duan et al., 2010). Excess Zn-induced growth inhibition and root death have been found in various plant species (Lingua et al., 2008; Ozdener and Aydin, 2010). However, whether Zn-induced root death occurs through PCD and its underlying mechanisms are poorly understood.In this study, we used a Zn-hyperaccumulator, Solanum nigrum, to study the effects of excess Zn on root system architecture and the roles of NO and ROS in these effects. S. nigrum is known to hyperaccumulate Zn and Cd in natural soil or in soils contaminated with Zn or Cd. In recent years, physiological characteristics of S. nigrum under Zn or Cd stress have been reported (Wei et al., 2004; Sun et al., 2007; Marques et al., 2008; Xu et al., 2009). The aim of this work was to study plant tolerance to excess Zn and the function of NO produced in Zn-treated plants. Our findings support the model in which NO contributes to rapid ROS accumulation and subsequent PCD in root tips in response to heavy metal stresses; our results also indicate that NO is an important regulator of Zn-modulated root system architecture. Potential mechanisms involved in this process are discussed.     

Effect of the Zinc Oxide Nanoparticles and Thiamine for the Management of Diabetes in Alloxan-Induced Mice: a Stereological and Biochemical Study

This research was carried out to evaluate the antidiabetic effects of zinc oxide nanoparticles (ZnO NPs) and thiamine following experimental diabetes. Fifty-six 6-week-old female mice were used and divided into seven groups of eight animals. Diabetes was induced in fasted mice by using intraperitoneal (IP) injection of alloxan (180 mg/kg). Groups included (I) non-diabetic control, (II) thiamine (30 mg/l, IP), (III) alloxan-induced diabetic mice, (IV) diabetes + ZnO NPs (0.1 mg/kg IP), (V) diabetes + ZnO NPs (0.5 mg/kg IP), (VI) diabetes + ZnO NPs (0.1 mg/kg IP) + thiamine (30 mg/l, IP), and (VII) diabetes + ZnO NPs (0.5 mg/kg IP) + thiamine (30 mg/l, IP). Coincident with pancreas recovery, in diabetic treated mice (groups IV to VII), the mean islet volume, islets per square micrometer, and volume density of the pancreas had increased than in alloxan-induced diabetic mice. ZnO NPs and thiamine induced a decreasing blood glucose, lower serum triglyceride (TG), LDL, and total cholesterol (TC) levels in alloxan-induced diabetic mice treated with ZnO NPs and thiamine, simultaneously increasing HDL as well. In conclusion, ZnO NPs and thiamine are potent antidiabetic factors, and that, these compound supplementation possesses hypoglycemic properties and have effect on serum lipid parameters in diabetes mice.     

Acute Toxicity of Amorphous Silica Nanoparticles in Intravenously Exposed ICR Mice

This study aimed to evaluate the acute toxicity of intravenously administrated amorphous silica nanoparticles (SNPs) in mice. The lethal dose, 50 (LD₅₀), of intravenously administrated SNPs was calculated in mice using Dixon''s up-and-down method (262.45±33.78 mg/kg). The acute toxicity was evaluated at 14 d after intravenous injection of SNPs at 29.5, 103.5 and 177.5 mg/kg in mice. A silicon content analysis using ICP-OES found that SNPs mainly distributed in the resident macrophages of the liver (10.24%ID/g), spleen (34.78%ID/g) and lung (1.96%ID/g). TEM imaging showed only a small amount in the hepatocytes of the liver and in the capillary endothelial cells of the lung and kidney. The levels of serum LDH, AST and ALT were all elevated in the SNP treated groups. A histological examination showed lymphocytic infiltration, granuloma formation, and hydropic degeneration in liver hepatocytes; megakaryocyte hyperplasia in the spleen; and pneumonemia and pulmonary interstitial thickening in the lung of the SNP treated groups. A CD68 immunohistochemistry stain indicated SNPs induced macrophage proliferation in the liver and spleen. The results suggest injuries induced by the SNPs in the liver, spleen and lungs. Mononuclear phagocytic cells played an important role in the injury process.     

Assessing the Potential Role of Zinc Oxide Nanoparticles for Mitigating Cadmium Toxicity in Capsicum annuum L. Under In Vitro Conditions

Journal of Plant Growth Regulation - The application of metal and metal-oxide nanoparticles (NPs) in agriculture to mitigate the abiotic environmental stress factors and pollutants has gained...     

Serum Calcium Response Following Oral Zinc Oxide Administrations in Dairy Cows

Six non-pregnant cows were allocated into 3 groups. Group 1 comprised a pair of lactating cows, whereas groups 2 and 3 each comprised a pair of non-lactating cows. The cows in groups 1 and 2 were dosed intraruminally by stomach tube with zinc oxide at 120 mg Zn per kg of bodyweight at weekly intervals for a period of 33 days. Each cow received a total of 4 doses of zinc oxide. Group 3 served as non-treated control group. Blood samples were collected from all 6 cows daily. Serum was analysed for concentration of calcium. Within 12–24 h of each zinc oxide administration the serum calcium of the lactating cows dropped dramatically indicating the existence of an antagonistic effect between Zn and Ca. The first Zn induced hypocalcaemic episode in the lactating cows was followed by a rise in serum calcium to a level above the pre-dosing level and above the mean value of the control group. The depth of the hypocalcaemic response decreased with the number of zinc oxide dosings. This effect was explained as a response from the stimulation of the calcium homeostatic mechanisms. In the Zn dosed non-lactating cows responses were similar but less clear. The perspective of these findings is discussed in relation to resistance towards parturient hypocalcaemia.     

Effects of Dietary Zinc Oxide Nanoparticles on Growth Performance and Antioxidative Status in Broilers

Broilers in four groups were fed a basal diet supplemented with 60 mg/kg zinc oxide (60-ZnO; control), or 20, 60, or 100 mg/kg ZnO nanoparticles (20-, 60-, and 100-nano-ZnO, respectively). Compared with the controls, after 14 days, birds in the 20- and 60-nano-ZnO groups had significantly greater weight gains and better feed conversion ratios. However, the body weight of birds in the 100-nano-ZnO group was dramatically reduced after 28 days. Relative to the control group, the total antioxidant capability (T-AOC) in serum and liver tissue was significantly higher in the 20-nano-ZnO group at all time points and also significantly higher in the 60- and 100-nano-ZnO groups in serum on days 28 and 35 and in liver tissues on days 21 and 28. Compared with the controls, the activity of copper-zinc superoxide dismutase (Cu-Zn-SOD) was significantly greater in the 60- and 100-nano-ZnO groups in serum on days 28 and 35 and in liver tissues after 21 days. Catalase activity in serum samples was significantly higher in the 20- and 60-nano-ZnO groups relative to the control and 100-nano-ZnO birds, but catalase activity in liver tissue was not affected by different nano-ZnO levels. Malondialdehyde content in serum and liver tissues was significantly reduced in the 20-, 60-, and 100-nano-ZnO groups compared with that in the control group at all time points except day 42. Taken together, our data indicate that appropriate concentration of dietary ZnO nanoparticles improves growth performance and antioxidative capabilities in broilers, and 20 mg/kg nano-ZnO is the optimal concentration.     

Long-Term Oral Administration of Hop Flower Extracts Mitigates Alzheimer Phenotypes in Mice

Coincident with the expanding population of aged people, the incidence of Alzheimer disease (AD) is rapidly increasing in most advanced countries. At present, no effective prophylactics are available. Among several pathological mechanisms proposed for AD, the “amyloid hypothesis” has been most widely accepted, in which accumulation or deposition of Aβ is considered to be the initial event. Thus, prevention of Aβ production would be an ideal strategy for the treatment or prevention of AD. Aβ is produced via the proteolytic cleavage of its precursor protein, APP (amyloid precursor protein), by two different enzymes, β and γ-secretases. Indeed, inhibitors against either or both enzymes have been developed and tested for clinical efficacy. Based on the “amyloid hypothesis”, we developed a luciferase-based screening method to monitor γ-secretase activity, screened more than 1,600 plant extracts, most of which have long been used in Chinese medicine, and observed that Hop extracts significantly inhibit Aβ production in cultured cells. A major component of the inhibitory activity was purified, and its chemical identity was determined by NMR to be Garcinielliptone HC. In vivo, oral administration of Hop extracts to AD model mice decreased Aβ depositions in the cerebral cortex of the parietal lobe, hippocampus, and artery walls (amyloid angiopathy) in the brains. In a Morris water maze test, AD model mice that had daily consumed Hop extracts in their drinking water showed significant mitigation of memory impairment at ages of 9 and 12 months. Moreover, in the open field test oral administration of Hop extracts also prevented an emotional disturbance that appeared in the AD mice at 18 months. Despite lifelong consumption of Hop extracts, no deleterious side effects were observed at any age. These results support the “amyloid hypothesis”, and indicate that Hop extract is a promising candidate for an effective prophylactic for AD.     

Uptake of Intact Copper Oxide Nanoparticles Causes Acute Toxicity in Cultured Glial Cells

Copper oxide nanoparticles (CuO-NPs) dispersions are known for their high cell toxic potential but contaminating copper ions in such dispersions are a major hurdle in the investigation of specific nanoparticle-mediated toxicity. In order to distinguish between the adverse effects exhibited by CuO-NPs and/or by contaminating ionic copper, the membrane-impermeable copper chelator bathocuproine disulfonate (BCS) was added in a low molar ratio (20% of the total copper applied) in order to chelate the copper ions that had been released extracellularly from the CuO-NPs before or during the incubation. Physicochemical characterization of synthesized CuO-NPs revealed that the presence of this low concentration of BCS did not alter the size or zeta potential of the CuO-NPs. Application of CuO-NPs to C6 glioma cells and primary astrocytes induced a concentration- and temperature-dependent copper accumulation which was accompanied by a severe loss in cell viability. The adverse consequences of the CuO-NP application were not affected by the presence of 20% BCS, while the copper accumulation and cell toxicity observed after application of ionic copper were significantly lowered in the presence of BCS. These results demonstrate that for the experimental conditions applied the adverse consequences of an exposure of cultured glial cells to dispersions of CuO-NPs are mediated by accumulated NPs and not caused by the uptake of contaminating copper ions.

     

Impact of Zinc Oxide Nanoparticles on Pomegranate Growth under In Vitro Conditions

Russian Journal of Plant Physiology - Nanotechnology is a promising tool to achieve great advancements in the global agricultural systems and food production. The widespread application of...     

Toxicity of Copper Oxide (CuO) Nanoparticles on Human Blood Lymphocytes

CuO nanoparticles (CuO-NPs) serve several important functions in human life, particularly in the fields of medicine, engineering, and technology. These nanoparticles have been utilized as catalysts, semiconductors, sensors, gaseous and solid ceramic pigments, and magnet rotatable devices. Further use for CuO-NPs has been employed in the pharmaceutical industry especially in the production of anti-microbial fabric treatments or prevention of infections caused by Escherichia coli and methicillin-resistant Staphylococcus aureus. Two key potential routes of exposure to CuO-NPs exist through inhalation and skin exposure. Toxicity of these nanoparticles has been reported in various studies; however, no study as of yet has investigated the complete cellular mechanisms involved in CuO-NPs toxicity on human cells. The aim of this study was to determine the cytotoxicity of CuO-NPs on human blood lymphocytes. Blood lymphocytes were obtained from healthy male subjects through the use of Ficoll polysaccharide subsequently by gradient centrifugation. The following parameters were assayed in blood lymphocytes after a 6-h incubation with different concentrations of CuO-NPs: cell viability, reactive oxygen species (ROS) formation, lipid peroxidation, cellular glutathione levels, and mitochondrial and lysosomal damage. Our results demonstrate that CuO-NPs, in particular, decreased cell viability in a concentration-dependent manner and the IC50 determined was 382 μM. CuO-NP cytotoxicity was associated with significant increase at intracellular ROS level and loss of mitochondrial membrane potential and lysosomal membrane leakiness. Hence, CuO-NPs are shown to effectively induce oxidative stress in addition to inflict damage on mitochondria and lysosomes in human blood lymphocytes.     

Evaluation of Induced Apoptosis by Biosynthesized Zinc Oxide Nanoparticles in MCF-7 Breast Cancer Cells Using Bak1 and Bclx Expression

Doklady Biochemistry and Biophysics - Zinc oxide nanoparticles (ZnO NPs) have peaked interests in many researches in these recent years due to their advantageous application in modern health care...     

Cerium Oxide Nanoparticles Attenuate Oxidative Stress and Inflammation in the Liver of Diethylnitrosamine-Treated Mice

Biological Trace Element Research - The catalytic activity of cerium oxide nanoparticles (CeO2NPs) is responsible for its application as an antitumor agent. This activity may be due to its ability...