Showing papers on "Toxicity published in 2013"
TL;DR: Recent investigations into the basis of CNT toxicity carried out by the team and by other laboratories are highlighted, highlighting several important factors that explain the disparities in the experimental results of nanotoxicity, such as impurities, amorphous carbon, surface charge, shape, length, agglomeration, and layer numbers.
Abstract: Because of their unique physical, chemical, electrical, and mechanical properties, carbon nanotubes (CNTs) have attracted a great deal of research interest and have many potential applications. As large-scale production and application of CNTs increases, the general population is more likely to be exposed to CNTs either directly or indirectly, which has prompted considerable attention about human health and safety issues related to CNTs. Although considerable experimental data related to CNT toxicity at the molecular, cellular, and whole animal levels have been published, the results are often conflicting. Therefore, a systematic understanding of CNT toxicity is needed but has not yet been developed. In this Account, we highlight recent investigations into the basis of CNT toxicity carried out by our team and by other laboratories. We focus on several important factors that explain the disparities in the experimental results of nanotoxicity, such as impurities, amorphous carbon, surface charge, shape, length, agglomeration, and layer numbers. The exposure routes, including inhalation, intravenous injection, or dermal or oral exposure, can also influence the in vivo behavior and fate of CNTs. The underlying mechanisms of CNT toxicity include oxidative stress, inflammatory responses, malignant transformation, DNA damage and mutation (errors in chromosome number as well as disruption of the mitotic spindle), the formation of granulomas, and interstitial fibrosis. These findings provide useful insights for de novo design and safe application of carbon nanotubes and their risk assessment to human health. To obtain reproducible and accurate results, researchers must establish standards and reliable detection methods, use standard CNT samples as a reference control, and study the impact of various factors systematically. In addition, researchers need to examine multiple types of CNTs, different cell lines and animal species, multidimensional evaluation methods, and exposure conditions. To make results comparable among different institutions and countries, researchers need to standardize choices in toxicity testing such as that of cell line, animal species, and exposure conditions. The knowledge presented here should lead to a better understanding of the key factors that can influence CNT toxicity so that their unwanted toxicity might be avoided.
617 citations
TL;DR: In-patient proof is provided that the observed "on-target" toxicity is antigen-directed and can be prevented by blocking antigenic sites in off-tumor organs and allowing higher T cell doses.
581 citations
TL;DR: This review identifies four key areas that explain the mechanism of the cytotoxicity of STZ in mammalian cell lines, investigates the practical aspects of using STz in experimental animals and investigates the potential risks of its exposure to human health.
Abstract: Streptozotocin (STZ) (2-deoxy-2-({[methyl(nitroso)amino]carbonyl}amino)-β-D-glucopyranose) is a naturally occurring diabetogenic compound, produced by the soil bacterium streptomyces achromogenes, that exhibits broad spectrum of antibacterial properties. Streptozotocin functions as a DNA synthesis inhibitor in both bacterial and mammalian cells. In mammalian cells, the actual mechanism and metabolic targets of STZ toxicity that results in cell death is not known. This review identifies four key areas that explain the mechanism of the cytotoxicity of STZ in mammalian cell lines, investigates the practical aspects of using STZ in experimental animals and the potential risks of its exposure to human health.
314 citations
TL;DR: The nano-ZnO was found to exert a dose-dependent toxicity to zebrafish embryos and larvae, reducing the hatching rate and inducing malformation and the acute toxicity toZn(2+) embryos was greater than that of the Zn( 2+) solution.
289 citations
TL;DR: CuO-nano toxicity is predominantly mediated by intracellular uptake and subsequent release of copper ions, whereas no toxicity is observed for Ag- nano due to low release of silver ions within short time periods.
Abstract: An increased understanding of nanoparticle toxicity and its impact on human health is essential to enable a safe use of nanoparticles in our society. The aim of this study is to investigate the role of a Trojan horse type mechanism for the toxicity of Ag-nano and CuO-nano particles and their corresponding metal ionic species (using CuCl2 and AgNO3), i.e., the importance of the solid particle to mediate cellular uptake and subsequent release of toxic species inside the cell. The human lung cell lines A549 and BEAS-2B are used and cell death/membrane integrity and DNA damage are investigated by means of trypan blue staining and the comet assay, respectively. Chemical analysis of the cellular dose of copper and silver is performed using atomic absorption spectroscopy. Furthermore, transmission electron microscopy, laser scanning confocal microscopy, and confocal Raman microscopy are employed to study cellular uptake and particle-cell interactions. The results confirm a high uptake of CuO-nano and Ag-nano compared to no, or low, uptake of the soluble salts. CuO-nano induces both cell death and DNA damage whereas CuCl2 induces no toxicity. The opposite is observed for silver, where Ag-nano does not cause any toxicity, whereas AgNO3 induces a high level of cell death. In conclusion: CuO-nano toxicity is predominantly mediated by intracellular uptake and subsequent release of copper ions, whereas no toxicity is observed for Ag-nano due to low release of silver ions within short time periods.
287 citations
TL;DR: The mechanism of degradation and excretion of the nanoMOFs has been evidenced and shows that the nanoparticles are rapidly sequestered by the liver and spleen, then further biodegraded and directly eliminated in urine or feces without metabolization and substantial toxicity.
Abstract: In vivo acute toxicity of high doses of nanoparticles of three different porous iron(III) carboxylate Metal–Organic Frameworks (nanoMOFs) was intravenously investigated in rats by evaluating their distribution, metabolism and excretion All studied parameters (serum, enzymatic, histological, etc) are in agreement with a low acute toxicity The mechanism of degradation and excretion of the nanoMOFs has been evidenced and shows that the nanoparticles are rapidly sequestered by the liver and spleen, then further biodegraded and directly eliminated in urine or feces without metabolization and substantial toxicity
279 citations
TL;DR: There is a trend for a clinically meaningful reduction in late G2+ GI toxicity with IMRT, and the occurrence of acute GI toxicity and large (>15%) volumes of rectum >70 Gy are associated with late rectal toxicity.
Abstract: Purpose To give a preliminary report of clinical and treatment factors associated with toxicity in men receiving high-dose radiation therapy (RT) on a phase 3 dose-escalation trial. Methods and Materials The trial was initiated with 3-dimensional conformal RT (3D-CRT) and amended after 1 year to allow intensity modulated RT (IMRT). Patients treated with 3D-CRT received 55.8 Gy to a planning target volume that included the prostate and seminal vesicles, then 23.4 Gy to prostate only. The IMRT patients were treated to the prostate and proximal seminal vesicles to 79.2 Gy. Common Toxicity Criteria, version 2.0, and Radiation Therapy Oncology Group/European Organization for Research and Treatment of Cancer late morbidity scores were used for acute and late effects. Results Of 763 patients randomized to the 79.2-Gy arm of Radiation Therapy Oncology Group 0126 protocol, 748 were eligible and evaluable: 491 and 257 were treated with 3D-CRT and IMRT, respectively. For both bladder and rectum, the volumes receiving 65, 70, and 75 Gy were significantly lower with IMRT (all P P =.039). On multivariate analysis, IMRT showed a 26% reduction in G2+ late GI toxicity ( P =.099). Acute G2+ toxicity was associated with late G3+ toxicity ( P =.005). With dose–volume histogram data in the multivariate analysis, RT modality was not significant, whereas white race ( P =.001) and rectal V70 ≥15% were associated with G2+ rectal toxicity ( P =.034). Conclusions Intensity modulated RT is associated with a significant reduction in acute G2+ GI/GU toxicity. There is a trend for a clinically meaningful reduction in late G2+ GI toxicity with IMRT. The occurrence of acute GI toxicity and large (>15%) volumes of rectum >70 Gy are associated with late rectal toxicity.
255 citations
TL;DR: The significance of hippurate excretion with respect to disease states including obesity, diabetes, gastrointestinal diseases, impaired renal function, psychological disorders and autism, as well as toxicity and parasitic infection are considered.
Abstract: Hippurate, the glycine conjugate of benzoic acid, is a normal constituent of the endogenous urinary metabolite profile and has long been associated with the microbial degradation of certain dietary components, hepatic function and toluene exposure, and is also commonly used as a measure of renal clearance Here we discuss the potential relevance of hippurate excretion with regard to normal endogenous metabolism and trends in excretion relating to gender, age, and the intestinal microbiota Additionally, the significance of hippurate excretion with respect to disease states including obesity, diabetes, gastrointestinal diseases, impaired renal function, psychological disorders and autism, as well as toxicity and parasitic infection, are considered
251 citations
TL;DR: Several leading paradigms in the field, such as on the roles of Na+ influx and tissue accumulation or the cytosolic K+/Na+ ratio in the development of toxicity, are currently insufficiently substantiated and require a new, critical approach.
Abstract: Sodium (Na+) is one of the most intensely researched ions in plant biology and has attained a reputation for its toxic qualities. Following the principle of Theophrastus Bombastus von Hohenheim (Paracelsus), Na+ is, however, beneficial to many species at lower levels of supply, and in some, such as certain C4 species, indeed essential. Here, we review the ion’s divergent roles as a nutrient and toxicant, focusing on growth responses, membrane transport, stomatal function, and paradigms of ion accumulation and sequestration. We examine connections between the nutritional and toxic roles throughout, and place special emphasis on the relationship of Na+ to plant potassium (K+) relations and homeostasis. Our review investigates intriguing connections and disconnections between Na+ nutrition and toxicity, and concludes that several leading paradigms in the field, such as on the roles of Na+ influx and tissue accumulation or the cytosolic K+/Na+ ratio in the development of toxicity, are currently insufficiently substantiated and require a new, critical approach.
248 citations
TL;DR: For nanosilver the most sensitive parameters for potential adverse responses were effects on the immune system and the most striking toxic effect was the almost complete suppression of the natural killer cell activity in the spleen at high doses.
245 citations
TL;DR: This model better detected in vivo drug-induced toxicity, including species-specific drug effects, when compared to monolayer hepatocyte cultures, and underline the importance of more complex and long lasting in vitro cell culture models that contain all liver cell types and allow repeated drug-treating for detection of in vivo-relevant adverse drug effects.
TL;DR: It could be concluded that spirulina administration able to minimize the toxic effects of deltamethrin by its free radical-scavenging and potent antioxidant activity.
Abstract: Deltamethrin is a broad-spectrum synthetic pyrethroid insecticide and acaricide widely used for agricultural and veterinary purposes. However, its human and animal exposure leads to hepatonephrotoxicity. Therefore, the present study was undertaken to examine the hepatonephroprotective and antioxidant potential of Spirulina platensis against deltamethrin toxicity in male Wistar albino rats. Deltamethrin treated animals revealed a significant increase in serum biochemical parameters as well as hepatic and renal lipid peroxidation but caused an inhibition in antioxidant biomarkers. Spirulina normalized the elevated serum levels of AST, ALT, APL, uric acid, urea and creatinine. Furthermore, it reduced deltamethrin-induced lipid peroxidation and oxidative stress in a dose dependent manner. Therefore, it could be concluded that spirulina administration able to minimize the toxic effects of deltamethrin by its free radical-scavenging and potent antioxidant activity.
TL;DR: It is concluded that ZnO-np leads to cell death through autophagic vacuole accumulation and mitochondria damage in normal skin cells via ROS induction and the results highlight and need for careful regulation of Zn O-np production and use.
TL;DR: Investigation of the effects of water chemistry on the toxicity evaluation of nano-ZnO and its toxicity to Escherichia coli showed that increasing solution pH, HPO(4)(2), and DOM reduced the concentration of free Zn(2+) released from nano- ZnNO, and thus lowered the toxicity of nano’s toxicity.
TL;DR: Hx prevented heme-iron loading in the cardiovascular system, thus limiting the production of reactive oxygen species, the induction of adhesion molecules, and the oxidative inactivation of nitric oxide synthase/nitric oxide, and promoted heme recovery and detoxification by the liver mainly through the inductionof heme oxygenase activity.
Abstract: Background—Hemolytic diseases are characterized by enhanced intravascular hemolysis resulting in heme-catalyzed reactive oxygen species generation, which leads to endothelial dysfunction and oxidative damage. Hemopexin (Hx) is a plasma heme scavenger able to prevent endothelial damage and tissue congestion in a model of heme overload. Here, we tested whether Hx could be used as a therapeutic tool to counteract heme toxic effects on the cardiovascular system in hemolytic diseases. Methods and Results—By using a model of heme overload in Hx-null mice, we demonstrated that heme excess in plasma, if not bound to Hx, promoted the production of reactive oxygen species and the induction of adhesion molecules and caused the reduction of nitric oxide availability. Then, we used β-thalassemia and sickle cell disease mice as models of hemolytic diseases to evaluate the efficacy of an Hx-based therapy in the treatment of vascular dysfunction related to heme overload. Our data demonstrated that Hx prevented heme-iron ...
TL;DR: The results show that TiO2 NPs induce different toxic effects on young and adult rats, and suggest that different ages may require different biomarkers for identifying and monitoring oral toxicity of nanoparticles.
Abstract: Titanium dioxide nanoparticles (TiO2 NPs) have potential applications as food additives, but concerns persist about their safety. Children are identified as having the highest exposure and may face the greatest health risks. However, the toxicological sensitivity of TiO2 NPs in different ages is not clear. Here, a comparative toxicity study of TiO2 NPs in 3-week (youth) and 8-week (adult) old Sprague-Dawley rats is reported following oral exposure at doses of 0, 10, 50, 200 mg kg(-1) body weight per day for 30 days. The organ mass and histology, blood biochemistry and redox state, intestinal function, and biodistribution of NPs are characterized. The results show that TiO2 NPs induce different toxic effects on young and adult rats. The liver edema, heart injuries and non-allergic mast cell activation in stomach tissues are found in young rats. On the other hand, only slight injury in the liver and kidney and decreased intestinal permeability and molybdenum contents are found in adult rats. Furthermore, TiO2 NP exposure can provoke reductive stress (i.e., increased reduced glutathione (GSH)/oxidized glutathione (GSSG) ratios) in plasmas through enhancing the glucose and GSH levels in young rats or reducing the glutathione peroxidase (GSH-Px) acitivity and GSSG levels in adult rats. These results suggest that different ages may require different biomarkers for identifying and monitoring oral toxicity of nanoparticles.
TL;DR: In this paper, the authors investigated the role of hydrogen sulfide (H2S) in Al toxicity in barley (Hordeum vulgare L) seedlings and found that H2S had significant rescue effects on Al-induced inhibition of root elongation which was correlated well with the decrease of Al accumulation in seedlings.
Abstract: Aluminum (Al) toxicity is one of the major factors that limit plant growth. Low concentration of hydrogen sulfide (H2S) has been proven to function in physiological responses to various stresses. The objective of this study is to investigate the possible role of H2S in Al toxicity in barley (Hordeum vulgare L) seedlings. Barley seedlings pre-treated with sodium hydrosulfide (NaHS), a H2S donor, and subsequently exposed to Al treatment were studied for their effects on root elongation, Al accumulation in seedlings, Al-induced citrate secretion and oxidative stress, and plasma membrane (PM) H+-ATPase expression. Our results showed that H2S had significant rescue effects on Al-induced inhibition of root elongation which was correlated well with the decrease of Al accumulation in seedlings. Meanwhile, Al-induced citrate secretion was also significantly enhanced by NaHS pretreatment. Al-induced oxidative stress as indicated by lipid peroxidation and reactive oxygen species burst was alleviated by H2S through the activation of the antioxidant system. Moreover, Al-induced reduction in PM H+-ATPase expression was reversed by exogenous NaHS. Altogether, our results suggest H2S plays an ameliorative role in protecting plants against Al toxicity by inducing the activities of antioxidant enzymes, increasing citrate secretion and citrate transporter gene expression, and enhancing the expression of PM H+-ATPase.
TL;DR: The reactivity of ebselen with protein thiols has helped to identify novel, selective targets for inhibitory actions on several enzymes of importance in pharmacology and toxicology, and initial concerns about selenium toxicity, fortunately, were unfounded.
TL;DR: The frequency and severity of cardiovascular toxicity in advanced renal cell carcinoma patients treated with targeted cancer therapies are high and early detection of asymptomatic patients could preempt symptomatic toxicity and reduce treatment-related morbidity and mortality.
Abstract: Objectives The purpose of this study was to document the incidence and extent of cardiovascular toxicity among advanced renal cell carcinoma patients treated with newer targeted cancer agents. Background The potential for targeted cancer agents to induce cardiovascular toxicity has been increasingly recognized, but the overall incidence and extent of toxicity have not been well characterized. Early detection of asymptomatic patients could preempt symptomatic toxicity and reduce treatment-related morbidity and mortality. Methods The incidence of hypertension, left ventricular dysfunction, and heart failure was assessed for all advanced renal cell carcinoma patients treated with targeted therapies at our institution between 2004 and 2011. Grading was performed according to the Common Terminology Criteria for Adverse Events version 4.0. Results Cardiovascular toxicity developed in 116 of 159 patients (73%), including 52 of 159 patients (33%) when hypertension was excluded. Toxicity varied from occurrences of asymptomatic drops in left ventricular ejection fraction to rises in N-terminal-pro-B-type natriuretic peptide to severe heart failure. The tyrosine kinase inhibitor sunitinib was the agent most frequently used, with 66 of 101 sunitinib-treated patients (65%) developing a form of cardiovascular toxicity, including 32 of 101 patients (32%), excluding hypertension. Other VEGF inhibitors such as bevacizumab, sorafenib, and pazopanib also elicited significant cardiovascular toxicity with incidences ranging from 51% to 68%. Conclusions The frequency and severity of cardiovascular toxicity in advanced renal cell carcinoma patients treated with targeted cancer therapies are high.
TL;DR: Coadministration of Nano-Se significantly improved the serum T, sperm quality, and spermatogenesis and reduced CIS-induced free radical toxic stress and sPermatic DNA damage.
TL;DR: The data suggest that prolonged exposure to GO may cause potential risk to environmental organisms after release into the environment, and GO toxicity may be due to the combinational effects of oxidative stress in the intestinal barrier, enhanced permeability of the biological barrier, and suppressed defecation behavior in C. elegans.
Abstract: Graphene oxide (GO) has been extensively studied for potential biomedical applications. Meanwhile, potential GO toxicity arises in both biomedical applications and non-biomedical products where environmental exposures may occur. In the present study, we examined the potential adverse effects of GO and the underlying mechanism using nematode Caenorhabditis elegans as the assay system. We compared the in vivo effects of GO between acute exposure and prolonged exposure, and found that prolonged exposure to 0.5-100 mg L(-1) of GO caused damage on functions of both primary (intestine) and secondary (neuron and reproductive organ) targeted organs. In the intestine, ROS production was significantly correlated with the formation of adverse effects on functions of both primary and secondary targeted organs. GO could be translocated into intestinal cells with loss of microvilli, and distributed to be adjacent to or surrounding mitochondria. Prolonged exposure to GO resulted in a hyper-permeable state of the intestinal barrier, an increase in mean defecation cycle length, and alteration of genes required for intestinal development and defecation behavior. Thus, our data suggest that prolonged exposure to GO may cause potential risk to environmental organisms after release into the environment. GO toxicity may be due to the combinational effects of oxidative stress in the intestinal barrier, enhanced permeability of the biological barrier, and suppressed defecation behavior in C. elegans.
TL;DR: It is suggested that at least two-fold higher doses of the cytotoxic agent are tolerated in T-DM1, supporting the premise of ADCs to improve the therapeutic index.
TL;DR: The findings offer a new avenue for the potential development of gold nanoparticles as a therapeutic agent in the treatment of such disorders, with the growing incidence of obesity and obesity-related diseases.
Abstract: Objectives Gold nanoparticles (AuNPs) of 21 nm have been previously well characterized in vitro for their capacity to target macrophages via active uptake However, the short-term impact of such AuNPs on physiological systems, in particular resident macrophages located in fat tissue in vivo, is largely unknown This project investigated the distribution, organ toxicity and changes in inflammatory cytokines within the adipose tissue after mice were exposed to AuNPs Methods Male C57BL/6 mice were injected intraperitoneally (IP) with a single dose of AuNPs (785 μg AuNPs/g) Body weight and energy intake were recorded daily Tissues were collected at 1 h, 24 h and 72 h post-injection to test for organ toxicity AuNP distribution was examined using electron microscopy Proinflammatory cytokine expression and macrophage number within the abdominal fat pad were determined using real-time PCR Results At 72 hours post AuNP injection, daily energy intake and body weight were found to be similar between Control and AuNP treated mice However, fat mass was significantly smaller in AuNP-treated mice Following IP injection, AuNPs rapidly accumulated within the abdominal fat tissue and some were seen in the liver A reduction in TNFα and IL-6 mRNA levels in the fat were observed from 1 h to 72 h post AuNP injection, with no observable changes in macrophage number There was no detectable toxicity to vital organs (liver and kidney) Conclusion Our 21 nm spherical AuNPs caused no measurable organ or cell toxicity in mice, but were correlated with significant fat loss and inhibition of inflammatory effects With the growing incidence of obesity and obesity-related diseases, our findings offer a new avenue for the potential development of gold nanoparticles as a therapeutic agent in the treatment of such disorders
TL;DR: These studies demonstrated that antioxidants are able to counteract the deleterious effects of chronic consumption or exposure to OTA and confirmed the potential effectiveness of dietary strategies to counteract OTA toxicity.
Abstract: Ochratoxin A (OTA) is a mycotoxin involved in the development of different types of cancers in rats, mice and humans. A growing number of in vitro and in vivo studies has been collected and has described evidence compatible with a role for oxidative stress in OTA toxicity and carcinogenicity. Because the contribution of the oxidative stress response in the development of cancers is well established, a role in OTA carcinogenicity is plausible. Several studies have been performed to try to counteract the adverse effects of oxygen radicals generated under OTA-exposure. A number of molecules with various antioxidant properties were tested, using in vivo or in vitro models. Protection against OTA-induced DNA damage, lipid peroxidation, as well as cytotoxicity were observed, further confirming the link between OTA toxicity and oxidative damage. These studies demonstrated that antioxidants are able to counteract the deleterious effects of chronic consumption or exposure to OTA and confirmed the potential effectiveness of dietary strategies to counteract OTA toxicity.
TL;DR: Evidence of the potential toxicity and inflammogenic potential of Ag NPs in the liver following ingestion is presented and the similarities between in vitro and in vivo responses are striking and encouraging for future reduction, refinement, and replacement of animal studies by the use of hepatocyte cell lines in particle risk assessment.
TL;DR: The results indicated that the observed toxicities of nano-ZnO were not likely a result solely of particle dissolution and identified as a function of particle toxicity and the possibility for a size dependence.
TL;DR: The results could lead to the conclusion that the long-term oral administration of E. hirta extract for 90 days does not cause sub-chronic toxicity, as well as food and water consumptions, body weight change, haematological and biochemical parameters, relative organ weights, and gross findings compared to the control group.
Abstract: DespiteEuphorbia hirta L. ethnomedicinal benefits, very few studies have described the potential toxicity. The aim of the present study was to evaluate the in vivo toxicity of methanolic extracts of E. hirta. The acute and subchronic oral toxicity of E. hirta was evaluated in Sprague Dawley rats. The extract at a single dose of 5000 mg/kg did not produce treatment related signs of toxicity or mortality in any of the animals tested during the 14-day observation period. Therefore, the LD 50 of this plant was estimated to be more than 5000 mg/kg. In the repeated dose 90-day oral toxicity study, the administration of 50 mg/kg, 250 mg/kg, and 1000 mg/kg/day ofE. hirta extract per body weight revealed no significant difference ( �� > 0.05 ) in food and water consumptions, body weight change, haematological and biochemical parameters, relative organ weights, and gross findings compared to the control group. Macropathology and histopathology examinations of all organs including the liver did not reveal morphological alteration. Analyses of these results with the information of signs, behaviour, and health monitoring could lead to the conclusion that the long-term oral administration of E. hirta extract for 90 days does not cause sub-chronic toxicity.
TL;DR: Evidence is slowly emerging that a low PON1 status may increase susceptibility to OP toxicity in humans, as shown by animal and human studies.
TL;DR: Assessment of the acute toxicity of 31 different nanomaterials to fish mature individuals Danio rerio and that to fish early life stages on using evaluation of the 48- and 96- hour LC50 values found no marked differences.
Abstract: At present, nanoparticles are beginning to influence our lives in many ways and understanding the environmental health and safety aspect of nanomaterials has become a crucial issue. The aim of the work was to assess and compare the acute toxicity of 31 different nanomaterials to fish mature individuals Danio rerio with that to fish early life stages on using evaluation of the 48- and 96- hour LC50 values. A further aim was to evaluate teratogenicity of the nanoparticles tested to fish eggs. The nanoparticles tested were: 8 pure metals, 10 metal oxides, 5 other metal compounds and their mixtures, 2 silicon compounds, 3 calcium compounds, and 3 carbon compounds. Using 48-h and 96-h tests of acute toxicity (according to OECD 203), we evaluated mortality data, LC50 values, occurrence of malformations, as well as hatching time. In our study, 6 kinds of nanoparticles - calcium oxide, copper, copper in the form of oxide and CuZnFe4O4, magnesium oxide, and nickel - caused cumulative mortality. Two kinds of nanoparticles - copper and silver - were toxic for fish with LC50 values of approximately 3 mg/L. We did not observe marked differences between the 48-hour and 96-hour acute toxicity LC50 values, yet the possibility to evaluate hatching time in the 96-h acute fish toxicity test seems to be an advantage against that of the 48-hour toxicity.
TL;DR: The chronic 21-day toxicity of silver NPs to D. magna in natural water was at the part-per-billion level, and adult mortality was more sensitive toxicity test endpoint than the reproduction (the number of offspring per adult).
Abstract: Although silver nanoparticles (NPs) are increasingly used in various consumer products and produced in industrial scale, information on harmful effects of nanosilver to environmentally relevant organisms is still scarce. This paper studies the adverse effects of silver NPs to two aquatic crustaceans, Daphnia magna and Thamnocephalus platyurus. For that, silver NPs were synthesized where Ag is covalently attached to poly(vinylpyrrolidone) (PVP). In parallel, the toxicity of collargol (protein-coated nanosilver) and AgNO3 was analyzed. Both types of silver NPs were highly toxic to both crustaceans: the EC50 values in artificial freshwater were 15–17 ppb for D. magna and 20–27 ppb for T. platyurus. The natural water (five different waters with dissolved organic carbon from 5 to 35 mg C/L were studied) mitigated the toxic effect of studied silver compounds up to 8-fold compared with artificial freshwater. The toxicity of silver NPs in all test media was up to 10-fold lower than that of soluble silver salt, AgNO3. The pattern of the toxic response of both crustacean species to the silver compounds was almost similar in artificial freshwater and in natural waters. The chronic 21-day toxicity of silver NPs to D. magna in natural water was at the part-per-billion level, and adult mortality was more sensitive toxicity test endpoint than the reproduction (the number of offspring per adult).