Direct embryotoxicity of chromium (III) exposure during preimplantation development.

Chromium in its trivalent form (chromium (III)) is an essential component of a balanced diet, and its deficiency disturbs glucose and lipid metabolism in humans and animals. The prevailing view is that chromium (III) is notably less toxic than chromium (VI), which is genotoxic and carcinogenic. Thus, the biotransformation of environmental chromium (VI) to chromium (III) is a promising and environmentally friendly detoxification method. However, increasing evidence suggests that chromium (III) induces considerable cytotoxicity. However, the toxicity of chromium (III) to early embryos remains largely unknown. In the present study, we used in vitro fertilization (IVF) to produce mouse embryos and identified the direct embryotoxicity of chromium (III). On exposure to high concentrations of CrCl3, blastocyst formation almost completely failed and a large proportion of embryos were arrested at the 2- to 4-cell stage. At low concentrations of CrCl3, IVF embryos showed a significant decrease in blastocyst formation, reduced total cell numbers, aberrant lineage differentiation, increased oxidative stress, and apoptosis. We also found that chromium (III) exposure during the preimplantation stage, even at low concentrations, led to impaired post-implantation development. Thus, our study substantiates the direct embryotoxicity of chromium (III) during preimplantation development and prolonged impairment of development potential. The results further highlight the potential adverse effects of chromium (III) on public reproductive health with respect to increased environmental enrichment of and dietary supplementation with chromium (III) complexes.

Evaluation of phototoxicity of tattoo pigments using the 3 T3 neutral red uptake phototoxicity test and a 3D human reconstructed skin model.

Phototoxicity due to dermally impregnated compounds exposed to ultraviolet radiation is associated with skin inflammation. The phototoxicity potential of active substances applied to the skin should be evaluated. Pigments are widely used for tattoos, and hypersensitivity reactions, such as photoallergic dermatitis, are possible tattoo-related complications. However, the phototoxicity of these chemicals is not well known. In this study, we evaluated the phototoxicity potential of six tattoo pigments, cadmium sulfide, carbazole, cadmium selenide, mercury (II) sulfide, chromium oxide, and cobalt aluminate, using in vitro methods-3 T3 neutral red uptake (NRU) phototoxicity test (PT) and a 3D human reconstructed skin model (EpiDerm). The validated 3 T3 NRU PT indicated the phototoxicity potential of carbazole and cadmium sulfide. The 3D human skin model confirmed that only carbazole was phototoxic. The 3 T3 NRU PT data corresponded well with those from the 3D skin model and suggested the need to employ several test systems for final phototoxicity assessment. In addition to the results obtained using 3 T3 NRU PT, further testing on 3D skin models may better reflect the bioavailability of a given chemical in the skin.

Changes in the gene expression profile of Arabidopsis thaliana under chromium stress.

Based on previous studies and preliminary test results, 200 µM was used as the test concentration of chromium (Cr), and changes in the gene expression profile of Arabidopsis thaliana in response to 24-h treatments of Cr(III) and Cr(VI) were analyzed using the Arabidopsis ATH1 Genome Array. The results were as follows. There were 238 upregulated genes and 858 downregulated genes in response to treatments with Cr(III) and Cr(VI). For Cr(III) and Cr(VI) treatments, there were 185 and 587 specifically upregulated genes as well as 220 and 956 specifically downregulated genes, respectively. Among the common differentially expressed genes (DEGs), the expression levels of genes involved in redox, secondary metabolism, and energy metabolism processes were significantly downregulated, while those of genes related to the stress response, photosynthesis, and sulfur metabolism were significantly upregulated. These findings indicated that Cr seriously affected the normal activities of A. thaliana cells. Some genes associated with stress and regulation were upregulated to adapt to the stress caused by Cr. Among the unique DEGs, the expression levels of genes involved in indole-3-acetic acid (IAA) regulatory pathway were significantly increased in response to Cr(III) treatment; the expression levels of genes involved in the abscisic acid (ABA) regulation pathway and carotenoid synthesis were significantly increased following Cr(VI) treatment. These results revealed some differences in response to Cr(III) and Cr(VI) in A. thaliana.

Hepatotoxicity and chromosomal abnormalities evaluation due to single and repeated oral exposures of chromium oxide nanoparticles in Wistar rats.

Metal oxide nanoparticles (NPs) have widespread uses ranging from nanoelectronics to nanotherapeutics. Because of their expanding industrial applications, a better understanding of their toxicity is needed. So far, limited reports are available on chromium oxide NPs (Cr2O3 NPs) toxicity. In this work, Cr2O3 NPs were synthesized and characterized in a sequential manner using X-ray diffraction (XRD), Fourier transform infrared (FTIR) spectroscopy, and transmission electron microscopy. Dose- and time-dependent toxicity assessment of Cr2O3 NPs was carried out in Wistar rats by examining liver function biomarkers, tissue histopathology, micronuclei (MN) formation, and chromosomal aberrations (CAs) in bone marrow along with sperm abnormalities. The results of this study demonstrated typical XRD and FTIR patterns of Cr2O3 NPs with a size of approximately 23.47 nm. Animals exposed to Cr2O3 NPs, exhibited a significant increase in aspartate transaminase, alanine transaminase, alkaline phosphatase, gamma glutamyltransferase, and total bilirubin, signifying liver injury. Histopathology data also supported the marked alterations in the liver biochemistry of NPs-exposed animals. Further, an increase in the frequency of MN, CA, and sperm abnormalities suggested Cr2O3 NPs-mediated genotoxicity. It is, therefore, suggested that possible safety issues of Cr2O3 NPs should be addressed promptly with limited future use in occupational settings.

Pulmonary toxicity and lung tumorigenic potential of surrogate metal oxides in gas metal arc welding-stainless steel fume: Iron as a primary mediator versus chromium and nickel.

In 2017, the International Agency for Research on Cancer classified welding fumes as "carcinogenic to humans" (Group 1). Both mild steel (MS) welding, where fumes lack carcinogenic chromium and nickel, and stainless steel (SS) increase lung cancer risk in welders; therefore, further research to better understand the toxicity of the individual metals is needed. The objectives were to (1) compare the pulmonary toxicity of chromium (as Cr(III) oxide [Cr2O3] and Cr (VI) calcium chromate [CaCrO4]), nickel [II] oxide (NiO), iron [III] oxide (Fe2O3), and gas metal arc welding-SS (GMAW-SS) fume; and (2) determine if these metal oxides can promote lung tumors. Lung tumor susceptible A/J mice (male, 4-5 weeks old) were exposed by oropharyngeal aspiration to vehicle, GMAW-SS fume (1.7 mg), or a low or high dose of surrogate metal oxides based on the respective weight percent of each metal in the fume: Cr2O3 + CaCrO4 (366 + 5 µg and 731 + 11 µg), NiO (141 and 281 µg), or Fe2O3 (1 and 2 mg). Bronchoalveolar lavage, histopathology, and lung/liver qPCR were done at 1, 7, 28, and 84 days post-aspiration. In a two-stage lung carcinogenesis model, mice were initiated with 3-methylcholanthrene (10 µg/g; intraperitoneal; 1x) or corn oil then exposed to metal oxides or vehicle (1 x/week for 5 weeks) by oropharyngeal aspiration. Lung tumors were counted at 30 weeks post-initiation. Results indicate the inflammatory potential of the metal oxides was Fe2O3 > Cr2O3 + CaCrO4 > NiO. Overall, the pneumotoxic effects were negligible for NiO, acute but not persistent for Cr2O3 + CaCrO4, and persistent for the Fe2O3 exposures. Fe2O3, but not Cr2O3 + CaCrO4 or NiO significantly promoted lung tumors. These results provide experimental evidence that Fe2O3 is an important mediator of welding fume toxicity and support epidemiological findings and the IARC classification.

Oxidative stress and DNA damage in a long-term hexavalent chromium-exposed population in North China: a cross-sectional study.

OBJECTIVE: The International Agency for Research on Cancer classifies hexavalent chromium (Cr(VI)) as a human carcinogen. As reported, cancer mortality was higher in Cr(VI)-contaminated areas. Scientists have recommended studying its health impact on people living in contaminated areas. This study aims to evaluate the health risk for people living in Cr(VI)-contaminated areas. DESIGN: We conducted a cross-sectional study in rural areas of north-eastern China. Malondialdehyde (MDA), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) were used as oxidative stress parameters, and 8-hydroxy-2 deoxyguanosine (8-OHdG) as a DNA damage biomarker. We collected information on demographics, lifestyles and length of residence from all participants using a questionnaire. Biological specimens and environmental media samples were collected on the same day as the survey was done. We used t-test, χ2 test, Wilcoxon rank-sum test and multivariate linear regression analysis. PARTICIPANTS: The study included 319 participants exposed to Cr(VI) and 307 unexposed participants, with 447 women and 179 men. These participants met the following criteria: (1) living in the areas for more than 10 years; (2) age older than 18 years; and (3) without occupational chromium exposure. RESULTS: Our study revealed that serum concentration of MDA (p<0.001), serum activities of CAT (p<0.001) and GSH-Px (p<0.001), as well as urine concentration of 8-OHdG (p=0.008) in the exposed group were significantly higher than those in the unexposed group. However, serum SOD activity was significantly lower in the exposed group, compared with that in the unexposed group (p<0.001). Cr(VI) exposure and smoking have an interaction effect on GSH-Px activity (p<0.05). Cr(VI) exposure and alcohol drinking also have an interaction effect on GSH-Px activity (p<0.05). Longer residence in the exposed areas increased the oxidative levels (p<0.05). CONCLUSIONS: The findings of this study showed elevated oxidative stress and DNA damage in people exposed to Cr(VI).

Effects of Cr2O3 nanoparticles on the chlorophyll fluorescence and chloroplast ultrastructure of soybean (Glycine max).

Chromic oxide nanoparticles (Cr2O3 NPs) are widely used in commercial factories and can cause serious environmental problems. However, the mechanism behind Cr2O3 NP-induced phytotoxicity remains unknown. In this study, the effects of Cr2O3 NPs on the growth, chlorophyll fluorescence, SEM-EDS analysis, and chloroplast ultrastructure of soybean (Glycine max) were investigated to evaluate its phytotoxicity. The growth of soybean treated with various Cr2O3 NP suspensions (0.01, 0.05, 0.1, and 0.5 g L-1) was significantly inhibited. Specially, shoot and root biomass decreased by 9.9 and 46.3%, respectively. Besides, the maximum quantum yield of PSII (Fv/Fm) as well as the photochemical quenching (qP) decreased by 8-22 and 30-37%, respectively, indicating that the photosynthetic system was damaged when treated with Cr2O3 NPs. Moreover, the inhibition was confirmed by the reduction of Rubisco and MDH enzyme activity (by 54.5-86.4 and 26.7-96.5%, respectively). Overall, results indicated that the damage was caused by the destruction of chloroplast thylakoid structure, which subsequently reduced the photosynthetic rate. Our research suggests that Cr2O3 NPs can be transported and cause irreversible damage to soybean plants by inhibiting the activity of electron acceptors (NADP+) and destroying ultrastructure of chloroplasts, providing insights into plant toxicity issues. Graphical abstract ᅟ.

Impact of chromium and boron compounds on the reproductive function in rats.

The purpose of this research is to study the process of mutagenesis and the reproductive function in male rats under separate and combined exposure to chromium and boron compounds. The experiment was conducted on two groups of animals. The first group was used to assess the ability of potassium dichromate and boric acid to induce mutation in germ and somatic cells under isolated and combined administration with the use of the dominant lethal mutations test and the micronuclei test in the polychromatophilic erythrocytes of the bone marrow. The second group was used to test the combined and separate effect of the compounds under consideration on the reproductive function of male rats during the spermatogenesis cycle. When used in specific doses, boron compounds are a promising means of preventing and correcting chromium-induced effects in chromium production facility workers and people who live in ecologically adverse regions.

Interactions between chromium(III) and iron(III), molybdenum(III) or nickel(II): Cytotoxicity, genotoxicity and mutagenicity studies.

The aim of this study was to examine the effect of chromium(III) and iron(III) and molybdenum(III) and nickel(II) and their combinations on cyto-, genotoxicity and mutagenicity in BALB/3T3 and HepG2 cells. The results obtained from cytotoxicity assays indicate that there are differences between BALB/3T3 and HepG2 cell lines in their sensitivity to chromium chloride, iron chloride, molybdenum trioxide and nickel chloride. The statistically significant increase of DNA damage of all used microelements in both cell lines was observed. The micronucleus assay performed with the use of all concentrations shows statistically significant induction of chromosomal aberrations in all tested microelements in both cell lines. Moreover, treated cells display characteristic apoptosis in comparison to control cells. In all tested microelements, the increase of number of reverse mutations was observed with and without metabolic activation. Additions of Cr(III) at 200 µM plus Fe(III) at 1000 µM showed synergistic effect in decrease of cell viability and increase of comets, micronuclei and number of revertants in both cell lines. In case of Cr(III) at 200 µM plus Mo(III) at 1000 µM, a protective effect of chromium against molybdenum at 1000 µM toxicity in both cell lines (assessed by MTT, LDH and NRU, comet, micronucleus and Ames assays) was observed. The protective effect of Cr(III) in decrease of cell viability was observed in pair of Cr(III) at 200 µM and Ni(II) at 1000 µM in BALB/3T3 and HepG2 cell lines assessed by MTT, LDH and NRU, comet, micronucleus and Ames assays.

[Cr3O(O2CCH2CH3)6(H2O)3]NO3·H2O (Cr3) Toxicity Potential in Bacterial and Mammalian Cells.

Chromium(III) has generally been considered to be essential for proper carbohydrate and lipid metabolism, and, despite recent evidence to the contrary, chromium(III)-containing compounds remain one of the most popular commercial dietary supplements. Cr3, or [Cr3O(O2CCH2CH3)6(H2O)3]NO3·H2O, is a trivalent chromium compound that is a promising chromium nutritional supplement. Studies with Cr3 have indicated that it is non-toxic in developmental and short- and long-term exposure studies in rodents, but the safety of this compound to chromosomes and cells has not been explored. The current study evaluates the mutagenicity, cytotoxicity, and clastogenicity of Cr3 in bacterial and mammalian cells and compares these results with similar studies using the bestselling Cr(III) nutritional supplement, chromium picolinate (CrPic). The mutagenicity of CrPic and Cr3 was tested in Escherichia coli FX-11 and Salmonella typhimurium (TA 98 and TA 100). Cytotoxicity was measured as a decrease in plating efficiency relative to controls after treatment with Cr3 and CrPic for 24 h in CHO K1 cells. Clastogenicity was measured by counting the number of metaphases damaged and of the total number chromosomal aberrations in CHO K1 cells. Mutagenesis assays in E. coli and S. typhimurium were negative. All treatments of Cr3 produced ≥ 84% plating efficiency except 80 µg/cm2, which reduced the plating efficiency to 62%. Cr3 at any treatment level did not produce a significant increase in the number of cells with abnormal metaphases, while treatments using ≥ 40 µg/cm2 of CrPic elevated the number significantly. These data suggest that Cr3 is significantly less mutagenic in bacteria cells and less clastogenic in CHO K1 cells, while CrPic is clastogenic in CHO K1 cells.

Antimutagenic action of the live yeast can be transmitted to the offspring of Drosophila melanogaster. A genetic study using the wing spot assay.

The present study evaluates whether the protective effect of live yeast (LY) against direct and indirect mutagenic agents, persists in the offspring from individuals fed with LY. The wing-spot test in Drosophila was used; four different mates were performed: a) neither females nor males were fed with LY-enriched food (NLYxNLY); b) only females were fed (LYxNLY); c) males were fed (NLYxLY) or d) both progenitors were fed (LYxLY). Results confirm that LY strongly stimulates fecundity in females but not in males and provides strength to the egg for survive. A greater reduction in mutation rate was observed when females were feed, in the following relationship: LYxNLY>LYxLY>NLYxLY. No protection was found against action in any of the promutagens tested. Results suggest that LY has a very powerful antimutagenic action, predominantly against the action of ionizing radiation and Chromium trioxide that can be transmitted mainly through the female.

Chromium oxide nanoparticle-induced biochemical and histopathological alterations in the kidneys and brain of Wistar rats.

Chromium oxide nanoparticles (Cr2O3 NPs) have a wide range of applications in industry. They are used as pigments, catalysts, wear-resistant or high-temperature-resistant coating material and are used in liquid crystal displays. In view of ever escalating use of NPs, risk assessment becomes obligatory to ensure the safety of both human health and the ecosystem. The present study was designed and conducted to evaluate biochemical changes and histopathological alterations in kidneys and brain of rats, following exposure to Cr2O3 NPs. Male Wistar rats were divided into low-dose (50 µg/100 g body weight (bwt) groups and high-dose (200 µg/100 g bwt) groups. Each group type received oral administration of Cr2O3 NPs for multiple durations (single dosing, once daily for 7 days and once daily for 14 days, respectively). According to our data, this allotment presented a meaningful picture of NPs behaviour in different scenarios. In the kidneys and brain of Cr2O3 NPs-exposed animals, reactive oxygen species (ROS) production caused a significant increase in malondialdehyde (MDA) concentration along with a significant decrease in superoxide dismutase and glutathione levels, as compared to controls. Histopathological changes in these organs confirmed cellular injury and functional damage due to exposure to Cr2O3 NPs. In this study, we have distinguished pathological alterations consequent to deleterious oxidative stress due to enhanced ROS generation after Cr2O3 NPs exposure.

Removal of Chromium from Soils Cultivated with Maize (Zea Mays) After the Addition of Natural Minerals as Soil Amendments.

The efficiency of natural minerals, i.e. zeolite, bentonite and goethite, regarding the retention of chromium, from maize was examined. Specifically, 1.0 kg of soil, 1.0 g of soil amendment and either 50 mg L-1 Cr(III) or 1 mg L-1 Cr(VI) were added in plant pots. Then, seeds of maize were cultivated. Each treatment was repeated three times. The statistical results of the experiments were analyzed by LSD test. Cr(III) addition in soil has shown that zeolite was the only amendment that increased the dry weight. Zeolite and bentonite reduced significantly the total chromium in plants after the addition of 50 mg L-1 Cr(III). The addition of Cr(VI) in soil has shown that bentonite was the only amendment that increased the dry weight of biomass and the plants' height. All soil amendments reduced to zero the total chromium concentration measured to plants after the addition of 1 mg L-1 Cr(VI).

Allergy-Inducing Chromium Compounds Trigger Potent Innate Immune Stimulation Via ROS-Dependent Inflammasome Activation.

Chromium allergy is a common occupational skin disease mediated by chromium (VI)-specific T cells that induce delayed-type hypersensitivity in sensitized individuals. Additionally, chromium (VI) can act as an irritant. Both responses critically require innate immune activation, but if and how chromium (VI) elicits this signal is currently unclear. Using human monocytes, primary human keratinocytes, and murine dendritic cells we show that chromium (VI) compounds fail to trigger direct proinflammatory activation but potently induce processing and secretion of IL-1ß. IL-1ß release required priming by phorbol-ester or toll-like receptor stimulation and was prevented by inhibition of K+ efflux, NLRP3 depletion or caspase-1 inhibition, identifying chromium (VI) as a hapten activator of the NLRP3 inflammasome. Inflammasome activation was initiated by mitochondrial reactive oxygen species production triggered by chromium (VI), as indicated by sensitivity to treatment with the ROS scavenger N-acetyl cysteine and a coinciding failure of K+ efflux, caspase-1, or NLRP3 inhibition to prevent mitochondrial reactive oxygen species accumulation. IL-1ß release further correlated with cytotoxicity that was secondary to reactive oxygen species, K+ efflux, and NLRP3 activation. Trivalent chromium was unable to induce mitochondrial reactive oxygen species production, inflammasome activation, and cytotoxicity, suggesting that oxidation state-specific differences in mitochondrial reactivity may determine inflammasome activation and allergic/irritant capacity of different chromium compounds.

Comparison of chromium III and VI toxicities in water using sulfur-oxidizing bacterial bioassays.

The toxicities of Cr (III) and Cr (VI) in water were evaluated using sulfur-oxidizing bacterial (SOB) bioassays both in batch and fed-batch conditions. Two days were enough for a quick buildup of SOB consortium in the master culture reactor (MCR). At concentrations up to 100 mg L(-1), Cr (III) was found to be nontoxic in both conditions, while Cr (VI) at very low concentrations (0.1-2 mg L(-1)) was very toxic to the SOB. Literature review suggested that the nontoxic nature of Cr (III) might be due to the absence of the iron uptake pathway in Acidithiobacillus caldus (the predominant bacteria in our reactors), which is required for Cr (III) uptake. The 2-h median effective concentration (EC50) values obtained for Cr (VI) in the batch and fed-batch tests were 2.7 mg L(-1) and 1.5 mg L(-1), respectively.

Mechanistic investigation of toxicity of chromium oxide nanoparticles in murine fibrosarcoma cells.

Chromium oxide nanoparticles (Cr2O3NPs) are widely used in polymers and paints. In the present study, we aimed to determine the toxicity of Cr2O3NPs in murine fibrosarcoma (L929) cells. The cytotoxicity of Cr2O3NPs was measured by MTT and neutral red uptake assays; Cr2O3NPs had significant cytotoxic effects on L929 cells. Enhancement of intracellular reactive oxygen species was observed in L929 cells after exposure to Cr2O3NPs. Cr2O3NPs produced caspase-3, indicating that exposure to Cr2O3NPs induced apoptosis. After exposure to Cr2O3NPs, the cellular glutathione level decreased and lipid peroxidation, superoxide dismutase, and catalase increased in a dose- and time-dependent manner. By using single-cell gel tests, we also observed increased DNA damage in a Cr2O3NP exposure-duration- and dose-dependent fashion. Cell toxicity and DNA damage may be useful biomarkers for determining the safety of Cr2O3NPs in human and animal health.

Oxidative Stress and Histological Alterations of Chicken Brain Induced by Oral Administration of Chromium(III).

This experiment was conducted to investigate the oxidative stress in chickens exposed to different concentrations of chromium trichloride (CrCl3) in drinking water. Seventy-two Hylan Brown male chickens were randomly divided into four groups: three experimental groups and one control group. The experimental groups were exposed to three different doses (50 % LD50, 25 % LD50, and 12.5 % LD50) of CrCl3 mg/kg body weight for 42 days, while the control group was given the equivalent water. The activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) and non-enzymatic index (glutathione, total antioxidant capacity, malondialdehyde, and hydrogen peroxide) were measured after obtaining the brain samples. Results suggested that 50 % LD50 chromium(III) significantly increased (P < 0.05) the contents of malondialdehyde and hydrogen peroxide. The antioxidant enzyme activities, total glutathione concentration, and total antioxidant capacity decreased significantly (P < 0.05) compared with those of the controls and were consistent with the increase in dosage and time. Additionally, extensive histological alterations were observed in the chicken brain, such as the vacuolization and nuclear condensation of the neurons. These results indicated that exposure to high-dose CrCl3 for a certain time could induce the occurrence of oxidative stress and histological alterations.

Synthesis, characterization and toxicological evaluation of Cr2O3 nanoparticles using Daphnia magna and Aliivibrio fischeri.

Chromium III oxide (Cr2O3) nanoparticles (NPs) are used in pigments for ceramics, dyes, paints and cosmetics. However, few studies addressing the toxic potential of these NPs have been reported in the literature. Thus, this research aimed to evaluate the acute and chronic effects of Cr2O3 NPs through acute toxicity tests with Daphnia magna and Aliivibrio fischeri and chronic toxicity tests with Daphnia magna. Cr2O3 NPs were synthesized by the sol-gel method and characterized through TEM, X-Ray diffraction (XRD), zeta potential (ZP) and surface area analysis. In the acute toxicity tests the EC(50,48h) value obtained with D. magna was 6.79 mg L(-1) and for A. fischeri the EC(50,15min) value was 16.10 mg L(-1) and the EC(50,30min) value was 12.91 mg L(-1). Regarding the chronic toxicity tests with D. magna, effects on longevity (OEC=1.00 mg L(-1)), reproduction (OEC=1.00 mg L(-1)) and growth (OEC=0.50 mg L(-1)) were observed. On the SEM and TEM images, ultrastructural alterations in the organelles of exposed organisms were also observed. Thus, toxicological studies with NPs are of great importance in order to reduce the risk of environmental contamination.

Effect of chromium oxide (III) nanoparticles on the production of reactive oxygen species and photosystem II activity in the green alga Chlamydomonas reinhardtii.

With the growth of nanotechnology and widespread use of nanomaterials, there is an increasing risk of environmental contamination by nanomaterials. However, the potential implications of such environmental contamination are hard to evaluate since the toxicity of nanomaterials if often not well characterized. The objective of this study was to evaluate the toxicity of a chromium-based nanoparticle, Cr2O3-NP, used in a wide diversity of industrial processes and commercial products, on the unicellular green alga Chlamydomonas reinhardtii. The deleterious impacts of Cr2O3-NP were characterized using cell density measurements, production of reactive oxygen species (ROS), esterase enzymes activity, and photosystem II electron transport as indicators of toxicity. Cr2O3-NP exposure inhibited culture growth and significantly lowered cellular Chlorophyll a content. From cell density measurements, EC50 values of 2.05±0.20 and 1.35±0.06gL(-1) Cr2O3-NP were obtained after 24 and 72h of exposure, respectively. In addition, ROS levels were increased to 160.24±2.47% and 59.91±0.15% of the control value after 24 and 72h of exposition to 10gL(-1) Cr2O3-NP. At 24h of exposure, the esterase activity increased to 160.24% of control value, revealing a modification of the short-term metabolic response of algae to Cr2O3-NP exposure. In conclusion, the metabolism of C. reinhardtii was the most sensitive to Cr2O3-NP after 24h of treatment.

Genotoxic effects of chromium oxide nanoparticles and microparticles in Wistar rats after 28 days of repeated oral exposure.

The nanotechnology industry has advanced rapidly in the last 10 years giving rise to the growth of the nanoparticles (NPs) with great potential in various arenas. However, the same properties that make NPs interesting raise concerns because their toxicity has not been explored. The in vivo toxicology of chromium oxide (Cr2O3)-NPs is not known till date. Therefore, this study investigated the 28-day repeated toxicity after 30, 300 and 1000 mg/kg body weight (bw)/day oral treatment with Cr2O3-NPs and Cr2O3 microparticles (MPs) in Wistar rats. The mean size of Cr2O3-NPs and Cr2O3-MPs was 34.89 ± 2.65 nm and 3.76 ± 3.41 µm, respectively. Genotoxicity was assessed using comet, micronucleus and chromosomal aberration (CA) assays. The results revealed a significant increase in DNA damage in peripheral blood leucocytes and liver, micronuclei and CA in bone marrow after exposure of 300 and 1000 mg/kg doses of Cr2O3-NPs and Cr2O3-MPs only at 1000 mg/kg bw/day. Cr biodistribution was observed in all the tissues in a dose-dependent manner. The maximum amount of Cr was found in the kidneys and least in the brain of the treated rats. More of the Cr was excreted in the faeces than in the urine. Furthermore, nanotreated rats displayed much higher absorption and tissue accumulation. These findings provide initial data of the probable genotoxicity and biodistribution of NPs and MPs of Cr2O3 generated through repeated oral treatment.