Improving the adoption of household health products: A sales experiment with chlorine tablets.

We test a door-to-door marketing intervention aimed to increase use of a targeted health product among poor households. Specifically, we examine three treatments in which this good-chlorine tablets for drinking water purification-is: (1) sold alone, (2) sold alongside a familiar and cheaper side good that is priced at its retail value, and (3) sold alongside the same side good that is priced on a promotional offer. The side good when sold at retail price is intended to be an "opt-out" good to reduce the marketing pressure, which should in turn reduce the amount of products sold that go unused. When the side good is sold on promotion, however, we hypothesize that it reintroduces marketing pressure due to the "gift" aspect of the promotion. Consistent with this hypothesis, we find that chlorine use is nearly double in the second condition compared to the other two conditions. Our results suggest that household valuation of a new product is shaped by both the presence and the price of a side good due to marketing pressure.

Investigating the underlying mechanism of cadmium-induced plant adaptive response to genotoxic stress.

Plants as sessile organisms have developed some unique strategies to withstand environmental stress and adaptive response (AR) is one of them. In the present study Cadmium (Cd)-induced AR was evaluated to ameliorate the genotoxicity of a known chemical mutagen ethyl methanesulphonate (EMS) based on cytotoxicity, genotoxicity and oxidative stress in two model plant systems Allium cepa L. and Vicia faba L. Priming the plants with cadmium chloride (CdCl2, 25 and 50 µM) reduced the genotoxicity of EMS (0.25 mM). Cd-induced AR was evident by the magnitude of adaptive response (MAR) values calculated for cytotoxicity, genotoxicity and biochemical parameters. In addition the involvement of some major metabolic pathways and epigenetic modifications in AR was investigated. Metabolic blockers of protein kinase cascades, DNA repair, oxidative stress and de novo translation interfered with the adaptive response implying their role in AR whereas, inhibitors involved in post-replication repair and autophagy were ineffective implicating that they probably have no role in the AR studied. Moreover to find the role of DNA methylation in AR, methylation-sensitive comet assay was carried out. Simultaneously 5-methyl- 2'-deoxycytidine (5mdC) levels were quantified by HPLC (high performance liquid chromatography). AR was eliminated in cells treated with a demethylating agent, 5-aza- 2'deoxycytidine (AZA). Results implied a contribution of DNA hypermethylation. To the best of our knowledge this is a first report correlating DNA methylation to Cd-induced adaptive response in plants undergoing genotoxic stress.

Effect of low-dose exposure of aluminium oxide nanoparticles in Swiss albino mice: Histopathological changes and oxidative damage.

Rapid growth in the use of aluminium oxide nanoparticles (Al2O3 NPs) in various fields such as medicine, pharmacy, cosmetic industries, and engineering creates concerns since the literature is replete with data regarding their toxicity in living organisms. The objective of the present study was to demonstrate the potential toxicological manifestations of repeated exposure to Al2O3 NP at low doses in vivo. In the present study, Al2O3 NP was orally administered at 15, 30 or 60 mg kg-1 body weight for 5 days to Swiss albino male mice. A battery of well-defined assays was undertaken to evaluate aluminium (Al) bioaccumulation, haematological and histological changes, oxidative damage and genotoxicity. Physico-chemical characterisation demonstrated increases in hydrodynamic diameter along the concentration gradient of Al2O3 NP dispersed in MilliQ water. Brain, liver, spleen, kidney and testes showed high Al retention levels. Histopathological lesions were prominent in the brain and liver. Al2O3 NP treatment increased levels of lipid peroxidation and decreased glutathione content in the test organs at all dose levels. The enzyme activities of catalase and superoxide dismutase were also significantly altered. DNA damage quantified using the comet assay was markedly increased in all the soft organs studied. Anatomical abnormalities, redox imbalance and DNA damage were positively correlated with Al retention in the respective organs. Size, zeta potential and colloidal state might have contributed to the bio-physico-chemical interactions of the NPs in vivo and were responsible for the non-linear dose response. The overall data indicate that Al2O3 NP exposure may result in adverse health consequences, inclusive of but not limited to disturbed redox homeostasis, hepatocellular toxicity, neurodegeneration and DNA damage.

Nanoscale zerovalent iron particles induce differential cytotoxicity, genotoxicity, oxidative stress and hemolytic responses in human lymphocytes and erythrocytes in vitro.

The growing usage of nanoscale zerovalent iron particles (nZVI) in the remediation of soil, ground/surface water has elicited large-scale environmental release triggering human exposure. The size of nanomaterials is a key regulator of toxicity. However, the effect of a variable size of nZVI on genotoxicity is unexplored in human cells. To the best of our knowledge, in this study, the cytotoxic, genotoxic and hemolytic potential of nZVI-1 (15 nm) and nZVI-2 (50 nm) at concentrations of 5, 10 and 20 µg/mL was evaluated for the first time in human lymphocytes and erythrocytes treated for 3 hours. In erythrocytes, spherocytosis and echinocytosis occurred upon exposure to nZVI-1 and nZVI-2, respectively, leading to hemolysis. Lymphocytes treated with 20 µg/mL nZVI-2 and 10 µg/mL nZVI-1, incurred maximum DNA damage, although nZVI-2 induced higher cyto-genotoxicity than nZVI-1. This can be attributed to higher Fe ion dissolution and time/concentration-dependent colloidal destabilization (lower zeta potential) of nZVI-2. Although nZVI-1 showed higher uptake, its lower genotoxicity can be due to lesser Fe content, Fe ion dissolution and superior colloidal stability (higher zeta potential) compared with nZVI-2. Substantial accumulation of Ca2+ , superoxide anions, hydroxyl radicals and H2 O2 leading to mitochondrial impairment and altered antioxidant enzyme activity was noted at the same concentrations. Pre-treatment with N-acetyl-cysteine modulated these parameters indicating the indirect action of reactive oxygen species in nZVI-induced DNA damage. The morphology of diffused nuclei implied the possible onset of apoptotic cell death. These results validate the synergistic role of size, ion dissolution, colloidal stability and reactive oxygen species on cyto-genotoxicity of nZVI and unlock further prospects in its environmental nano-safety evaluation.

Role of cerium oxide nanoparticle-induced autophagy as a safeguard to exogenous H2O2-mediated DNA damage in tobacco BY-2 cells.

The effect of cerium oxide nanoparticle (CeNP) in plants has elicited substantial controversy. While some investigators have reported that CeNP possesses antioxidant properties, others observed CeNP to induce reactive oxygen species (ROS). In spite of considerable research carried out on the effects of CeNP in metazoans, fundamental studies that can unveil its intracellular consequences linking ROS production, autophagy and DNA damage are lacking in plants. To elucidate the impact of CeNP within plant cells, tobacco BY-2 cells were treated with 10, 50 and 250 µg ml-1 CeNP (Ce10, Ce50 and Ce250), for 24 h. Results demonstrated concentration-dependent accumulation of Ca2+ and ROS at all CeNP treatment sets. However, significant DNA damage and alteration in antioxidant defence systems were noted prominently at Ce50 and Ce250. Moreover, Ce50 and Ce250 induced DNA damage, analysed by comet assay and DNA diffusion experiments, complied with the concomitant increase in ROS. Furthermore, to evaluate the antioxidant property of CeNP, treated cells were washed after 24 h (to minimise CeNP interference) and challenged with H2O2 for 3 h. Ce10 did not induce genotoxicity and H2O2 exposure to Ce10-treated cells showed lesser DNA breakage than cells treated with H2O2 only. Interestingly, Ce10 provided better protection over N-acetyl-L-cysteine against exogenous H2O2 in BY-2 cells. CeNP exposure to transgenic BY-2 cells expressing GFP-Atg8 fusion protein exhibited formation of autophagosomes at Ce10. Application of vacuolar protease inhibitor E-64c and fluorescent basic dye acridine orange, further demonstrated accumulation of particulate matters in the vacuole and occurrence of acidic compartments, the autophagolysosomes, respectively. BY-2 cells co-treated with CeNP and autophagy inhibitor 3-methyladenine exhibited increased DNA damage in Ce10 and cell death at all assessed treatment sets. Thus, current results substantiate an alternative autophagy-mediated, antioxidant and geno-protective role of CeNP, which will aid in deciphering novel phenomena of plant-nanoparticle interaction at cellular level.

In planta genotoxicity of nZVI: influence of colloidal stability on uptake, DNA damage, oxidative stress and cell death.

Nanoremediation of soil, ground and surface water using nanoscale zerovalent iron particles (nZVI) has facilitated their direct environmental exposure posing ecotoxicological concerns. Numerous studies elucidate their phytotoxicity in terms of growth and their fate within the plant system. However, their potential genotoxicity and cytotoxicity mechanisms are not known in plants. This study encompasses the physico-chemical characterisation of two forms of nZVI (nZVI-1 and nZVI-2) with different surface chemistries and their influence on uptake, root morphology, DNA damage, oxidative stress and cell death in Allium cepa roots after 24 h. To our knowledge, this is the first report on the cyto-genotoxicity of nZVI in plants. The adsorption of nZVI on root surfaces caused root tip, epidermal and root hair damage as assessed by Scanning Electron Microscopy. nZVI-1, due to its colloidal destabilisation (low zeta potential, conductivity and high polydispersity index), smaller size and high uptake imparted enhanced DNA damage, chromosome/nuclear aberrations (CAs/NAs) and micronuclei formation compared to nZVI-2. Although nZVI-2 exhibited high zeta potential and conductivity, its higher dissolution and substantial uptake induced genotoxicity. nZVI incited the generation of reactive oxygen species (ROS) (hydrogen peroxide, superoxide and hydroxyl radicals) leading to membrane lipid peroxidation, electrolyte leakage and mitochondrial depolarisation. The inactivation of catalase and insignificant glutathione levels marked the onset of oxidative stress. Increased superoxide dismutase and guaiacol peroxidase enzyme activities, and proline content indicated the activation of antioxidant defence machinery to alleviate ROS. Moreover, ROS-mediated apoptotic and necrotic cell death occurred in both nZVI-1 and nZVI-2-treated roots. Our results open up further possibilities in the environmental safety appraisal of bare and modified nZVI in correlation with their physico-chemical characters.

Genotoxicity of antiobesity drug orlistat and effect of caffeine intervention: an in vitro study.

CONTEXT: Obesity is a major global health problem associated with various adverse effects. Pharmacological interventions are often necessary for the management of obesity. Orlistat is an FDA-approved antiobesity drug which is a potent inhibitor of intestinal lipases. OBJECTIVE: In the current study, orlistat was evaluated for its genotoxic potential in human lymphocyte cells in vitro and was compared with that of another antiobesity drug sibutramine, presently withdrawn from market due its undesirable health effects. Caffeine intake may be an additional burden in people using anorectic drugs, therefore, further work is needed to be carried out to evaluate the possible effects of caffeine on orlistat-induced DNA damage. MATERIALS AND METHODS: Human lymphocytes were exposed to orlistat (250, 500 and 1000 µg/ml), sibutramine (250, 500 and 1000 µg/ml) and caffeine (25, 50, 75, 100, 125 and 150 µg/ml) to assess their genotoxicity by comet assay in vitro. In addition, lymphocytes were co-incubated with caffeine (50, 75 and 100 µg/ml) and a single concentration of orlistat (250 µg/ml). RESULTS: Orlistat and sibutramine were genotoxic at all concentrations tested, sibutramine being more genotoxic. Caffeine was found to be genotoxic at concentrations 125 µg/ml and above. Co-treatment of orlistat with non-genotoxic concentrations (50, 75 and 100 µg/ml) of caffeine lead to a decrease in DNA damage. DISCUSSION AND CONCLUSION: Orlistat can induce DNA damage in human lymphocytes in vitro and caffeine was found to reduce orlistat-induced genotoxicity.

Toxicity assessment of zero valent iron nanoparticles on Artemia salina.

The present study deals with the toxicity assessment of two differently synthesized zero valent iron nanoparticles (nZVI, chemical and biological) as well as Fe2+ ions on Artemia salina at three different initial concentrations of 1, 10, and 100 mg/L of these particles. The assessment was done till 96 h at time intervals of 24 h. EC50 value was calculated to evaluate the 50% mortality of Artemia salina at all exposure time durations. Between chemically and biologically synthesized nZVI nanoparticles, insignificant differences in the level of mortality were demonstrated. At even 24 h, Fe2+ ion imparted complete lethality at the highest exposure concentration (100 mg/L). To understand intracellular oxidative stress because of zero valent iron nanoparticles, ROS estimation, SOD activity, GSH activity, and catalase activity was performed which demonstrated that ionic form of iron is quite lethal at high concentrations as compared with the same concentration of nZVI exposure. Lower concentrations of nZVI were more toxic as compared with the ionic form and was in order of CS-nZVI > BS-nZVI > Fe2+ . Cell membrane damage and bio-uptake of nanoparticles were also evaluated for all three concentrations of BS-nZVI, CS-nZVI, and Fe2+ using adult Artemia salina in marine water; both of which supported the observations made in toxicity assessment. This study can be further explored to exploit Artemia salina as a model organism and a biomarker in an nZVI prone aquatic system to detect toxic levels of these nanoparticles. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1617-1627, 2017.

Malathion and dithane induce DNA damage in Vicia faba.

The increasing use of pesticides such as malathion and dithane in agriculture causes environmental mutagenicity. However, their genotoxicity in edible crops is seldom assessed. In this study, the genotoxic potential of malathion and dithane was evaluated in the roots of Vicia faba L. All three concentrations (0.05, 0.1, and 0.2%) of malathion and dithane tested resulted in a significant decrease in root length and inhibited seed germination. Cytological observations showed that the mitotic frequency in the root meristematic cells decreased parallel to the increase in concentrations, and the increase in chromosome aberrations and micronuclei frequency was concentration dependent. Alkaline comet assay revealed significant onset of DNA damage at all tested concentrations. For the randomly amplified polymorphic (RAPD)-polymerase chain reaction (PCR) analyses, 10 random RAPD primers were found to produce 116 unique polymorphic RAPD band fragments of 223-3139 bp. Each primer generated 3-15 RAPD bands on an average. The percentage of polymorphic DNA fragments was higher in malathion-exposed plants than dithane ones. The changes in RAPD profiles included disappearance and/or appearance of DNA bands in malathion and dithane treatment. Hence, DNA damage observed by the cytogenetic endpoints and comet assay corroborated with RAPD-PCR analysis. A total of 15 new protein bands of molecular weight ranging 11.894-226.669 kDa were observed in roots of Vicia plants that were exposed to the pesticides. The number of new protein bands was higher in malathion-treated DNA samples than in dithane-treated ones. Based on the results, we conclude that the pesticides can alter genomic template stability and change protein profiles. Malathion was more genotoxic than dithane. Therefore, RAPD assays can be useful in determining genotoxicity of pesticides in V. faba and other crops along with other quantitative parameters.

Evaluation of genetic damage in tobacco and arsenic exposed population of Southern Assam, India using buccal cytome assay and comet assay.

Ground water is the principal source of drinking water in Assam. Ground water contamination of arsenic in drinking water is a great concern for human health and considered as a human carcinogen. The present cytogenetic biomonitoring study was undertaken to investigate the genotoxic effects associated with people of southern Assam consuming arsenic contaminated water and chewing tobacco. Employing the buccal cytome assay, exfoliated cells were analyzed in 138 individuals of age range 22-42 years and divided into four groups. Group I (n=54) are participants residing in localities where ground water contains arsenic concentration below the permissible limit (<10µg/l) and without any tobacco chewing history. Group II (n=32) participants from the same area but they are tobacco chewers. Group III (n=24) participants from localities where significantly high arsenic contamination in ground water were observed. Whereas the Group IV (n=28) consists of participants from the arsenic contaminated area and also tobacco chewers. Body mass index (BMI) in all the groups are found to be nearly same and in normal range. Statistically significant (P<0.001) increase in genotoxic, cell death parameters and cell proliferation biomarkers were observed in the Group IV compared to other groups. In the comet assay, percent of tail DNA gradually increases among the groups and has statistical significance. Spearman correlation revealed strong positive correlation between the arsenic exposed peoples and the binucleated cells (r=0.4763; P<0.001). Amount of chewing tobacco had significant positive correlation with micronucleus frequency (r=0.268; P<0.05) and karyolitic cells (r=0.217; P<0.05) and also in the percentage of tail DNA (r=0.5532, P<0.001). A statistically significant increase in glucose content and decrease in hemoglobin content as well as acetylcholine esterase in the blood of exposed individuals was observed. Our preliminary study indicate that population exposed to arsenic through drinking water may become more susceptible towards chewing tobacco induced nuclear damage as evaluated by buccal cytome assay and comet assay.

Argemone oil induces genotoxicity in mice.

CONTEXT: Argemone mexicana L. is native to Mexico and the plant extracts are used in traditional medicine in India and South American countries. Argemone oil (AO) is a common adulterant of mustard oil in India and causes serious pathophysiological consequences leading to outbreaks of epidemic dropsy among consumers. In vivo cytogenetic studies on the toxicological effects of AO and its component alkaloids are limited. OBJECTIVE: The present study was undertaken to evaluate the safety of AO by assessment of their in vivo genotoxic potential in bone marrow cells of mice. MATERIALS AND METHODS: AO mixed in corn oil in the proportions of 0.01, 0.1, and 1 ml AO/kg body weight in a total volume of 10 ml/kg body weight and a single undiluted dose of AO (10 ml/kg body weight) were administered intraperitoneally in separate groups of male Swiss Albino mice for 24 h. In addition, a single concentration of sanguinarine (SG) (50 mg/kg body weight) was also administered. Genotoxicity was evaluated by chromosome aberration (CA) and sister chromatid exchange (SCE) tests. Bromodeoxyuridine (BrdU) differential technique was used to study the effect on cell replication by the calculation of average generation time (AGT). RESULTS: The minimum effective concentrations that produced significant frequencies of CA and SCE were 0.1 and 0.01 ml/kg, respectively. AO and SG induced an insignificant increase of AGT indicating that they are non-cytotoxic in the concentrations tested. DISCUSSION AND CONCLUSION: Our results confirm that AO is genotoxic even at low concentrations and its usage should be checked.

Late Life Immigration and Quality of Life among Asian Indian Older Adults.

Late-life immigration among seniors for purposes of family reunification is a growing phenomenon in developed countries. Using the World Health Organization's Quality of Life instrument short form (WHOQOL-BREF) and other psychosocial measures related to the political/legal context of immigration, and personal and environmental autonomy (mastery, immigration status, access to transportation, and language barrier), this study examined quality of life (QoL) in Asian Indian seniors (N = 109), who immigrated to the United States to reunite with their adult children. The sample scores on Overall QoL and QoL domains (physical and psychological health, social relationships, and environment) were similar to established norms. Although all QoL domains correlated significantly with Overall QoL at the bivariate level, multivariate analysis showed that only environmental domain contributed significantly to Overall QoL. Linear regressions indicated: Mastery contributed significantly to Overall QoL and all QoL domains; access to transport contributed to Overall QoL, physical health, and environmental QoL; immigration status (a proxy for political/legal context) contributed to environmental QoL whereas language barrier contributed to none. Implications for improving perceptions of QoL, mastery, access to transport and other services are discussed.

Antimutagenic and genoprotective effects of Saraca asoca bark extract.

AIM OF THE STUDY: Traditionally herbal formulations have been used effectively for the management of disorders that are now being accepted worldwide. Saraca asoca bark extract (SAE) finds use in traditional herbal medicine. In the present study, SAE were studied for their antioxidant, antimutagenic, and antigenotoxic properties. METHODS: SAE were evaluated for antimutagenic property in Salmonella strains (TA97a, TA98, TA100, and TA102), in the presence and absence of metabolic activation (S9). The SAE was also studied for antigenotoxic property against cyclophosphamide (CP) in Swiss albino male mice in vivo. The extract was analyzed using high-performance liquid chromatography (HPLC). RESULTS: The study reveals antimutagenic property of the bark extract in Salmonella strains in the presence and absence of metabolic activation (S9). The study reports antigenotoxic property of the bark extract against CP in vivo. Thiobarbituric acid reactive species assay on the bark extract revealed antioxidant property. HPLC revealed the presence of two peaks corresponding to gallic acid and (-)-epicatechin, respectively. CONCLUSION: The study clearly reveals the antimutagenic and antigenotoxic properties of SAE.

Cytogenetic studies of chromium (III) oxide nanoparticles on Allium cepa root tip cells.

The current study evaluates the cytogenetic effects of chromium (III) oxide nanoparticles on the root cells of Allium cepa. The root tip cells of A. cepa were treated with the aqueous dispersions of Cr2O3 nanoparticles (NPs) at five different concentrations (0.01, 0.1, 1, 10, and 100µg/mL) for 4hr. The colloidal stability of the nanoparticle suspensions during the exposure period were ascertained by particle size analyses. After 4hr exposure to Cr2O3 NPs, a significant decrease in mitotic index (MI) from 35.56% (Control) to 35.26% (0.01µg/mL), 34.64% (0.1µg/mL), 32.73% (1µg/mL), 29.6% (10µg/mL) and 20.92% (100µg/mL) was noted. The optical, fluorescence and confocal laser scanning microscopic analyses demonstrated specific chromosomal aberrations such as-chromosome stickiness, chromosome breaks, laggard chromosome, clumped chromosome, multipolar phases, nuclear notch, and nuclear bud at different exposure concentrations. The concentration-dependent internalization/bio-uptake of Cr2O3 NPs may have contributed to the enhanced production of anti oxidant enzyme, superoxide dismutase to counteract the oxidative stress, which in turn resulted in observed chromosomal aberrations and cytogenetic effects. These results suggest that A. cepa root tip assay can be successfully applied for evaluating environmental risk of Cr2O3 NPs over a wide range of concentrations.

Sodium fluoride promotes apoptosis by generation of reactive oxygen species in human lymphocytes.

Fluoride generated the attention of toxicologists due to its deleterious effects at high concentrations in human populations suffering from fluorosis and with in vivo experimental models. Interest in its undesirable effects has resurfaced due to the awareness that this element interacts with cellular systems even at low doses. This study focused on examining the adverse effects of inorganic fluoride (NaF) on human lymphocyte cells in vitro. Mitochondrial function, oxidative stress, cell cycle progression, and mode of cell death were combined with genotoxic endpoints. Data demonstrated that NaF at lower concentrations, although not significantly cytotoxic and genotoxic, induced oxidative stress leading to apoptotic cell death. The results also suggested that at low concentrations (<1 µg/ml), NaF may affect cell cycle progression. Taken together, our findings confirm earlier reports on mechanisms involved in NaF-induced apoptosis.

Biosynthesis and safety evaluation of ZnO nanoparticles.

The secrets gleaned from nature have led to the development of biomimetic approaches for the growth of advanced nanomaterials. Biological methods for nanoparticle synthesis using microorganisms, enzymes, and plants or plant extracts have been suggested as possible ecofriendly alternatives to chemical and physical methods. Here, we report extracellular mycosynthesis of ZnO-NPs by Alternaria alternata (Fr.) Keissl (1912). On treating zinc sulfate solution with fungal culture filtrate, rapid reduction of ZnSO4 was observed leading to the formation of highly stable ZnO-NPs in the solution and up-to-date literature survey showed this was the first report of biosynthesis of ZnO-NPs using this fungus. The particles thereby obtained were characterized by different analytical techniques. EDX-spectrum revealed the presence of zinc and oxygen in the nanoparticles. FTIR spectroscopy confirmed the presence of a protein shell outside the nanoparticles which in turn also support their stabilization. DLS and TEM analysis of the ZnO-NPs indicated that they ranged in size from 45 to 150 nm with average size of 75 ± 5 nm. But potential negative impacts of nanomaterials are sometimes overlooked during the discovery phase of research. Therefore, in the present study, bio-safety of mycosynthesized ZnO-NPs were evaluated by using cytotoxicity and genotoxicity assays in human lymphocyte cells, in vitro. Cytotoxicity studied as function of membrane integrity and mitochondrial dehydrogenase activity revealed significant (P < 0.05) toxicity at treatment concentration of 500 µg/ml and above. Additionally, DNA damaging potential was also studied using comet assay. The results revealed significant genotoxicity at the highest concentration (1,000 µg/ml).

Genotoxicity evaluation of 4-carboxyl- 2,6-dinitrophenylazohydroxynaphthalenes in mice.

A short-term in vivo genotoxicity evaluation of 4-carboxyl-2,6-dinitrophenylazohydronaphthalenes (AZ-01 to AZ-04) has been carried out in mice. Aqueous colloidal solutions of the dyes were administered to mice on each day for 5 successive days using gastric gavages. Two end point assessments of the genotoxicity potentials of the dyes were assessed using comet assay and chromosomal aberration studies using the mice bone marrow cells. The dyes were well tolerated at the doses investigated, as there were no deaths or any adverse pharmacotoxic events. Dose-dependent DNA damage (in terms of percentage of tail DNA and Olive tail moment) occurred with AZ-01 and AZ-02, although the effects were significant only with the highest doses. AZ-03 gave similar patterns with those of AZ-01 and AZ-02, while replacement with butanone in AZ-04 altered the observed pattern. Minimal chromosomal damages were obtained for the four dyes, with AZ-01 and AZ-02 giving nonsignificant damages, while the highest dose of AZ-03 produced significant aberrations in terms of breaks. Some minor isochromatid breaks and gaps were also noticed in the dye-treated mice. Mitotic indices in all cases were not significantly different from concomitantly administered vehicle control showing lack of cytotoxicity of the monoazo dyes at these doses. The monoazo dyes show the potential of being utilized as colorants, pending further required tests.

Evaluation of multi-endpoint assay to detect genotoxicity and oxidative stress in mice exposed to sodium fluoride.

Fluoride compounds are naturally present in soil, water and food. The objective of this study was to investigate the genotoxic and oxidative damage induced by chronic fluoride exposure on mammalian cells in vivo. For this purpose, the genotoxic potential was investigated in bone marrow cells by the micronucleus test, chromosome aberration assay and comet assay (DNA strand breaks). In addition, DNA damage was evaluated in soft tissues and organs like spleen, liver and kidney cells. The oxidative damage was assessed by selective biochemical parameters by the measurement of lipid peroxidation, reduced glutathione (GSH), glutathione S-transferase (GST) and catalase (CAT) activity in liver. Adult Swiss albino male mice were exposed to sodium fluoride in drinking water at the concentrations of 4, 12 and 20mg/L for 30 consecutive days. Control groups (vehicle and positive) were also included. Animals were sacrificed; bone marrow and soft tissue samples were collected and subjected to series of assays respectively. We observed that NaF exposure, at the various concentrations tested caused a significant increase in the frequency of micronucleus (MN) in polychromatic erythrocytes (PCEs), structural chromosome aberrations in bone marrow cells. With the exception of the spleen cells, DNA damage was observed in bone marrow cells as well as in kidney and liver cells. We found an increase in lipid peroxidation, and catalase activity as well as decrease in glutathione activity (GSH and GST) in liver of mice respectively which were exposed to sodium fluoride. In conclusion, the data obtained clearly documents that NaF exhibits genotoxic activity and enhanced oxidative damage in mouse model.

Cytotoxic, genotoxic and the hemolytic effect of titanium dioxide (TiO2 ) nanoparticles on human erythrocyte and lymphocyte cells in vitro.

With the increasing clinical use of titanium dioxide (TiO2 ) nanoparticles, a better understanding of their safety in the blood stream is required. The present study evaluates the toxic effect of commercially available TiO2 nanoparticles (~100 nm) using a battery of cytotoxic, genotoxic, hemolytic and morphological parameters. The cytotoxic effects of TiO2 nanoparticles in human lymphocyte cells were studied with respect to membrane damage, mitochondrial function, metabolic activity and lysosomal membrane stability. Genotoxicity in lymphocyte cells was quantitated using a comet assay. The mode of cell death (apoptosis/necrosis) was evaluated using PI/Annexin V staining. TiO2 nanoparticles were also evaluated for their hemolytic properties, osmotic fragility and interaction with hemoglobin. Human erythrocyte cells were studied for morphological alterations using atomic force microscopy (AFM). Results suggest that the particles could induce a significant reduction in mitochondrial dehydrogenase activity in human lymphocyte cells. Membrane integrity remained unaffected by nanoparticle treatment. DNA damage and apoptosis were induced by TiO2 nanoparticles in a dose-dependent manner. A study on human erythrocyte cells revealed a hemolytic property of TiO2 nanoparticles characterized by spherocytosis and echinocytosis. Spectral analysis revealed a hemoglobin TiO2 nanoparticle interaction. Our in vitro study results suggest that commercially available blood contacting nanoparticles (TiO2 nanoparticle) should be carefully evaluated for their toxic potential.

Inequality in the golden years: Wealth gradients in disability-free and work-free longevity in the United States.

We study the relationship of wealth with the "quality" of longevity as measured by years after age 65 containing disability or work. By comparing cohorts turning 65 in 1996 and 2006, we observe strong within-cohort gradients of wealth in which the more wealthy live more years disability-free and work more years, yet also experience more work-free years. We document that these gradients steepened over the decade we study. We explore robustness using education as an alternative indicator for socioeconomic status, and rule out certain explanations for these trends by analyzing the effect of health shocks on wealth accumulation.