Acute toxicity and environmental risk of teflubenzuron to Daphnia magna, Poecilia reticulata and Lemna minor in the absence and presence of sediment

This study aimed to estimate the acute toxicity of teflubenzuron (1-(3,5-dichloro-2,4-difluorophenyl)-3-(2,6-difluorobenzoyl)urea) (TFB) for Daphnia magna, Lemna minor and Poecilia reticulata, in the absence and presence of sediment; evaluate the effect of sediment on the TFB bioavailability; and to classify this insecticide according to its environmental poisoning risk for agricultural and aquaculture uses. The tests of TFB acute toxicity were conducted in static system in a completely randomized design with increasing TFB concentrations, and a control group. The TFB has been classified according to the estimated values of EC50 and LC50 by its acute toxicity and environmental risk. The sediment significantly reduced toxicity and bioavailability of TFB in water column. Therefore, the insecticide can be classified as being highly toxic to Daphnia magna, which means the agricultural and aquacultural uses of TFB pose a high risk of environmental toxicity to non-target organisms. However, it was practically non-toxic to L. minor and P. reticulata. © 2013 Copyright Taylor and Francis Group, LLC.

Risk assessment of cadmium toxicity on hepatic and renal tissues of rats

Pollution and industrial practices result in concentrations of metals and other environmental agents that are related to environmental toxicity. A rat bioassay was utilized for the identification of toxic effects of cadmium intake. This demonstrated increased total urinary proteins and increased kidney weights in rats exposed to CdCl2, for 7 days, in drinking water (100 mg/L). Serum creatinine, total and direct bilirubin concentrations and alanine transaminase activity were increased in Cd-exposed rats, indicating renal and hepatic toxicity. It was also observed that lipoperoxide concentrations were increased, while Cu-Zn superoxide dismutase activity was decreased in rats treated with cadmium. This indicated that the renal and hepatic toxicity induced by cadmium involved superoxide radicals. (C) 1998 Academic Press.

草甘膦的土壤酶效应研究

为了探讨当今世界使用量最大的除草剂——草甘膦的土壤环境效应,本文采用室内模拟方法,较为系统地研究了我国4类土壤:褐土、黄绵土、风沙土和红壤,共11个土样中4种主要酶类(脲酶、转化酶、磷酸酶以及脱氢酶)活性与草甘膦间的关系,计算并得到了能够表征土壤轻度污染的生态剂量值ED10。结果表明:非缓冲液法较好地反映了土壤酶的实际情况;草甘膦总体上激活土壤脲酶、转化酶和脱氢酶活性,最大增幅分别为190%、1372%和42%;抑制磷酸酶活性,最大幅度为35%;磷酸酶与草甘膦间为完全抑制作用机理;激活脱氢酶活性揭示出草甘膦导致了土壤中微生物活性增强,从侧面反映出草甘膦是一种毒性较低的农药。计算获得4类供试土壤褐土、黄绵土、风沙土和红壤ED10值分别为168.3、438.5、35.1和141.4mg·kg-1;在一定程度上用土壤酶活性比生物来表征土壤污染程度更敏感。土壤性质对草甘膦的毒性有重要影响。

Proteomic approach to oxidative stress in Daphnia magna

The keystone aquatic organism Daphnia magna is extensively used to assess the toxicity of chemicals. This has recently lead to an increase in the omics literature focusing on daphnids, an increase fuelled by the sequencing of the Daphnia pulex genome. Yet, no omics study has looked directly at oxidative stress (OS) in daphnids, even though OS is of primary importance in the response of aquatic organisms to their changing environment and is often induced by anthropogenic xenobiotics. This thesis thus focuses on the application of redox-proteomics, the study of the oxidative modification of proteins, to D. magna Specifically, daphnids were exposed to copper or paraquat, two well studied prooxidants, and protein carbonyls were labelled with fluorescein-5-thiosemicarbazide prior to twodimensional electrophoresis (2DE). This showed clearly that both compounds affect a different portion of the proteome. The identified proteins indicated that energy metabolism was affected by paraquat, while copper induced a reduction of the heat shock response (heat shock proteins, proteases and chaperones) a counterintuitive result which may be adaptative to metal toxicity in arthropods. The same approach was then applied to the study of the toxicity mechanism of silver nanoparticles (AgNP), an increasingly utilised form of silver with expected environmental toxicity, and its comparison to silver nitrate. The results demonstrate that, although less toxic than silver ions, AgNP toxicity functions through a different mechanism. AgNP toxicity is thus not a product of silver dissolution and increased protein carbonylation indicates that AgNP cause OS. Interestingly three of the four tested compounds altered vitellogenin levels and oxidation. Vitellogenins could thus represent an interesting subproteome for the detection of stress in daphnids. Finally, an experiment with oxidised BSA demonstrates the applicability of solid phase hydrazide in the enrichment of undigested carbonylated proteins.

Avaliação ecotoxicológica de solos contaminados por ibuprofeno

Os produtos farmacêuticos são substâncias químicas muito utilizados em medicina, veterinária e ainda na agricultura. Nos anos 90, foi descoberta a presença de fármacos em meio aquático, verificando-se que a sua remoção nas Estações de Tratamento de Águas Residuais (ETAR) não era completa. Durante as duas últimas décadas foi identificada a presença de mais de oitenta compostos no meio ambiente e actualmente são considerados poluentes emergentes. Podem contaminar solos e águas, depois de serem usados e excretados (inalterados ou metabolizados) por humanos e animais, ou quando são indevidamente lançados directamente no meio ambiente. Os estudos ecotoxicológicos efectuados com estes poluentes têm sido direccionados, sobretudo, para as águas, existindo uma ausência de trabalhos sobre solos. O Ibuprofeno (IB) é um anti-inflamatório não esteróide, utilizado também como analgésico e antipirético, sendo um dos produtos farmacêuticos mais vendidos em todo o mundo, o que justifica a sua forte presença no meio ambiente. Por isso, e dada a ausência de trabalhos ecotoxicológicos de solos contaminados por fármacos, o IB foi o produto farmacêutico selecionado para a realização deste trabalho. A ecotoxicidade pode ser avaliada através de bioensaios. Estes têm a capacidade de avaliar a toxicidade de uma determinada substância de forma global, usando organismos vivos que funcionam como bio-indicadores. O presente trabalho tem como objectivos avaliar o impacte causado nos solos pelo IB, testar a toxicidade de dois processos de descontaminação para remover o referido fármaco dos solos assim como avaliar a toxicidade provocada por águas residuais, de três unidades hospitalares e de uma indústria farmacêutica. Esta avaliação foi efectuada através de ensaios de toxicidade aguda de germinação e de alongamento de raiz de sementes de alface, variedade bola de manteiga (Lactuca sativa), em solo arenoso. Os ensaios de ecotoxicidade aguda em solos contaminados por IB foram realizados para uma gama de concentrações entre 0,1 e 1000 μg/L. Verificou-se uma redução do número de sementes germinadas e do comprimento médio da planta no solo contaminado com 0,5 e 20 μg/L de IB. No solo contaminado com 1000 μg/L de IB observou-se uma redução da germinação, acompanhada por uma indução de crescimento da raiz da espécie Lactuca sativa. Os dois tratamentos de descontaminação de solos, reagente de Fenton e Nanopartículas de ferro zero valente, revelaram toxicidade, tendo-se obtido uma percentagem de germinação entre 32,2 ± 3,5 e 48,5 ± 6,2 e inibição do crescimento da raiz do organismo teste em cerca de 85,0 %. Em relação às águas residuais hospitalares verificou-se uma redução da percentagem de germinação entre 31,1 ± 5,0 e 72,3 ± 12,4 e uma inibição do crescimento da raiz situada entre 13,0 ± 6,4 e 20,2 ± 10,0 %. Para a água residual industrial ocorreu uma inibição da percentagem de germinação de 60,5 ± 13,1, contudo nas plantas germinadas observou-se uma indução do crescimento da raiz de 14,9 ± 7,7 %.

Changing bodies, changing discourses : women's experiences of early menopause

Early menopause has been constructed by discourses of biological determinism as an untimely, but natural, failure of the female body. Medical discourses in particular have interpreted early menopause as a congenital irregularity and a rare anomaly of menopause at midlife. In this thesis I challenge the notion that early menopause is an innate imperfection related only to women’s age. I propose that early menopause is dependent upon the cultural interpretations of individual women and is constituted through the mercurial and multiple discourses of women who have this embodied experience. Moreover, I reveal that early menopause is a contemporary condition and that its location in history is inextricably bound to discourses of risk, naturalism and the self. Further I make the assumption that having an early menopause both affects and is an effect of women’s fertility, sexuality and subjectivity. I have drawn upon a broad range of sources to provide a sociological analysis of early menopause. Literature on early menopause is dominated by positivist discourses, yet many alternate discourses negotiate these influential constructions. I suggest here that the perception of early menopause as a natural fault is merely a construction by medical discourses and does not incorporate the dynamic discourses of early-menopausal women. Moreover, the restriction of early menopause to a genetic female failure excludes the majority of women who have an early menopause through iatrogenisis. This omission occurs through the failure of positivist discourses to accommodate diversity in discourses. Recent sociological and feminist studies have vindicated menopausal women. They have reconstructed menopause through notions of embodiment and have removed the veil of negativity used by the medical sciences to contain menopausal women (Komesaroff, Rothfield and Daly 1997). The visibility of menopausal women, however, remains connected to age. Menopause has been created as a predictable consequence of aging and as such has come to be synonymous with middle age. Nowadays, even men are said to experience menopause at midlife (Carruthers 1996). But early menopause is constituted within the discourses of women who have this experience. Medico-scientific discourses, based upon theories of genetic inevitability, disregard this perspective. Consequently early menopause is subsumed by naturalistic discourses that relate menopause to midlife. Such restraint reflects the unease created by menopause that does not coincide with prescribed life stages. Women's experiences of their changing bodies are largely unheard. Thus, women who have an early menopause are faced with a chasm of ‘cultural non-recognition’ (Fraser 1997). Conjointly with this discursive repression early-menopausal women face social imbalances that are transacted as both cause and consequence of early menopause. In particular the contemporary creation of early menopause is bound to the social and historical location of women as a group. Women are exploited by the institution of medicine, ‘exposure to environmental toxicity’ (Fraser 1997: 11) and commercialization as causes of early menopause. Yet the corporeal effects of practices of risk avoidance (Beck 1993), social practices (Shilling 1993) and Western consumerism (Lupton 1994) fail to be recognized. I address these problematics through a poststructural and feminist critique that assumes moments of commonality among women, while at the same time recognizes shifting and multiple differences (Nicholson 1999). I suggest here that early menopause falls into cultural misrecognition in Fraser's (1997) terms and argue that it is united concurrently with the gender injustice of androcentrism (Fraser 1997: 21). Fraser (1997: 16) suggests that it is only by relating these dual problematics that we are able to make sense of current dilemmas. Thus I have critiqued early menopause through a connection between individual embodied experiences of early menopause and early menopause as a modern phenomenon that is specific to women. I have attempted to unravel these arguments that simultaneously call to ‘... abolish gender differentiation and to valorize gender specificity’ (Fraser 1997: 21) while at the same time acknowledging their interconnectedness. An approach of merely combining women’s discourses with overarching social issues would be inadequate as not only do these problematics intersect but they also can be opposed. As Fraser (1997: 25) notes with her theory, redressing one aspect of cultural or social analysis can further imbalance another. For instance making visible the diversity and uniqueness of individual experiences of early menopause could detract from acknowledging the contemporary construction of early menopause through social inequality. Crucial to this understanding is a destabilizing of the binary construction of differences between the sexes that makes way for a reconstruction of early menopause through ‘sexual slippage’ (Matus 1995). In this thesis I look for a subtlety between the particular and the collective that views early menopause as concurrently a singular and changeable experience as well as imbedded in social practice. I suggest that these concepts are entwined as interactive effects of early menopause. Thus I have analyzed the bivalent problematics of the embodiment and social location of early menopause as imbricated, dynamic and unending discourses. From this perspective I reviewed the literature that was available on early menopause. In Chapter One I look to descriptions of early menopause and note that it has disappeared into a conglomeration of disparate, mostly medical, discourses that are contradictory. Nevertheless medical discourses offer ‘conclusive’ definitions of early menopause that are based on naturalistic views of the body (Shilling 1994). The determinants used are inconsistent and do not include women's discourses of early menopause. Thus, dominant medical discourses obscure women’s embodied experiences of early menopause and ignore the contemporary causes of early menopause. In Chapter Two I examine the causes of early menopause as a way of explaining the disparity between medical discourses and my anecdotal observations of early menopause as a fairly common contemporary occurrence. The relatively recent escalation in gynaecological surgery, especially hysterectomy, appears to account almost single-handedly for early menopause as a current phenomenon. Moreover, the extraordinary number of women who have their uterus removed at hysterectomy can be interpreted as a modern implementation of ancient anxieties. Women's sexuality has been constructed throughout history as problematic and this unease has been translated through women's bodies as dangerous and in need of control (Greer 1992). Thus social concerns which have evolved historically have emerged through the representation of a woman's uterus as an unseen, dark and mysterious risk (Beck 1993). Medical discourses define this risk and are able to negate the so-called dangers of women's sexuality through the surgical removal of their organs. Widespread negotiation of medical discourses is apparent, as hysterectomy in the modern Western world is the most common of all surgical operations (Hufnagel 1989). It is overwhelmingly the most common cause of early menopause as well. I examine also the historical condemnation of infertile women and how this anxiety has been transposed to the modern world through the commercialization of reproduction. Transactions of this social unease can cause early menopause. For instance the medical technology of in-vitro fertilization (I.V.F.) has been offered as a panacea for the infertility of early menopause but, paradoxically, can cause early menopause as well. Conception through technology has been normalized as a viable option for women who are unable to conceive and understandings of I.V.F. have moved into everyday discourse. Medical discourses have constructed fertility as a saleable item and infertile women expect that they can purchase this merchandise. Human eggs have become lucrative commodities that now are available in the market place. Egg ‘donation’ for I.V.F. programs can hasten the attrition rate of eggs and can cause early menopause in some pre-menopausal women (Rowland 1992: 24). Even the recycling of a woman’s uterus supposedly has become a possibility through the transferring of this ‘used’ organ at hysterectomy to a recipient woman who can use the other woman’s uterus as a ‘gestational garage’ (Rogers 1998). In this way women have been disembodied as mechanical systems with inter-changeable body parts and the potentially detrimental consequences of these commercial transactions are ignored. In addition I show how early menopause can be caused by the connection between the self and the social structure. Women's subjectivity is constituted through the cultural discourses available to them and these discourses affect social behaviour (Lupton 1995). For instance smoking and dieting have been identified as causes of early menopause. These activities have been related to the creation of women’s bodies as hetero-sexually desirable and are endemic to young women (Evans-Young 1995). This suggests that cultural causes of early menopause are transactions of sexual politics. Yet there is a paucity of literature that acknowledges the relationship between women’s subjectivity and early menopause. Thus the second chapter exposes a link between sexual politics and causes of early menopause through women's relationships with risk, naturalism and the self. In Chapter Three I deconstruct early menopause through theoretical considerations. I rely on an overarching poststructuralism that embraces the concept of fragmented plural discourses and the subjectivity of menopausal women as a continuous process (Komesaroff 1997: 61). I have woven these variables through broad feminist critiques (Leonard 1997). Through this eclectic approach I hoped to find some loose alignment between the corporeal, ontological and embodied dimensions of early menopause. The recurring themes of sexuality, fertility and subjectivity emerge through deconstructing discourses of sexual difference as immutable and non-negotiable; exposing ‘premature ovarian failure’ as a discursive construction that censures early-menopausal women; and acknowledging the discourses of individual women as unique, diverse and dynamic. I looked to a method of exposing some of these individual discourses and in Chapter Four I describe a critical research process aimed at understanding early menopause as a lived experience. In the remaining chapters I align these ontological arguments with an analysis of the discourses of women who had experienced or were experiencing an early menopause. This section partly relieves the ‘cultural non-recognition’ of the discourses of early-menopausal women. I recorded the narratives of fifty early-menopausal women through in-depth interviews and used this empirical data to direct the study. This data provides the opportunity to understand early menopause as an assortment of embodied experiences. For instance women’s experiences of age at commencement of menopause spanned over three and half decades. They did not reflect the age specifications prescribed by medical discourses. Rather women interpreted their experiences within their own discourses and determined their menopause as early based upon the expectations of their cultural context. Many of the women experienced changes attributed to menopause at midlife. It was not these changes that were significant to early-menopausal women it was how each woman translated these changes that provided meanings of early menopause. In Chapter Five I introduce the women through a table that connects the varying experiences of each woman. This profile shows that, in the main, the women’s experiences of early menopause were unexpected. I suggest that this is due to the disparity between early-menopausal women’s experiences and the current age and social norms of menopause. By bracketing the women into cohorts patterns emerged displaying differences between women who had menopause in their teens, twenties, thirties and forties. Adolescent women had intense feelings of abnormality and despair. Women who were in their twenties were less devastated by menopause than the younger women but described their sexuality and self-identity as changing. And although some women in their thirties were shocked or dismayed to have an early menopause others were ambivalent or happy. These women also described their sexuality and self-identity through changing discourses. A number of the women who were in their forties said that they were ‘too young for the menopause’ but were far less despondent than the younger women. It seemed that the greater the distance between age norms and social norms the more negatively women responded. Age norms that determine the social norms of women's lives through a ‘biological clock’ are constructed to reflect social values. But age is a social construction that changes over time. Thus it would appear that women’s changing bodies and changing discourses of early menopause are in the process of recreating age and social norms around menopause. In Chapter Six I draw upon women’s narratives that describe a connection between early menopause and sexuality. Yet the respondents were not unified in their constructions of sexuality. For instance a number of the women rejected the containment of their sexuality as absolute and defined in terms of bi-lateral hetero-sexual opposition. The discourses of these women constructed their sexuality as continuously flexible. Some early-menopausal women described this sexual mobility as an equivocal relationship between their sexuality, reproductive capacity and female organs. Other women articulated their sexuality as vacillating, ambiguous and unrepresentative of the so-called ‘true woman’. Several felt that they were not meant to have female reproductive organs at all. Nearly one third of the women had had their uterus removed at hysterectomy and the reproductive organs of two women were rudimentary. Women’s narratives showed that the social value of fertility influences constructions of early menopause. In Chapter Seven I record the contrast between the poignant responses of women who wished to have a baby of their own and other women who resisted discourses that entwine reproductivity with being a woman. For instance some women negotiated fertility through economic discourses of consumerism with the expectation that they could purchase conception as a commodity. Other women welcomed their early menopause as freedom from contraceptive concerns and others had no interest in reproduction at all. Thus discord arose through discourses that problematize early-menopausal women as non-reproductive and discourses that value variability. In addition many of the women’s accounts constructed their subjectivity as mobile, challenging the notion that discourses of the self are immutable. Chapter Eight presents narratives which suggest that the subjectivity of many women was altered continuously by early menopause. Yet some of the women rejected the construction of their subjectivity as unfluctuating. These contradictions reflect the uncertainties of the contemporary world. Nevertheless most respondents found that the tethering of menopause to constructions of midlife was incongruous with their own experiences. Many women refused to accept the label of social redundancy attached to middle-aged women. They moved their subjectivity beyond the reproductive body to a shifting and tractable identity of the self. This thesis demonstrates that the medical construction of early menopause as a rare and natural female flaw varies from women's experiences which suggest that early menopause is common and discursively constructed. This disparity has occurred through the privilege placed upon the construction of bodies as immutable and sexually static. This privileging has obscured the multi-dimensional causes of early menopause and given preference to a mono-causal theory. By exposing the variety of causes of early menopause the medical construction of women through a universal and unalterable body of reproduction is challenged. Moreover, women's discourses of early menopause demonstrate that the medical reduction of early menopause to a spontaneous bio-chemical malfunction has ignored the volatility of women’s embodied experiences. Women experience early menopause variously and through mercurial discourses. I suggest here that women's discourses of their experiences of early menopause reflect recurring and restructuring philosophical quandaries of fertility, sexuality and subjectivity. While there can be no representative claims made from this thesis it contributes to an understanding of the embodied experiences of early menopause. It provides an understanding of the creation of early menopause through social practices and goes part way to redressing the problematics of what Fraser terms ‘cultural non-recognition’. But, more importantly, it acknowledges early menopause as a variety of experiences where women interpret their changing bodies through changing discourses.

An investigation of porphyrinuria in Australian children with autism

Two recent studies, from France (Nataf et al., 200614. Nataf, R., Skorupka, C., Amet, L., Lam, A., Springbett, A. and Lathe, R. 2006. Porphyrinuria in childhood autistic disorder: Implications for environmental toxicity. Toxicol. Appl. Pharmacol., 214: 99–108. [CrossRef], [PubMed], [Web of Science ®] View all references) and the United States (Geier & Geier, 20079. Geier, D. A. and Geier, M. R. 2007. A prospective study of mercury toxicity biomarkers in autistic spectrum disorders. J. Toxicol. Environ. Health, A, 70: 1723–1730. [Taylor & Francis Online], [PubMed], [Web of Science ®] View all references), identified atypical urinary porphyrin profiles in children with an autism spectrum disorder (ASD). These profiles serve as an indirect measure of environmental toxicity generally, and mercury (Hg) toxicity specifically, with the latter being a variable proposed as a causal mechanism of ASD (Bernard et al., 20012. Bernard, S., Enayati, A., Redwood, L., Roger, H. and Binstock, T. 2001. Autism: A novel form of mercury poisoning. Med. Hypoth., 56: 462–471. [CrossRef], [PubMed], [Web of Science ®] View all references; Mutter et al., 200515. Mutter, J., Naumann, J., Schneider, R., Walach, H. and Haley, B. 2005. Mercury and autism: Accelerating evidence?. Neuroendocrinol. Lett., 26: 439–446. [PubMed], [Web of Science ®] View all references). To examine whether this phenomenon occurred in a sample of Australian children with ASD, an analysis of urinary porphyrin profiles was conducted. A consistent trend in abnormal porphyrin levels was evidenced when data was compared with those previously reported in the literature. The results are suggestive of environmental toxic exposure impairing heme synthesis. Three independent studies from three continents have now demonstrated that porphyrinuria is concomitant with ASD, and that Hg may be a likely xenobiotic to produce porphyrin profiles of this nature.

Are urinary porphyrins a valid diagnostic biomarker of autism spectrum disorder?

A fundamental challenge to the timely diagnosis of Autism Spectrum Disorder (ASD) is the reliance on the observation of a set of aberrant behavior. Consequently, the diagnostic process requires that the child reach an age where the behaviors would typically be exhibited. The identification of a reliable biological marker (biomarker) could be of considerable benefit to the diagnostic process. As a diagnostic biomarker, porphyrins present an attractive prospect as previous studies have reported consistent findings of children with ASD showing significant elevations in porphyrin levels in contrast to controls. Furthermore, there is some evidence that ASD severity may be associated with porphyrins, which would be a valuable characteristic of any ASD biomarker. Importantly, for practical use, porphyrins can be tested non-invasively via a sample of urine. The present study sought to investigate whether porphyrin profiles can reliably be used to (a) differentiate ASD cases from healthy controls; and (b) predict ASD severity. The study compared the porphyrin levels of three groups of children aged 2-6 years: Group 1-children diagnosed with ASD (n = 70); Group 2-healthy, normally developing siblings of children diagnosed with ASD (n = 36); and Group 3-healthy, normally developing children with no known blood relative diagnosed with ASD (n = 54). The results of logistic regression analyses failed to find support for the hypotheses that porphyrin levels could be used as a valid tool to detect ASD cases or predict severity. Autism Res 2014, 7: 535-542. © 2014 International Society for Autism Research, Wiley Periodicals, Inc.

Controlled release system for ametryn using polymer microspheres: Preparation, characterization and release kinetics in water

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Differential/combined effect of water contamination with cadmium and nickel on tissues of rats

The contamination of water by metal compounds is a worldwide environmental problem. Concentrations of metals are widely related to biochemical values which are used in disease diagnosis due to environmental toxicity. The acute combined effects of cadmium and nickel on biochemical parameters were determined and compared with those of Cd2+ or Ni2+ alone in rats. Male adult rats were given drinking solutions of CdCl2 [Cd(II) cation, 100 mg/liter] or NiSO4 [Ni(II) cation, 100 mg/liter]. For the combined treatment, the animals (Ni+Cd) received both Ni(II)) cation (100 mg/liter) and Cd(II) cation (100 mg/liter). Nickel treatment induced increased alanine transaminase (ALT) activity and hepatotoxicity, but not renal injury. In contrast, cadmium exposure produced hepatic, renal and myocardial damage, characterized by increased creatinine, total and direct bilirubin concentrations and increased ALT and lactate dehydrogenase (LDH) activities. The combined effect Ni-Cd is less toxic than cadmium alone, suggesting antagonism between these toxicants. The toxicity of nickel and cadmium, alone and in combination, decreased Cu-Zn superoxide dismutase (SOD) activity and increased lipoperoxide formation. (C) 1998 Elsevier B.V. Ltd. All rights reserved.

TOXIC EFFECTS OF WATER EUTROPHICATION ON PANCREATIC, HEPATIC AND OSTEOGENIC TISSUES OF RATS

Pollution, industrial solvents, concentrations of metals and other environmental agents are widely related to biochemicals values which are used in disease diagnosis of environmental toxicity. A rat bioassay validated for the identification of toxic effects of eutrophication revealed increased serum activities of amylase, alanine transaminase (BLT) and alkaline phosphatase (ALP) in rats that received algae, filtered water and nickel or cadmium from drinking water. Serum Cu-Zn superoxide dismutase activity decreased from its basal level of 40.8 +/- 2.3 to 26.4 U/mg protein, at 7 days of algae and at 48 hr of nickel and cadmium water ingestion. The observation that lipoperoxide concentration was not altered in rats treated with filtered water, while amylase, ALT and ALP were increased in these rats and in those treated with nickel or cadmium, indicated that pancreatic, hepatic and osteogenic lesions by eutrophication were not related to superoxide radicals, and might be due to a novel toxic environmental agent found in filtered and non-filtered algae water.

Evaluation of Cyto- and Genotoxicity of Poly(lactide-co-glycolide) Nanoparticles

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Superoxide radical and nephrotoxic effect of cadmium exposure

Pollution and industrial practices result in concentrations of metals and other environmental agents that are related to environmental toxicity. Concentrations of metals are widely related to biochemicals values which are used in disease diagnosis due to environmental toxicity. This work was carried out in order to verify the nephrotoxic effect of cadmium and to clarify the contribution of reactive oxygen species (ROS) in this process. Cadmium chloride was tested for nephrotoxic damage in rats by a single intraperitoneal (i.p.) injection Cd 2+ (2 mg/kg) and oral intake (Cd2 +-100 mg/l-from CdCl 2). The cadmium-induced biochemical alterations included significant increased levels of serum creatinine concentrations, in rats with i.p. injection. Total urinary protein concentrations were only increased in rats with cadmium intake. Lipoperoxide was also increased after 3 and 7 days of the Cd 2+ treatment. No changes were observed in glutathione peroxidase activities. Cadmium-induced damage might be due to superoxide radicals (O 2 -), since Cu-Zn superoxide dismutase activities were decreased by Cd 2+ treatment. This study allows tentative conclusions to be drawn regarding which reactive oxygen metabolites play a role in cadmium nephrotoxicity. We concluded that the superoxide radical may be produced as a mediator of nephrotoxic action of cadmium.

Organotypic Modeling Platform for Adverse Outcome Pathways of Male Reproductive and Developmental Processes

Thesis (Master's)--University of Washington, 2016-06

Real-time biosensor for the assessment of nanotoxicity and cancer electrotherapy

Knowledge of cell electronics has led to their integration to medicine either by physically interfacing electronic devices with biological systems or by using electronics for both detection and characterization of biological materials. In this dissertation, an electrical impedance sensor (EIS) was used to measure the electrode surface impedance changes from cell samples of human and environmental toxicity of nanoscale materials in 2D and 3D cell culture models. The impedimetric response of human lung fibroblasts and rainbow trout gill epithelial cells when exposed to various nanomaterials was tested to determine their kinetic effects towards the cells and to demonstrate the biosensor's ability to monitor nanotoxicity in real-time. Further, the EIS allowed rapid, real-time and multi-sample analysis creating a versatile, noninvasive tool that is able to provide quantitative information with respect to alteration in cellular function. We then extended the application of the unique capabilities of the EIS to do real-time analysis of cancer cell response to externally applied alternating electric fields at different intermediate frequencies and low-intensity. Decreases in the growth profiles of the ovarian and breast cancer cells were observed with the application of 200 and 100 kHz, respectively, indicating specific inhibitory effects on dividing cells in culture in contrast to the non-cancerous HUVECs and mammary epithelial cells. We then sought to enhance the effects of the electric field by altering the cancer cell's electronegative membrane properties with HER2 antibody functionalized nanoparticles. An Annexin V/EthD-III assay and zeta potential were performed to determine the cell death mechanism indicating apoptosis and a decrease in zeta potential with the incorporation of the nanoparticles. With more negatively charged HER2-AuNPs attached to the cancer cell membrane, the decrease in membrane potential would thus leave the cells more vulnerable to the detrimental effects of the applied electric field due to the decrease in surface charge. Therefore, by altering the cell membrane potential, one could possibly control the fate of the cell. This whole cell-based biosensor will enhance our understanding of the responsiveness of cancer cells to electric field therapy and demonstrate potential therapeutic opportunities for electric field therapy in the treatment of cancer.