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Exposure Leads (exposure + lead)
Selected AbstractsMethanol exposure interferes with morphological cell movements in the Drosophila embryo and causes increased apoptosis in the CNSDEVELOPMENTAL NEUROBIOLOGY, Issue 3 2004Dervla M. Mellerick Abstract Despite the significant contributions of tissue culture and bacterial models to toxicology, whole animal models for developmental neurotoxins are limited in availability and ease of experimentation. Because Drosophila is a well understood model for embryonic development that is highly accessible, we asked whether it could be used to study methanol developmental neurotoxicity. In the presence of 4% methanol, approximately 35% of embryos die and methanol exposure leads to severe CNS defects in about half those embryos, where the longitudinal connectives are dorsally displaced and commissure formation is severely reduced. In addition, a range of morphological defects in other germ layers is seen, and cell movement is adversely affected by methanol exposure. Although we did not find any evidence to suggest that methanol exposure affects the capacity of neuroblasts to divide or induces inappropriate apoptosis in these cells, in the CNS of germ band retracted embryos, the number of apoptotic nuclei is significantly increased in methanol-exposed embryos in comparison to controls, particularly in and adjacent to the ventral midline. Apoptosis contributes significantly to methanol neurotoxicity because embryos lacking the cell death genes grim, hid, and reaper have milder CNS defects resulting from methanol exposure than wild-type embryos. Our data suggest that when neurons and glia are severely adversely affected by methanol exposure, the damaged cells are cleared by apoptosis, leading to embryonic death. Thus, the Drosophila embryo may prove useful in identifying and unraveling mechanistic aspects of developmental neurotoxicity, specifically in relation to methanol toxicity. © 2004 Wiley Periodicals, Inc. J Neurobiol 60: 308,318, 2004 [source] Ethanol preference in C. elegansGENES, BRAIN AND BEHAVIOR, Issue 6 2009J. Lee Caenorhabditis elegans senses multiple environmental stimuli through sensory systems and rapidly changes its behaviors for survival. With a simple and well-characterized nervous system, C. elegans is a suitable animal model for studying behavioral plasticity. Previous studies have shown acute neurodepressive effects of ethanol on multiple behaviors of C. elegans similar to the effect of ethanol on other organisms. Caenorhabditis elegans also develops ethanol tolerance during continuous exposure to ethanol. In mammals, chronic ethanol exposure leads to ethanol tolerance as well as increased ethanol consumption. Ethanol preference is associated with the development of tolerance and may lead to the development of ethanol dependence. In this study, we show that C. elegans is a useful model organism for studying chronic effects of ethanol, including the development of ethanol preference. We designed a behavioral assay for testing ethanol preference after prolonged ethanol exposure. Despite baseline aversive responses to ethanol, animals show ethanol preference after 4 h of pre-exposure to ethanol and exhibit significantly enhanced preference for ethanol after a lifetime of ethanol exposure. The cat-2 and tph-1 mutant animals have defects in the synthetic enzymes for dopamine and serotonin, respectively. These mutants are deficient in the development of ethanol preference, indicating that dopamine and serotonin are required for this form of behavioral plasticity. [source] Behind the Third-Person Effect: Differentiating Perceptual Processes for Self and OtherJOURNAL OF COMMUNICATION, Issue 4 2001Douglas M. McLeod This study investigated factors related to two types of judgments that make up the third-person perception: media effects on others and effects on self. Specifically, separate regression path models revealed that estimates of effects on others are based on a relatively naive schema for media effects that is similar to the "magic bullet" model of media effects (i.e., more exposure leads to greater effects). On the other hand, assessing effects on self involves a more complex, conditional effects model. The different pattern of results for the self and other models reflect the "fundamental attribution error" from attribution theory. The path models also extend results from the perceptual component to the behavioral component of the third-person effect by linking the explanatory variables to support for censorship. Both models showed that paternalistic attitudes were the strongest predictor of support for censorship. [source] Changes in endoplasmic reticulum stress proteins and aldolase A in cells exposed to dopamineJOURNAL OF NEUROCHEMISTRY, Issue 1 2008April A. Dukes Abstract In Parkinson's disease, oxidative stress is implicated in protein misfolding and aggregation, which may activate the unfolded protein response by the endoplasmic reticulum (ER). Dopamine (DA) can initiate oxidative stress via H2O2 formation by DA metabolism and by oxidation into DA quinone. We have previously shown that DA quinone induces oxidative protein modification, mitochondrial dysfunction in vitro, and dopaminergic cell toxicity in vivo and in vitro. In this study, we used cysteine- and lysine-reactive fluorescent dyes with 2D difference in-gel electrophoresis, mass spectrometry, and peptide mass fingerprint analysis to identify proteins in PC12 cell mitochondrial-enriched fractions that were altered in abundance following DA exposure (150 ,M, 16 h). Quantitative changes in proteins labeled with fluorescent dyes indicated increases in a subset of proteins after DA exposure: calreticulin, ERp29, ERp99, Grp58, Grp78, Grp94 and Orp150 (149,260%), and decreased levels of aldolase A (39,42%). Changes in levels of several proteins detected by 2D difference in-gel electrophoresis were confirmed by western blot. Using this unbiased proteomics approach, our findings demonstrated that in PC12 cells, DA exposure leads to a cellular response indicative of ER stress prior to the onset of cell death, providing a potential link between DA and the unfolded protein response in the pathogenesis of Parkinson's disease. [source] Fetal alcohol syndrome and developing craniofacial and dental structures , a reviewORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 4 2006LB Sant'Anna Structured abstract Authors ,, Sant'Anna LB, Tosello DO Objectives ,, Fetal alcohol syndrome (FAS) is a collection of signs and symptoms seen in children exposed to alcohol in the prenatal period. It is characterized mainly by a distinct pattern of craniofacial malformations, physical and mental retardation. However, with the increased incidence of FAS, there is a great variation in the clinical features of FAS. Design ,, Narrative review. Results ,, This review describes data from clinical and experimental studies, and in vitro models. Experimental studies have shown that alcohol has a direct toxic effect on the ectodermal and mesodermal cells of the developing embryo, particularly in the cells destined to give rise to dentofacial structures (i.e. cranial neural crest cells). Other effects, such as, abnormal pattern of cranial and mandibular growth and altered odontogenesis are described in detail. The exact mechanism by which alcohol induces its teratogenic effects remains still unknown. The possible mechanisms are outlined here, with an emphasis on the developing face and tooth. Possible future research directions and treatment strategies are also discussed. Conclusion ,, Early identification of children affected by prenatal alcohol exposure leads to interventions, services, and improved outcomes. FAS can be prevented with the elimination of alcohol consumption during pregnancy. We need to provide education, target high-risk groups, and make this issue a high priority in terms of public health. [source] Effect of UVA or UVB Irradiation on Cutaneous Lipids in Films or in SolutionPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2010Chloé Merle The barrier function of the skin is largely due to the stratum corneum which is essentially composed of lipids. Different external factors, such as UV irradiation, affect this skin layer and are responsible for a destabilization of the supramolecular organization of its constituted lipids. In this work, mass spectrometry and infrared spectroscopy are combined to study the correlation between the formation of oxidative compounds by UV irradiation and the lipid organization. Experiments were carried out on unsaturated lipids in film or solution form, exposed to UVA or UVB irradiation. UV exposure leads to the formation of oxygenated entities in the case of lipids with an unsaturated fatty acid moiety, resulting in a decrease in their packing which is greater when the lipids are in solution. The packing decrease is even greater following UVB irradiation. [source] Gestational stage sensitivity to ultrasound effect on postnatal growth and development of miceBIRTH DEFECTS RESEARCH, Issue 8 2006Suresh Rao Abstract BACKGROUND: An experiment was conducted to find out whether ultrasound exposure leads to changes in postnatal growth and development in the mouse. METHODS: A total of 15 pregnant Swiss albino mice were exposed to diagnostic levels of ultrasound (3.5 MHz, 65 mW/cm2, ISPTP = 1 mW/cm2 Intensity(Spatial Peak-Temporal Peak), ISATA = 240 mW/cm2 Intensity(Spatial Average-Temporal Average)) for 30 min for a single day between days 10 and 18 of gestation (GD 10,18). Virgin female mice were placed with same age group males for mating in the ratio 2 females : 1 male and examined the next morning for the presence of vaginal plug, a sign of successful copulation. The females with vaginal plugs were separated and labeled as 0-day pregnant. Maternal vaginal temperature was also measured. A sham exposed control group of 15 pregnant mice was maintained for comparison. All exposed as well as control animals were left to complete gestation and parturition. Their offspring were used in our further studies. They were monitored during early postnatal life for standard developmental markers, postnatal mortality, body weight, body length, head length, and head width, and growth restriction was recorded up to 6 weeks of age. RESULTS: An exposure to ultrasound induced nonsignificant deviations in the maternal vaginal temperature or developmental markers. Significant low birth weight was observed in the present study, after exposure at GD 11, 12, 14, and 16. However, 14 and 16 days postcoitus during the fetal period appears to be the most sensitive to the ultrasound effect, in view of the number of different effects as well as severity of most of the observed effects when exposed on these gestation days. CONCLUSIONS: The results indicate that diagnostic ultrasound can induce harmful effects on mouse growth and development when given at certain critical periods of gestation. Birth Defects Research (Part A) 76:602,608, 2006. © 2006 Wiley-Liss, Inc. [source] Interleukin1-Induced apoptosis of keratocytes: effect of biglycanACTA OPHTHALMOLOGICA, Issue 2007M KOULIKOVSKA Purpose: Biglycan is absent in the normal cornea, but UVR exposure leads to a significant expression of the biglycan gene in the rabbit cornea, an effect that decreases after healing is completed, indicating the envolvement of biglycan in the corneal repair process. In the present study, we have investigated possible involvement of biglycan in the modulation of the survival of keratocytes. Methods: Keratocytes were grown either under serum free conditions to obtain quiescent keratocyte cell culture or in the presence of 10% fetal bovine serum to induce keratocyte transformation into myofibroblasts. Myofibroblastic phenotype was confirmed by immunocytochemistry with anti-alpha-smooth muscle actin antibodies. Cell death was induced in both cell cultures by interleukin-1 in the presence or absence of biglycan. Histone-associated DNA fragments were assayed by using a cell death detection ELISA. Results: Quantification of histone-associated DNA fragments by the cell death detection ELISA showed that biglycan strongly protected quiescent keratocytes from dying whereas it enhanced the death rate of transformed keratocytes. Apoptotic death rate was elevated after the addition of IL-1 in both keratocyte and myofibroblast cell cultures. Co-incubation with biglycan markedly reduced the number of apoptotic keratocytes but markedly increased the number of apoptotic myofibroblasts. Conclusions: IL-1-induces apoptosis of both quiescent and transformed keratocytes. However, biglycan has differential effect on apoptosis of these two cell types. [source] | |||||||||||||