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ABSTRACT: INTRODUCTION: Sleep disorders are associated with various human pathologies and interfere with biological processes essential for health and quality of life. On the other hand, cancer is one of the most common diseases worldwide with an average of 1,500 deaths per day in the USA. Is there a factor common to both sleep disorders and cancer that serves to link these conditions? DISCUSSION: It is a normal process for cellular metabolism to produce reactive oxidant series (ROS). However, when the production of ROS overcomes the antioxidant capacity of the cell to eliminate these products, the resulting state is called oxidative stress. Oxidative DNA damage may participate in ROS-induced carcinogenesis. Moreover, ROS are also produced in the sleep deprivation process. The aim of this article is to review pathways and mechanisms that may point to oxidative stress as a link between sleep deprivation and cancer.
Sleep And Breathing 02/2013; · 1.84 Impact Factor
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ABSTRACT: Oral cancer is a common neoplasm worldwide. Its incidence and mortality have also increased over the past decades. It is characterized by poor prognosis and a low survival rate despite sophisticated surgical and radiotherapeutic modalities. Metastasis of oral cancer is a complex process involving detachment of cells from tumor tissue, regulation of cell motility and invasion, proliferation and evasion through the lymphatic system or blood vessels. In this review, we will focus on the current knowledge in metastasis from oral cancer regarding facts, such as incidence; stage, histopathology and grade of primary tumor; clinical manifestations; diagnosis; and treatment. Certainly, such information will contribute to the understanding of oral cancer pathogenesis.
Cancer genomics & proteomics. 09/2012; 9(5):329-35.
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ABSTRACT: The aim of the present study was to comparatively evaluate genomic damage (micronucleus) and cellular death (pyknosis, karyolysis and karyorrhexis) in exfoliated oral mucosa cells from hairdressers using two different anatomic buccal sites: cheek mucosa and lateral border of the tongue. A total of 28 hairdressers and 30 health controls (non-exposed individuals) were included in this setting. Individuals had epithelial cells from the cheek and lateral border of the tongue mechanically exfoliated, placed in fixative and dropped in clean slides that were checked for the previously mentioned nuclear phenotypes. The results pointed out statistically significant differences (p < 0.05) of micronucleated oral mucosa cells from hairdressers in the lateral border of the tongue. Exposure to hair dyes caused an increase of other nuclear alterations closely related to cytotoxicity, such as karrhyorexis, pyknosis and karyolysis in both the oral sites evaluated. In summary, these data indicate that hairdressers are occupationally exposed to agents that are genotoxic and cytotoxic. It seems that the lateral border of the tongue is a more sensitive site to the genotoxic and cytotoxic effects of hair dyes.
Toxicology mechanisms and methods 08/2012; · 1.03 Impact Factor
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ABSTRACT: Titanium is known to possess excellent biocompatibility as a result of corrosion resistance, lack of allergenicity when compared with many other metals. Fluoride is well known as a specific and effective caries prophylactic agent and its systemic application has been recommended widely over recent decades. Nevertheless, high fluoride concentrations impair the corrosion resistance of titanium. The purpose of this article is to summarize the current data regarding the influence of fluoride on titanium corrosion process in the last 5 years. These data demonstrate noxious effects induced by high fluoride concentration as well as low pH in the oral cavity. Therefore, such conditions should be considered when prophylactic actions are administrated in patients containing titanium implants or other dental devices.
Biology of Metals 07/2012; 25(5):859-62. · 3.17 Impact Factor
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ABSTRACT: This study assessed the genotoxic and cytotoxic potential of three different glass ionomer cements used in Orthodontics (Vidrion C, OptiBand, and Band-Lok).
The tested cements were exposed in vitro to mouse fibroblast cells for 1 h at 37°C. The genotoxicity and cytotoxicity were evaluated by means of the single cell gel (Comet Assay) and the trypan blue exclusion test, respectively. All data were assessed by the Kruskal-Wallis non-parametric test, followed by Dunn's test. P < 0.05 was considered for statistical significance.
Significant statistically differences (P < 0.05) in cytotoxicity were observed for both Vidrion C powder and liquid at the tested concentrations, with exception to the group presenting the lowest powder concentration. OptiBand similarly presented induced cellular death at the highest tested concentration for paste A (P < 0.05). Band-Lok paste B was also able to induce cytotoxicity at the highest tested concentration. Regarding the comet assay, Band-Lok paste B and OptiBand paste A resulted in increased DNA injury (P < 0.05).
The obtained results support the thought that some glass ionomer cement components present both genotoxic and cytotoxic effects when in high concentrations. Since DNA damage and cellular death are important events during oncogenesis, this study represents relevant contribution to estimate the real risks induced by these materials upon cellular systems.
Dental research journal 07/2012; 9(4):393-8.
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ABSTRACT: Skin performs a host of primordial functions that keep the body alive. Morphine is a drug with immunosuppressant properties whose chronic use may lead to increased infection and delayed wound healing. Sleep is a fundamental biological phenomenon that promotes the integrity of several bodily functions. Sleep deprivation adversely affects several systems, particularly the immune system. The aim of this study was to perform an immunohistochemical evaluation on the expression of inducible nitric oxide synthase and cyclooxygenase-2 in skin of sleep-deprived mice and mice chronically treated with morphine. Adult hairless male mice were distributed into the following groups: Control, morphine, sleep-deprived, and morphine + SD. Morphine (10 mg/kg, subcutaneous) was injected every 12 h for 9 days. Morphine induced immunoexpression of cyclooxygenase-2 and nitric oxide synthase. Sleep deprivation did not modulate outcomes induced by morphine. Morphine, not sleep loss, induces cyclooxygenase-2 and nitric oxide synthase immunoexpression in the skin of hairless mice.
Toxicology mechanisms and methods 06/2012; 22(8):577-83. · 1.03 Impact Factor
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ABSTRACT: Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alfa-iduronidase (IDUA), which leads to intralysosomal accumulation
of glycosaminoglycans. Some studies have revealed that oxidative stress plays an important role in MPS I. However, the mechanisms
by which these alterations occur are still not fully understood. The aim of this study was to analyze genomic instability
in blood cells from murine model of MPS I by single cell gel (comet) assay and micronucleus test. The results pointed out
genetic damage in blood cells as depicted by the single cell gel (comet) assay results. By contrast, no increase of micronucleated
cells were found in mouse blood cells when compared to negative control. Taken together, our results suggest that IDUA deficiency
induces genomic damage in blood cells. Certainly, this finding offers new insights into the mechanisms underlying the relation
between IDUA deficiency and clinical manifestations that can occur in MPS I patients.
KeywordsMucopolysaccharidosis–Blood cells–Genomic damage
Journal of Molecular Histology 04/2012; 42(6):575-578. · 1.48 Impact Factor
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ABSTRACT: The interaction between sleep deprivation and epilepsy has been well described in electrophysiological studies, but the mechanisms underlying this association remain unclear. The present study evaluated the effects of sleep deprivation on locomotor activity and genetic damage in the brains of rats treated with saline or pilocarpine-induced status epilepticus (SE). After 50 days of pilocarpine or saline treatment, both groups were assigned randomly to total sleep deprivation (TSD) for 6 h, paradoxical sleep deprivation (PSD) for 24 h, or be kept in their home cages. Locomotor activity was assessed with the open field test followed by resection of brain for quantification of genetic damage by the single cell gel electrophoresis (comet) assay. Status epilepticus induced significant hyperactivity in the open field test and caused genetic damage in the brain. Sleep deprivation procedures (TSD and PSD) did not affect locomotor activity in epileptic or healthy rats, but resulted in significant DNA damage in brain cells. Although PSD had this effect in both vehicle and epileptic groups, TSD caused DNA damage only in epileptic rats. In conclusion, our results revealed that, despite a lack of behavioral effects of sleep deprivation, TSD and PSD induced genetic damage in rats submitted to pilocarpine-induced SE.
Neuroscience Letters 03/2012; 515(2):137-40. · 2.11 Impact Factor
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ABSTRACT: Oral cancer is a common neoplasm worldwide. The incidence and mortality have also increased in recent decades. It is characterized by poor prognosis and a low survival rate despite sophisticated surgical and radiotherapeutic modalities. The WNTs comprise a large family of highly conserved growth factors associated with a number of functions. In this review, we focus largely on the canonical pathway, revealing the recent findings, in oral cancer research, thereby raising our understanding of the mechanisms of this crucial signaling in several cellular activities.
Anticancer research 03/2012; 32(3):873-8. · 1.73 Impact Factor
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ABSTRACT: The aim of this study was to evaluate alkylation induced genotoxicity as a result of DNA repair deficiency during 4-nitroquinoline 1-oxide (4NQO)-induced rat tonguecarcinogenesis by means of single cell gel (comet)assay. Male Wistar rats were distributed into three groups of 10 animals each and treated with 50 ppm 4NQO solution through their drinking water for 4, 12, and 20 weeks.Ten animals were used as negative control. Blood samples and oral mucosa cells collected from all animals were divided into two aliquots of 20 lL each to study basal DNA damage and DNA damage due to genotoxin sensitivity.The first aliquot was processed immediately for comet assay to assess basal DNA damage. The second aliquot was treated with a known genotoxin, methylmetanesulfonate.Significantly greater DNA damage was noticed to oral mucosa cells from 4, and 12 weeks posttreatment.Peripheral blood cells did show statistically significant differences (P\0.05) after 20 weeks-group(squamous cell carcinoma). In conclusion, alkylation induced genotoxicity as a result of DNA repair deficiency is present in oral mucosa cells following oral experimental carcinogenesis.
Journal of molecular histology 01/2012; 43(2):145-50. · 1.75 Impact Factor
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ABSTRACT: The goal of this study was to investigate the expression of some metalloendopeptidases in squamous cell carcinomas of the oropharynx as well as its relation to histological differentiation, staging of disease, and prognosis. Paraffin blocks from 21 primary tumors were obtained from archives of the Department of Pathology, Paulista Medical School, Federal University of Sao Paulo, UNIFESP/EPM. Immunohistochemistry was used to detect the expression of EP24.15 and EP24.16 by means of tissue microarrays. Expression of EP24.15 or EP24.16 was not correlated with the stage of disease, histopathological grading or recurrence in squamous cell carcinomas of the oropharynx. In summary, our results support the notion that EP24.15 and EP24.16 are expressed in carcinoma of the oropharynx; however, these do not appear to be suitable biomarkers for histological grading, disease stage or recurrence as depicted by tissue microarrays and immunohistochemistry.
Cancer genomics & proteomics. 11/2011; 8(6):307-10.
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ABSTRACT: Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of alfa-iduronidase (IDUA), which leads to intralysosomal accumulation of glycosaminoglycans. Some studies have revealed that oxidative stress plays an important role in MPS I. However, the mechanisms by which these alterations occur are still not fully understood. The aim of this study was to analyze genomic instability in blood cells from murine model of MPS I by single cell gel (comet) assay and micronucleus test. The results pointed out genetic damage in blood cells as depicted by the single cell gel (comet) assay results. By contrast, no increase of micronucleated cells were found in mouse blood cells when compared to negative control. Taken together, our results suggest that IDUA deficiency induces genomic damage in blood cells. Certainly, this finding offers new insights into the mechanisms underlying the relation between IDUA deficiency and clinical manifestations that can occur in MPS I patients.
Journal of molecular histology 10/2011; 42(6):575-8. · 1.75 Impact Factor
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ABSTRACT: The aim of this study was to investigate oxidative DNA damage during 4-nitroquinoline 1-oxide (4NQO)-induced rat tongue carcinogenesis. For this purpose, male Wistar rats were distributed into three groups of 10 animals each and treated with 50 ppm 4NQO solution through their drinking water for 4, 12, and 20 weeks. Ten animals were used as negative control. The alkaline Comet assay modified with lesion-specific enzymes was used to detect single and double strand breaks, labile sites (SBs), and oxidised purines and pyrimidines. Although no histopathological abnormalities were induced in the epithelium after 4 weeks of carcinogen exposure, oxidative DNA damage was detected in the 'normal' oral epithelium. In pre-neoplastic lesions and squamous cell carcinomas induced after 12 and 20 weeks following carcinogen exposure, respectively, oxidative DNA damage was also increased (P < 0.05) when compared to negative control. In conclusion, our results suggest that oxidative DNA damage is an early event during multistep carcinogenesis assay induced by 4NQO. This kind of approach should be considered to persons with high risk of oral cancer, such as in smokers or alcohol consumers.
Journal of molecular histology 03/2011; 42(2):181-6. · 1.75 Impact Factor
