ABSTRACT
Background: Malva sylvestris L. [M. sylvestris] has antioxidant property and is widely used in the traditional medicine to treat gastrointestinal, respiratory, skin and urological disorders
Objective: In this study, the protective effect of M. sylvestris against sodium fluoride-induced nephrotoxicity in the rat was evaluated
Methods: The M. sylvestris flower extract was prepared and injected intraperitoneally at the doses of 100, 200, 400 mg/kg/day to rat groups [10 in each group] for 1 week and subsequently 600 ppm sodium fluoride was added to the rats drinking water for 1 additional week. After these steps, the rat serum levels of urea, creatinine, reduced glutathione, catalase and malondialdehyde were determined. The histopathology of the rats' kidney was also studied. In this study, vitamin C [10 mg/kg/day] was used as positive control
Results: Sodium fluoride administration increased levels of BUN, creatinine, glutathione, catalase activity and decreased malondialdehyde levels indicating induction of nephrotoxicity in the rats. M. sylvestris extract pretreatment significantly decreased the BUN and creatinine levels [P<0.05]. Catalase activity and glutathione levels were significantly increased by M. sylvestris [P<0.05]. All three doses of the M. sylvestris decreased the malondialdehyde level, but it was significant only for the dose of 400 mg/kg/day [P<0.05]. The Malva sylvestris effects were comparable with those of vitamin C. Histopathological findings also showed protective effects of M. sylvestris against the renal damage induced by sodium fluoride
Conclusion: The results suggest that M. sylvestris has protective effects against sodium fluorideinduced nephrotoxicity which maybe mediated by the antioxidant activity of the plant flavonoids
Subject(s)
Adult , Animals, Laboratory , Male , Malva , Sodium Fluoride/toxicity , Phytotherapy , Rats, Wistar , Models, AnimalABSTRACT
O trato gastrointestinal (TGI) é a principal rota de exposição ao fluoreto (F) e o seu mais importante sítio de absorção. Acredita-se que a toxicidade do F comprometa a fisiologia do intestino, devido à relevante sintomatologia gastrointestinal relatada em consequência da exposição excessiva ao F. A função intestinal é controlada por uma complexa rede neuronal interligada e incorporada à parede deste órgão, denominada Sistema Nervoso Entérico (SNE). Embora os efeitos tóxicos do F sobre o Sistema Nervoso Central sejam descritos na literatura, não há estudos relacionados à sua toxicidade sobre o SNE. Neste estudo realizado em ratos, foi avaliado o efeito da exposição aguda ou crônica ao F, sobre a população geral de neurônios entéricos e sobre as subpopulações que expressam os principais neurotransmissores entéricos: Acetilcolina (ACh), Óxido Nítrico (NO), Peptídeo Vasoativo Intestinal (VIP), Peptídeo Relacionado ao Gene da Calcitonina (CGRP) e Substância P (SP). Os animais foram divididos em 5 grupos: 3 destinados à exposição crônica (0 ppm, 10 ppm ou 50 ppm de F na água de beber) e 2 à exposição aguda (0 ou 25 mgF/Kg por gavagem gástrica). Foram coletados os 3 segmentos do intestino delgado (duodeno, jejuno e íleo) e processados para a detecção da HuC/D, ChAT, nNOS, VIP, CGRP e SP, através de técnicas de imunofluorescência, no plexo mioentérico. Foram obtidas imagens para a realização da análise quantitativa dos neurônios da população geral (HuC/D) e nitrérgicos (imunorreativos à nNOS); e morfométrica dos neurônios imunorreativos à HuC/D ou nNOS; e das varicosidades imunorreativas à ChAT, VIP, CGRP ou SP. Amostras dos 3 segmentos intestinais foram preparadas e coradas em Hematoxilina e Eosina para análise histológica da morfologia básica. O segmento intestinal considerado mais afetado na análise morfométrica da população geral de neurônios, o duodeno, foi selecionado para a realização da análise proteômica, com o objetivo de oferecer o seu perfil proteico...
The gastrointestinal tract (GIT) is the main route of fluoride (F) exposure, and the most important site of its absorption. It is believed that F toxicity compromises the intestine physiology, due to the relevant gastrointestinal symptomatology reported in consequence to excessive exposure. The intestinal function is controlled by a complex neuronal net, which is interconnected and embedded in the wall of this organ, named Enteric Nervous System (ENS). Although the toxic effects of F on the Central Nervous system are described in the literature, there are no studies related to its toxicity on the ENS. Therefore, in this study performed in rats, the effects of chronic and acute F exposure were evaluated, on the general population of enteric neurons and on the subpopulations that express the main enteric neurotransmitters: Acetylcholine (Ach), Nitric Oxide (NO), Vasoactive Intestinal Peptide (VIP), Calcitonin gene related peptide (CGRP), and Substance P (SP). The animals were divided into 5 groups: 3 designed to the chronic exposure (0 ppm, 10 ppm ou 50 ppm de F in the drinking water) and 2 to the acute exposure (0 ou 25 mgF/Kg - gastric gavage). Three intestinal segments were collected (duodenum, jejunum, and ileum) and processed for the immunofluorescence techniques to detect HuC/D, ChAT, nNOS, VIP, CGRP and SP, on the myenteric plexus. Images were obtained for the quantitative analysis of the general population of neurons (HuC/D immunoreactive) and the nitrergic neurons (nNOS immunoreactive), for the morphometric analysis of the general population and nitrergic neurons and also for the immunoreactive varicosities to ChAT, VIP, CGRP or SP. Samples of the 3 intestinal segments were prepared and stained with hematoxylin and eosin for histological analysis of the basic morphology. Duodenum, the intestinal segment considered the most affected in the morphological analysis of the general population of neurons, was selected for the proteomic analysis...
Subject(s)
Animals , Male , Rats , Sodium Fluoride/administration & dosage , Sodium Fluoride/toxicity , Intestine, Small , Proteins/analysis , Enteric Nervous System , Fluorescent Antibody Technique , Intestine, Small/chemistry , Proteomics , Rats, Wistar , Reference ValuesABSTRACT
O trato gastrointestinal (TGI) é a principal rota de exposição ao fluoreto (F) e o seu mais importante sítio de absorção. Acredita-se que a toxicidade do F comprometa a fisiologia do intestino, devido à relevante sintomatologia gastrointestinal relatada em consequência da exposição excessiva ao F. A função intestinal é controlada por uma complexa rede neuronal interligada e incorporada à parede deste órgão, denominada Sistema Nervoso Entérico (SNE). Embora os efeitos tóxicos do F sobre o Sistema Nervoso Central sejam descritos na literatura, não há estudos relacionados à sua toxicidade sobre o SNE. Neste estudo realizado em ratos, foi avaliado o efeito da exposição aguda ou crônica ao F, sobre a população geral de neurônios entéricos e sobre as subpopulações que expressam os principais neurotransmissores entéricos: Acetilcolina (ACh), Óxido Nítrico (NO), Peptídeo Vasoativo Intestinal (VIP), Peptídeo Relacionado ao Gene da Calcitonina (CGRP) e Substância P (SP). Os animais foram divididos em 5 grupos: 3 destinados à exposição crônica (0 ppm, 10 ppm ou 50 ppm de F na água de beber) e 2 à exposição aguda (0 ou 25 mgF/Kg por gavagem gástrica). Foram coletados os 3 segmentos do intestino delgado (duodeno, jejuno e íleo) e processados para a detecção da HuC/D, ChAT, nNOS, VIP, CGRP e SP, através de técnicas de imunofluorescência, no plexo mioentérico. Foram obtidas imagens para a realização da análise quantitativa dos neurônios da população geral (HuC/D) e nitrérgicos (imunorreativos à nNOS); e morfométrica dos neurônios imunorreativos à HuC/D ou nNOS; e das varicosidades imunorreativas à ChAT, VIP, CGRP ou SP. Amostras dos 3 segmentos intestinais foram preparadas e coradas em Hematoxilina e Eosina para análise histológica da morfologia básica. O segmento intestinal considerado mais afetado na análise morfométrica da população geral de neurônios, o duodeno, foi selecionado para a realização da análise proteômica, com o objetivo de oferecer o seu perfil proteico...
The gastrointestinal tract (GIT) is the main route of fluoride (F) exposure, and the most important site of its absorption. It is believed that F toxicity compromises the intestine physiology, due to the relevant gastrointestinal symptomatology reported in consequence to excessive exposure. The intestinal function is controlled by a complex neuronal net, which is interconnected and embedded in the wall of this organ, named Enteric Nervous System (ENS). Although the toxic effects of F on the Central Nervous system are described in the literature, there are no studies related to its toxicity on the ENS. Therefore, in this study performed in rats, the effects of chronic and acute F exposure were evaluated, on the general population of enteric neurons and on the subpopulations that express the main enteric neurotransmitters: Acetylcholine (Ach), Nitric Oxide (NO), Vasoactive Intestinal Peptide (VIP), Calcitonin gene related peptide (CGRP), and Substance P (SP). The animals were divided into 5 groups: 3 designed to the chronic exposure (0 ppm, 10 ppm ou 50 ppm de F in the drinking water) and 2 to the acute exposure (0 ou 25 mgF/Kg - gastric gavage). Three intestinal segments were collected (duodenum, jejunum, and ileum) and processed for the immunofluorescence techniques to detect HuC/D, ChAT, nNOS, VIP, CGRP and SP, on the myenteric plexus. Images were obtained for the quantitative analysis of the general population of neurons (HuC/D immunoreactive) and the nitrergic neurons (nNOS immunoreactive), for the morphometric analysis of the general population and nitrergic neurons and also for the immunoreactive varicosities to ChAT, VIP, CGRP or SP. Samples of the 3 intestinal segments were prepared and stained with hematoxylin and eosin for histological analysis of the basic morphology. Duodenum, the intestinal segment considered the most affected in the morphological analysis of the general population of neurons, was selected for the proteomic analysis...
Subject(s)
Animals , Male , Rats , Sodium Fluoride/administration & dosage , Sodium Fluoride/toxicity , Intestine, Small , Proteins/analysis , Enteric Nervous System , Fluorescent Antibody Technique , Intestine, Small/chemistry , Proteomics , Rats, Wistar , Reference ValuesABSTRACT
Fluoride compounds are naturally present in soil, water, and food. Furthermore, fluoride in amounts exceeding the standard therapeutic dosage accumulates in hard and soft tissues, where it disturbs the metabolic processes and produces noticeable changes in multiple organs. The study was designed to investigate the effects of sodium fluoride [NaF] on the lung of adult albino rats and the possible protective role of vitamin E on these changes. Twenty-six adult albino rats were divided into three groups: group I [control], group II receiving NaF alone [10 mg/kg body weight], and group III receiving the same NaF dose together with vitamin E supplementation [3 mg/day orally for 35 days]. Tissue homogenates were collected for biochemical study, and the lung tissues were excised for histological, immunohistochemical, and biochemical studies. The results of biochemical and immunohistochemical studies were measured and statistically analyzed. Lung sections of rats treated with NaF showed congestion and injury in the endothelium of blood vessels, with hemorrhage and injury in the alveolar epithelium. Proliferation of pneumocytes type II and interstitial septal cells were seen. Thickening of interalveolar septum by cellular infiltration and red blood cells with subsequent decrease in the alveolar space was observed. Some area showed compensatory dilated alveolar ducts. A significant increase in the mean area% of cyclooxygenase-2-immunopositive cells was observed when compared with other groups. There was a significant decrease in the catalase activity and an increase in malondialdehyde concentration in group II. In vitamin E-treated group, most fields showed normal lung structure and some fields showed thickened interalveolar septa and dilated air spaces. The use of vitamin E has a beneficial effect on the protection of lung against NaF-induced injury
Subject(s)
Male , Animals, Laboratory , Sodium Fluoride/toxicity , Lung/pathology , RatsABSTRACT
O flúor tem sido amplamente usado na Odontologia, pois é um agente profilático efetivo e específico contra a cárie dentária. Entretanto, o flúor em excesso pode representar perigos à saúde humana, especialmente por causar agressão ao material genético. Testes de genotoxicidade representam uma importante parte da pesquisa do câncer para a avaliação de risco de possíveis carcinógenos. Neste presente estudo, danos ao DNA associados à exposição ao flúor foram avaliados pelo teste de células individualizadas em gel de agarose (teste do cometa) in vitro. Células de ovário de hamster chinês foram expostas ao fluoreto de sódio (NaF) nas concentrações finais de 7 a 100 µg/ml, durante 3 h, a 37ºC. Os resultados mostraram que o NaF não contribuiu para os danos no DNA em todas as concentrações testadas, conforme demonstrado pelas médias do momento da cauda e da intensidade da cauda dos cometas. Esses achados são clinicamente importantes, uma vez que representam uma importante contribuição para a correta avaliação do potencial risco à saúde associada à exposição aos agentes odontológicos.
Subject(s)
Cricetinae , Animals , Female , CHO Cells/drug effects , DNA Damage , Sodium Fluoride/toxicity , Comet Assay , CricetulusABSTRACT
Wistar albino rats were exposed to 30 or 100 ppm fluoride in drinking water during their fetal, weanling and post-weaning stages of life up to puberty. Extent of lipid peroxidation and response of the antioxidant systems in red blood cells and plasma to prolonged fluoride exposure were assessed in these rats in comparison to the control rats fed with permissible level (0.5 ppm) of fluoride. Rats treated with 100 ppm fluoride showed enhanced lipid peroxidation as evidenced by elevated malondialdehyde (MDA) levels in red blood cells but, 30 ppm fluoride did not cause any appreciable change in RBC MDA level. 30 ppm fluoride-intake resulted in increased levels of total and reduced glutathione in red blood cells and ascorbic acid in plasma while 100 ppm fluoride resulted in decreases in these levels. The activity of RBC glutathione peroxidase was elevated in both the fluoride-treated groups, more pronounced increase was seen with 100 ppm. Reduced to total glutathione ratio in RBC and uric acid levels in plasma decreased in both the groups. RBC superoxide dismutase activity decreased significantly on high-fluoride treatment. These results suggest that long-term high-fluoride intake at the early developing stages of life enhances oxidative stress in the blood, thereby disturbing the antioxidant defense of rats. Increased oxidative stress could be one of the mediating factors in the pathogenesis of toxic manifestations of fluoride.
Subject(s)
Administration, Oral , Animals , Ascorbic Acid/blood , Dose-Response Relationship, Drug , Erythrocytes/drug effects , Female , Glutathione/blood , Lipid Peroxidation/drug effects , Malondialdehyde/blood , Pregnancy , Prenatal Exposure Delayed Effects , Rats , Rats, Wistar , Sodium Fluoride/toxicity , Superoxide Dismutase/blood , Uric Acid/bloodABSTRACT
Se presenta una revisión de la literatura en la que se detectó que los resultados de las investigaciones en relación con la capacidad potencial de los fluoruros de producir daño en los sistemas genéticos celulares, pueden ser agrupadas en 3 categorías: um grupo de investigadores sostiene que los fluoruros son agentes mutágenos capaces de dañar el DNA y los cromosomas; otros estiman que no tienen tales potencialidades genotóxicas y un último criterio sustentado por pocos trabajos experimentales, considera que poseen sinergismo o efectos antagónicos con algunos mutágenos conocidos. El análisis de los artículos publicados pone de manifestio que los polémicos resultados de la década del sesenta y setenta han ido aclarándose en la medida en que la genotoxicología se ha desarrollado como ciencia y han aparecido pruebas más precisas y confiables. Queda claro en la literatura que la exposición aguda a los fluoruros no causa alteraciones en los sistemas biológicos celulares en los que han sido realizadas las pruebas y que en el caso de la exposición crónica, los estudios más recientes y mejor diseñados coinciden en que no producen efectos deletéreos al nivel de las dosis empleadas en la prevención de la caries dental; pero en este aspecto, a juicio de algunos científicos, debe investigarse más para llegar a una conclusión definitiva