Efeitos citotóxicos da exposição ao mercúrio e a cisplatina: estudo hemodinâmico

• Autor(a) principal: Silva, Daniele Angeli da
• Data de Publicação: 2014
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
• Texto Completo: http://repositorio.ufes.br/handle/10/7998
• topic: Chromosomal aberrations; Bone marrow; Arterial pressure; Cytogenetics; Clastogenicity; Aberrações cromossômicas; Medula óssea; Pressão arterial; Citogenética; Clastogenicidade; Hemodinâmica; Quimioterapia; Frequência cardíaca; Fisiologia; 612

Metal with unique characteristics and wide use, mercury became a global concern from the moment that its environmental and human health risks were known. Reference values for plasma concentrations were established, but studies have shown the occurrence of adverse effects of the metal, even at near, or below, considered safe concentration levels. To better understand the effects of mercury on the physiology of various biological systems, chronic tests have been developed in models to simulate human poisoning. The results of these studies have clarified points of metabolic pathways that directly or indirectly participate in the transformation, accumulation or excretion of mercury. Even with these advances, there are few studies of genotoxicity associated with chronic models of metal intoxication. We began a study to verify the occurrence and to identify the types of chromosomal aberrations (CA) in a model of exposure of Wistar rats to mercuric chloride (HgCl2) for 15 and 30 days. Another purpose was to record possible changes in hemodynamic parameters. The animals were divided into three groups, negative control, positive control and a treatment with mercury. After anesthesia, records from arterial pressure showed no change in arterial pressure and heart rate of the animals treated with HgCl2. Classical cytogenetic alowed to observe the presence of aberrations such as breakage and gap, both in bone marrow samples from animals treated for 15 days and 30 days. The absolute frequency of chromosomal aberrations (AFCA) the total gaps and breaks (TG and TB) and total chromosomes with gaps and breaks (CG and CB) was recorded. From all results, only samples of 30 days showed statistically noticeable difference for all evaluated citogenetic parameters when compared with the negative control. Two metabolic pathways that suffer direct influence of mercury may be related to the results obtained. The first is the way in which acts the dUTPase enzyme that, when unbalanced, makes DNA strand breakable. The other one is the Glutathione pathway, which is related to the control of the levels of free radicals, and whose imbalance increases the production of reactive oxygen species, leading to oxidative stress. Based on these results, it was concluded that the low concentration of mercury used in the chronic exposure model was genotoxic, clastogenic and potentially mutagenic to cells of bone marrow from female Wistar rats treated for 30 days.