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Doctoral Thesis
Full name
Tania Cristina Higashi Sawada
Knowledge Area
Date of Defense
São Paulo, 2004
Barros, Silvia Berlanga de Moraes (President)
Campa, Ana
Capitani, Eduardo Mello de
Silva, Carlos Sergio da
Tenuta Filho, Alfredo
Title in Portuguese
Influência da N-acetilcisteína no estresse oxidativo hepático e cerebral e na cinética de mercúrio em ratos expostos ao cloreto de metilmercúrio
Keywords in Portuguese
Estresse oxidativo
Abstract in Portuguese
Trabalhos experimentais demonstram o envolvimento de estresse oxidativo como mecanismo responsável pelas lesões cerebrais e hepáticas que acompanham a intoxicação pelo cloreto de metilmercúrio (CH3HgCI). A N-acetilcisteína (NAC) é capaz de ligar-se a metais e sequestrar radicais livres. O objetivo deste trabalho foi avaliar a influência da NAC sobre os níveis de mercúrio (Hg) e no estresse oxidativo induzido pelo metilmercúrio. Neste trabalho em ratos preconizamos a exposição oral a 20 mg de CH3HgCl/kg e intraperitoneal (ip) a 200 mg/kg de NAC, avaliados após 6, 12 e 24 horas e exposição oral a 0,5 mg de CH3HgCI/kg e doses de NAC (i.p.). Não houve aumento de TBARS hepático e cerebral após exposição aguda e sub-crônica. Dos antioxidantes apenas o ácido ascórbico mostrou-se diminuído após 12 horas da exposição. A NAC apresentou-se eficaz apenas na exposição sub-crônica com animais apresentando níveis de Hg reduzidos em fígado e cérebro
Title in English
Influence of N-acetylcysteine on cerebral and hepatic oxidative stress and the kinetics of mercury in rats exposed to methylmercury chloride
Keywords in English
Oxidative stress
Abstract in English
Experimental studies show oxidative stress to cause cerebral and hepatic lesions after methylmercury intoxication. N-acetylcysteine (NAC) is capable of binding to metals and scavenges free radicals. In this study we evaluated the influence of NAC on the levels of mercury (Hg) and on oxidative stress parameters after methylmercury chloride (CH3HgCI) exposure. A group of rats were treated by gavage with 20mg of CH3HgCl/kg body weight (b.w.) and 200mg/kg b.w. of NAC by intraperitoneal (ip) injection. These animals were killed after 6, 12 and 24hours. A second group received 0,5mg of CH3HgCl/kg b.w. by gavage during four weeks and five doses of NAC (200mg/kg b.w. ip) in the last week of exposure to CH3HgCI. There was no increase in hepatic and cerebral TBARS after the acute and subchronic exposure. Considering antioxidants, only ascorbic acid was reduced in liver after 12hours. NAC was effective decreasing mercury levels in brain, liver and kidney after subchronic exposure to CH3HgCI.
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