ABC | Volume 112, Nº4, April 2019

Original Article Vassallo et al Mercury increases ACE activity and oxidative stress Arq Bras Cardiol. 2019; 112(4):374-380 Table 4 – Malondialdehyde (MDA) (mM/mg of protein) concentrations in plasma, heart, aorta, lung, brain and kidney of untreated and Mercury (HgCl 2 )-treated Wistar rats and spontaneously hypertensive rats (SHRs) Wistar Control n = 6 Wistar HgCl 2 -treated n = 6 SHR Control n = 6 SHR HgCl 2 -treated n = 7 Plasma 0.93 ± 0.15 1.28 ± 0.44* 0.89 ± 0.22 0.92 ± 0.05 Heart 0.22 ± 0.03 0.28 ± 0.03* 0.45 ± 0.05 0.55 ± 0.05 & Aorta 0.13 ± 0.03 0.12 ± 0.05 0.96 ± 0.27 1.51 ± 0.37 & Lung 0.18 ± 0.05 0.14 ± 0.03 0.21 ± 0.03 0.12 ± 0.03 & Brain 0.13 ± 0.03 0.09 ± 0.03 0.54 ± 0.07 0.34 ± 0.03 & Kidney 0.38 ± 0.07 0.14 ± 0.03* 0.96 ± 0.07 0.51 ± 0.03 & Values are expressed in mM/mg of protein (MDA). The results represent the mean ± SD. N-Number of animals used. One-way ANOVA, post hoc Tukey’s. *p < 0.05 vs Wistar Control and & p < 0.05 vs SHR Control. Table 5 – Angiotensin converting enzyme (ACE) activity levels in plasma, heart, aorta, lung, brain and kidney of untreated and Mercury (HgCl 2 )-treated Wistar rats and spontaneously hypertensive rats (SHRs) Wistar Control n = 6 Wistar HgCl 2 -treated n = 6 SHR Control n = 6 SHR HgCl 2 -treated n = 6 Plasma 187 ± 39.2 235 ± 34.3* 114 ± 27.9* 163 ± 38.7 & Heart 3.4 ± 0.5 4.1 ± 0.3* 17.9 ± 2.7* 14.8 ± 1.4 & Aorta 213 ± 53.9 221 ± 61.3 670 ± 39.9* 535 ± 47.0 & Lung 95 ± 6.1 99.4 ± 11.3 87.6 ± 5.4 75.1 ± 9.8 & Brain 46.4 ± 7.9 42.6 ± 9.9 40.3 ± 5.6 27.8 ± 4.4 & Kidney 47.8 ± 16.2 45.4 ± 14.2 80.0 ± 15.4* 61.4 ± 6.9 & Values are expressed in nmol/mL/min/mg of protein in tissues and in nmol/mL of plasma/min in plasma (ACE). Results represent the mean ± SD. N-Number of animals used. One-way ANOVA, post hoc Tukey’s. *p < 0.05 vs Wistar Control and & p < 0.05 vs SHR Control. depend on mercury concentration in each of them? Would a pre-existing cardiovascular disorder be aggravated by exposure to inorganicmercury? These questions can be considered limitations of our study, and issues for further studies. Conclusions Results described here allow us to affirm that chronic exposure to inorganic mercury, similarly to that we previously reported, produces blood concentrations compatible with those found in exposed humans, and do represent a cardiovascular risk factor. Such exposure influenced ACE activity, increased oxidative stress and promoted hypertension in SHRs (which had a higher blood pressure increment compared with untreated SHRs), as well as increased the LVEDP in Wistar rats. This controlled exposure affected the cardiovascular system , produced more expressive changes of ACE activity and oxidative stress in SHRs representing a risk factor for the development of cardiovascular disorders in normotensive rats and a contributing factor to pre-existing risks in high blood pressure condition. Author contributions Conception and design of the research: Vassallo DV, Simões MR, Giuberti K, Stefanon I; acquisition of data: Giuberti K, Azevedo BF, Ribeiro Junior RF; analysis and interpretation of the data and statistical analysis: Vassallo DV, Simões MR, Giuberti K, Azevedo BF, Ribeiro Junior RF, Salaices M, Stefanon I; obtaining funding: Vassallo DV, Salaices M; writing of the manuscript: Vassallo DV, Simões MR; critical revision of the manuscript for intellectual content: Vassallo DV, Simões MR, Salaices M, Stefanon I. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding This study was funded by FAPES, CAPES, CNPq, Ministério da Economia e Competitividade (SAF 2016-80305-P). Study Association This article is part of the thesis of Doctoral submitted by Maylla Ronacher Simões, from Universidade Federal do Espírito Santo. Ethics approval and consent to participate This study was approved by the Ethics Committee on Animal Experiments of the Escola Superior de Ciências da Santa Casa de Misericórdia de Vitória under the protocol number CEUA-EMESCAM 003/2007. 378