Jacobs Journal of Anatomy and Physiology

Influence of Periodontal IgG on The Antioxidant Enzyme System in Rat Atria Myocardium

*Enri Borda
Department Of Dentistry, Buenos Aires University, Buenos Aires, Argentina

*Corresponding Author:
Enri Borda
Department Of Dentistry, Buenos Aires University, Buenos Aires, Argentina

Published on: 2018-09-25


In this paper, we demonstrate that circulating antibodies from the serum of periodontitis patients presenting atria β1 adrenoceptors (AR) induce changes upon antioxidant superoxide dismutase (SOD) and catalase (CAT) enzymes and the release of nitrites during early hypoxia. We also demonstrate the existence of reactivity against the second extracellular loop of human myocardial β1 AR by means of the ELISA, using the β1 synthetic peptide with an amino acid sequence identical to that of the second loop of human myocardial β1 AR as a coating antigen. These autoantibodies in the serum of chronic periodontitis patients have two complementary results, i.e., a decrement of SOD’s activity and an increment of CAT’s activity. These phenomena are accompanied by a further one; namely, the stimulation of the generation of nitrites by rat atria myocardium during hypoxia. The effect of the presence of isoproterenol (ISO) resembles those observed in the presence of autoantibodies. The actions of β1 IgG and ISO are blunted by atenolol, L-NMMA, and β1 synthetic peptide, respectively. Normal IgG (n IgG) is without effect in our study system. These results indicate that the presence of β1 IgG in atria myocardium modifies the activities of SOD and CAT during early hypoxia; a modification which is accompanied by an increment of the nitrate levels. This increment may, in turn, be the cause of an increment of the levels of reactive oxygen species (ROS) and may be one of the factors that subsequently trigger radioprotection or myocardial injury, leading to irreversible cellular and tissue damage.


Myocardium, Hypoxia, Normoxia, Nitrites, Antioxidant Enzymes


To introduce our study let’s recall some facts: the release of catecholamine activates the β1 adrenoceptor during myocardial ischemia injury when this is abundantly expressed on cardiomyocytes. Increased reactive oxygen species (ROS) and myocardial apoptosis are thought to be mediated by the β1 adrenoceptor in vitro and in vivo. When this adrenoceptor is stimulated by β1 IgG in cardiac atria it appears through a canonical cyclic adenosine monophosphate (cAMP) dependent protein kinase A (PKA) pathway The β1 adrenoceptor’s antagonists can preserve the membrane’s phospholipids, by scavenging free radicals and reducing the lipid peroxidation. This being the case, seeking for β1 adrenoceptor’s antagonists based on a target receptor and fully understanding the protective mechanisms are necessary for the treatment of myocardial ischemia injury.