Lipoteichoic acid reduces antioxidant enzymes in H9c2 cells

Berenice Fernández-Rojas; Gustavo I Vázquez-Cervantes; José Pedraza-Chaverri; Gloria Gutiérrez-Venegas

doi:10.1016/j.toxrep.2019.12.007

Lipoteichoic acid reduces antioxidant enzymes in H9c2 cells

Toxicol Rep. 2019 Dec 30:7:101-108. doi: 10.1016/j.toxrep.2019.12.007. eCollection 2020.

Authors

Berenice Fernández-Rojas¹, Gustavo I Vázquez-Cervantes², José Pedraza-Chaverri², Gloria Gutiérrez-Venegas¹

Affiliations

¹ Laboratorio de Bioquímica de la División de Estudios de Posgrado e Investigación, Facultad de Odontología, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510 Ciudad de México, México.
² Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, Circuito interior s/n, Ciudad Universitaria, 04510, Ciudad de México, México.

Abstract

Infective endocarditis (IE) is an illness where the heart is invaded by bacteria, like Streptococcal and Staphylococcal species that contain lipoteichoic acid (LTA) related to an essential role in this disease. This study is the first in evaluating antioxidant enzyme levels in embryonic cardiomyocyte cell line (H9c2) induced by LTA from Streptococcus sanguinis. LTA increased reactive oxygen species (ROS) and reduced the levels of the antioxidant enzymes glutathione peroxidase, superoxide dismutase (SOD)-1 and catalase (CAT) but did not affect glutathione content. At the highest LTA concentration (15 μg/ml), SOD-1 and CAT levels did not change, and this effect was related to the induction of mRNA levels of Nrf2 induced by LTA. These results suggest that low antioxidant enzyme levels and ROS production could be related to IE.

Keywords: AKT, protein kinase B; Antioxidant enzymes; CAT, catalase; Carboxy-H2DCFDA, 6-carboxy-2´,7´ dichlorodihydrofluorescein diacetate; DHE, dihydroethidium; ERK, extracellular signal-regulated kinases; FDA, fluorescein diacetate; GPx-1, glutathione peroxidase-1; GSH, glutathione; H2O2, hydrogen peroxide; IE, infective endocarditis; Infective endocarditis; JNK, c-jun N-terminal kinases; LTA, lipoteichoic acid; Lipoteichoic acid; MAPK, mitogen-activated protein kinase; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; NO, nitric oxide; NOS, nitric oxide synthase; Nrf2, nuclear factor (erythroid-derived 2)-like 2; O2•¯, superoxide radical; OH•, hydroxyl radical; ONOO¯, peroxynitrite anion; Oxidative stress; RNS, reactive nitrogen species; ROS production; ROS, reactive oxygen species; SOD-1, superoxide dismutase-1.