This study aims to analyze post-mortem human cardiac specimens, to verify and evaluate the existence or extent of oxidative stress in subjects whose cause of death has been traced to sepsis, through immunohistological oxidative/nitrosative stress markers. Indeed, in the present study, i-NOS, NOX2, and nitrotyrosine markers were higher expressed in the septic death group when compared to the control group, associated with also a significant increase in 8-OHdG, highlighting the pivotal role of oxidative stress in septic etiopathogenesis. In particular, 70% of cardiomyocyte nuclei from septic death specimens showed positivity for 8-OHdG. Furthermore, intense and massive NOX2-positive myocyte immunoreaction was noticed in the septic group, as nitrotyrosine immunostaining intense reaction was found in the cardiac cells. These results demonstrated a correlation between oxidative and nitrosative stress imbalance and the pathophysiology of cardiac dysfunction documented in cases of sepsis. Therefore, subsequent studies will focus on the expression of oxidative stress markers in other organs and tissues, as well as on the involvement of the intracellular pattern of apoptosis, to better clarify the complex pathogenesis of multi-organ failure, leading to support the rationale for including therapies targeting redox abnormalities in the management of septic patients.

Oxidative stress in sepsis: a focus on cardiac pathology / Bertozzi, Giuseppe; Ferrara, Michela; Di Fazio, Aldo; Maiese, Aniello; Delogu, Giuseppe; Di Fazio, Nicola; Tortorella, Vittoria; La Russa, Raffaele; Fineschi, Vittorio. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 25:5(2024), pp. 1-11. [10.3390/ijms25052912]

Oxidative stress in sepsis: a focus on cardiac pathology

Ferrara, Michela;Maiese, Aniello;Delogu, Giuseppe;Di Fazio, Nicola;Tortorella, Vittoria;La Russa, Raffaele;Fineschi, Vittorio
2024

Abstract

This study aims to analyze post-mortem human cardiac specimens, to verify and evaluate the existence or extent of oxidative stress in subjects whose cause of death has been traced to sepsis, through immunohistological oxidative/nitrosative stress markers. Indeed, in the present study, i-NOS, NOX2, and nitrotyrosine markers were higher expressed in the septic death group when compared to the control group, associated with also a significant increase in 8-OHdG, highlighting the pivotal role of oxidative stress in septic etiopathogenesis. In particular, 70% of cardiomyocyte nuclei from septic death specimens showed positivity for 8-OHdG. Furthermore, intense and massive NOX2-positive myocyte immunoreaction was noticed in the septic group, as nitrotyrosine immunostaining intense reaction was found in the cardiac cells. These results demonstrated a correlation between oxidative and nitrosative stress imbalance and the pathophysiology of cardiac dysfunction documented in cases of sepsis. Therefore, subsequent studies will focus on the expression of oxidative stress markers in other organs and tissues, as well as on the involvement of the intracellular pattern of apoptosis, to better clarify the complex pathogenesis of multi-organ failure, leading to support the rationale for including therapies targeting redox abnormalities in the management of septic patients.
2024
8-OHdG; NOX-2; NT; death; heart; iNOS; oxidative stress; sepsis
01 Pubblicazione su rivista::01a Articolo in rivista
Oxidative stress in sepsis: a focus on cardiac pathology / Bertozzi, Giuseppe; Ferrara, Michela; Di Fazio, Aldo; Maiese, Aniello; Delogu, Giuseppe; Di Fazio, Nicola; Tortorella, Vittoria; La Russa, Raffaele; Fineschi, Vittorio. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 25:5(2024), pp. 1-11. [10.3390/ijms25052912]
File allegati a questo prodotto
File Dimensione Formato  
Bertozzi_Oxidative_2024.pdf

accesso aperto

Tipologia: Documento in Post-print (versione successiva alla peer review e accettata per la pubblicazione)
Licenza: Creative commons
Dimensione 3.47 MB
Formato Adobe PDF
3.47 MB Adobe PDF

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1721047
Citazioni
  • ???jsp.display-item.citation.pmc??? 2
  • Scopus 3
  • ???jsp.display-item.citation.isi??? 3
social impact