Oxidative, Reductive, and Nitrosative Stress Effects on Epigenetics and on Posttranslational Modification of Enzymes

I Pérez-Torres1, M E Soto2, V Castrejón-Tellez3

  • 1Cardiovascular Biomedicine Department, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, Tlalpan, Mexico City 14080, Mexico.

Insights

Oxidative, reductive, and nitrosative stresses induce epigenetic changes impacting cardiometabolic health. These stress-induced modifications to DNA and proteins are reversible and potentially treatable.

Area of Science:

  • Biochemistry
  • Epigenetics
  • Molecular Biology

Background:

  • Oxidative (OS), reductive (RS), and nitrosative (NSS) stresses involve interconnected reactions like carbonylation and nitration.
  • These stresses arise from imbalances in antioxidant systems and nitric oxide (NO) metabolism.

Purpose of the Study:

  • To explore the general characteristics of OS, RS, and NSS.
  • To detail how these stresses induce DNA damage, histone modification, and alter epigenetic enzyme activities.
  • To discuss the role of these stresses in cardiometabolic disorders and health heritability.

Main Methods:

  • Review of biochemical reactions induced by OS, RS, and NSS.
  • Analysis of posttranslational modifications on DNA, histones, and enzymes.
  • Examination of the link between early-life stress exposure and adult cardiometabolic disease programming.

Main Results:

  • OS, RS, and NSS induce DNA damage (e.g., 8-oxo-d guanosine) and modify histones.
  • These stresses alter the activity of epigenetic enzymes (DNMTs, HMTs, HATs, HDACs) and DNA repair enzymes.
  • Stress-induced epigenetic marks are established through reversible chemical modifications.

Conclusions:

  • OS, RS, and NSS significantly impact cardiometabolic health through epigenetic reprogramming.
  • Early-life environmental exposures mediated by these stresses can influence long-term health and heritability.
  • The reversible nature of these epigenetic modifications offers potential therapeutic targets for cardiometabolic diseases.

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