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

Table 1

Changes induced by OS, RS, and NSS on DNA and associated proteins and on proteins that establish classical epigenetic cues.

Effects on DNA and associated proteins	OS	-Activation of DNMTs [74, 98]
		-Depletion of SAM [99–101]
		-Inhibition of TET enzymes [99–101]
		-Methylation through formation of methionine sulfoxide [124–126]
	RS	- Activation of DNMT by H2S [137]
		- Inhibition of SAM by GSH [129, 130]
		-Decreased production of methionine sulfoxide [135]
		-Damage to DNA repair mechanisms [23, 50]
	NSS	-Inhibition of HDAC by NO [138]
		-Inhibition of JmjC demethylases [142]
		-Activation PARP-1 [23, 50]
Effects on proteins that establish epigenetic cues	OS	-Controversial effects on methylation of lysines by HMT [102]
		-Increased acetylation through inhibition of HDAC [107–109]
		-Increased acetylation through inactivation of SIRT1 [111, 112]
		-Degradation of SIRT3 [113, 114]
		-Increased phosphorylation [119]
	RS	-Glutathionylation of H3 causing instability of the nucleosome [133, 134]
		-Inactivation of SIRT1 by GSH [136]
		-Upregulation of SIRT3 by H2S [136]
	NSS	-Increased histone acetylation by NO [138]
		-Controversial effects on HDAC [143]
		-Inactivation of SIRT1 and 6 [143, 146]

OS: oxidative stress; RS: reductive stress; NSS: nitrosative stress; DNMT: DNA methyltransferase; SAM: S-adenosyl methionine; TET enzymes: ten-eleven translocation (TET) methylcytosine dioxygenases; GSH: glutathione; H₂S: sulfhydric acid; HDAC: histone deacetylase; NO: nitric oxide; JmjC: Jumonji C; PARP1: poly [ADP-ribose] polymerase 1; HMT: histone methyl transferase; SIRT: sirtuin deacetylase.