Abstract
Oxidative (OS), reductive (RS), and nitrosative (NSS) stresses produce carbonylation, glycation, glutathionylation, sulfhydration, nitration, and nitrosylation reactions. OS, RS, and NSS are interrelated since RS results from an overactivation of antioxidant systems and NSS is the result of the overactivation of the oxidation of nitric oxide (NO). Here, we discuss the general characteristics of the three types of stress and the way by which the reactions they induce (a) damage the DNA structure causing strand breaks or inducing the formation of 8-oxo-d guanosine; (b) modify histones; (c) modify the activities of the enzymes that determine the establishment of epigenetic cues such as DNA methyl transferases, histone methyl transferases, acetyltransferases, and deacetylases; (d) alter DNA reparation enzymes by posttranslational mechanisms; and (e) regulate the activities of intracellular enzymes participating in metabolic reactions and in signaling pathways through posttranslational modifications. Furthermore, the three types of stress may establish new epigenetic marks through these reactions. The development of cardiometabolic disorders in adult life may be programed since early stages of development by epigenetic cues which may be established or modified by OS, RS, and NSS. Therefore, the three types of stress participate importantly in mediating the impact of the early life environment on later health and heritability. Here, we discuss their impact on cardiometabolic diseases. The epigenetic modifications induced by these stresses depend on union and release of chemical residues on a DNA sequence and/or on amino acid residues in proteins, and therefore, they are reversible and potentially treatable.
Highlights
Mammalian cells contain two different genomes: the nucleic genome and a smaller mitochondrial genome, and both genomes may be epigenetically modified
The three types of stress modify proteins including histones, enzymes participating in the establishment of the classical epigenetic cues, DNA damage reparation enzymes, and proteins participating in intracellular pathway through posttranslational regulation
These stresses participate in the nongenomic tuning of the phenotype modifying previously existing epigenetic cues, having beneficial effects, or increasing or decreasing the risk of diseases later in life including cardiometabolic disorders
Summary
Mammalian cells contain two different genomes: the nucleic genome and a smaller mitochondrial genome, and both genomes may be epigenetically modified. The three types of stress modify proteins including histones, enzymes participating in the establishment of the classical epigenetic cues, DNA damage reparation enzymes, and proteins participating in intracellular pathway through posttranslational regulation. They induce changes that may act as new epigenetic marks. RNS, in proper concentrations, function as second messengers, participate in signal transduction pathways, and serve as nonspecific defenses forming part of the immune responses When their concentrations are increased, RNS elevate the level of toxic molecules and may induce cellular damage in the presence of an oxidative environment [27, 28]. The following molecules are considered RNS: peroxynitrite (ONOO-), nitrogen dioxide (·NO2), peroxynitrous acid ((ynNHnitiONrtirc3Oo-u)a3,)scn,iaddictirin(diOtite(r2Oo(NNgNOeOnOO2tO-Hr)i,H)oa,x)n,niddpietenr(oriNotsrox2oynOxniy3uil)tm,raannticietoar(ontiOxo(y2nNlN(O(OHN-)ONO[-O+8),)]),.p, npereitorroxaxyte--
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