TY - JOUR
T1 - Gene regulation by melatonin linked to epigenetic phenomena
AU - Korkmaz, Ahmet
AU - Rosales-Corral, Sergio
AU - Reiter, Russel J.
PY - 2012/7/15
Y1 - 2012/7/15
N2 - Many exogenous (e.g., toxins, chemicals, ultraviolet, cigarette smoke) and endogenous (e.g., hyperglycemia, dyslipidemia, cytokines, chemokines) agents disrupt the intracellular environment and result in a massive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS). The molecular damage that ROS/RNS induce is referred to as nitrooxidative stress. The cellular consequences of nitrooxidative stress include lipid peroxidation, protein oxidation and DNA damage. Additionally, ROS and RNS deplete cellular defenses and initiate inflammation. It is widely accepted that nitrooxidative stress and inflammation play important roles in the pathogenesis of a variety of human diseases and sequelae. Several processes are crucial to overcome the damaging cellular events caused by nitrooxidative stress, e.g., scavenging both ROS and RNS, induction of defense mechanisms and alleviating/suppressing inflammation are essential. Both endogenous and pharmacological concentrations of melatonin have long been known to play role in the direct scavenging of ROS and RNS as well as inducing antioxidant defense mechanisms and ameliorating inflammation. The current review summarizes research related to two major transcription factors that participate in these processes and summarizes how melatonin regulates antioxidant and pro-inflammatory genes via epigenetic on/off mechanisms.
AB - Many exogenous (e.g., toxins, chemicals, ultraviolet, cigarette smoke) and endogenous (e.g., hyperglycemia, dyslipidemia, cytokines, chemokines) agents disrupt the intracellular environment and result in a massive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS). The molecular damage that ROS/RNS induce is referred to as nitrooxidative stress. The cellular consequences of nitrooxidative stress include lipid peroxidation, protein oxidation and DNA damage. Additionally, ROS and RNS deplete cellular defenses and initiate inflammation. It is widely accepted that nitrooxidative stress and inflammation play important roles in the pathogenesis of a variety of human diseases and sequelae. Several processes are crucial to overcome the damaging cellular events caused by nitrooxidative stress, e.g., scavenging both ROS and RNS, induction of defense mechanisms and alleviating/suppressing inflammation are essential. Both endogenous and pharmacological concentrations of melatonin have long been known to play role in the direct scavenging of ROS and RNS as well as inducing antioxidant defense mechanisms and ameliorating inflammation. The current review summarizes research related to two major transcription factors that participate in these processes and summarizes how melatonin regulates antioxidant and pro-inflammatory genes via epigenetic on/off mechanisms.
KW - Cytokines
KW - Epigenetics
KW - Free radicals
KW - Melatonin
KW - Oxidative stress
KW - Transcription
UR - http://www.scopus.com/inward/record.url?scp=84861764997&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84861764997&partnerID=8YFLogxK
U2 - 10.1016/j.gene.2012.04.040
DO - 10.1016/j.gene.2012.04.040
M3 - Review article
C2 - 22569208
AN - SCOPUS:84861764997
SN - 0378-1119
VL - 503
SP - 1
EP - 11
JO - Gene
JF - Gene
IS - 1
ER -