Crosstalk between DNA damage and inflammation can play an important role in cancer development
Chronic infections, inflammatory diseases and physicochemical factors can induce inflammation.
25% of cancer is caused by chronic inflammation.
Chronic inflammation damages DNA, which leads to mutations and genomic instability if not properly repaired.
The DNA damage response can also induce an inflammatory microenvironment, which is characterized by hypoxia.
A state of hypoxia also induces hypoxia-inducible factor and iNOS (inducible nitric oxide synthase), resulting in further progressive DNA damage resulting in a poor prognosis.
This study suggests that crosstalk between DNA damage and inflammation can play an important role in cancer development.
A proposed mechanism for the crosstalk may explain why aspirin decreases the long-term risk of cancer mortality.
Inflammatory disease, infectious agents, and physicochemical factors cause DNA damage via chronic inflammation, leading to mutations and genomic instability.
Thus, inflammation is an important cause of cancer and it is promoted in the cancer microenvironment. In this microenvironment, DNA damage and mutations accumulate, leading to carcinogenesis via genomic instability.
The DNA damage response also simultaneously induces inflammation, forming a vicious cycle.Inflammation appears to be a key tool in understanding the long-standing concept that inflammation is a precancerous symptoms.
Oxidative stress play an important role in degenerative changes of systemic tissues in aging
Another study conducted showed that oxidative stress plays an important role in degenerative changes of systemic tissues in aging.
In fact, high levels of oxidative damage results in key cellular changes including a reduction in available NAD+, an essential molecule required for a number of vital cellular processes including DNA repair, immune signaling and epigenetic processing.
In this study, experts quantify changes in NAD+ and markers of inflammation and oxidative damage in the cerebrospinal fluid of healthy humans between the ages of 24 and 91.
The cerebrospinal fluid of those aged over 45, was found to have a higher level of lipid peroxidation and inflammation, with a decreased level of both antioxidant capacity, compared to their younger counterparts.
A correlation with alcohol consumption was also identified. Those who consumed more than 1 drink per day, had lower levels of NAD+, compared to the ones who consumed no alcohol.This data suggest that as we ageing, there is an increase in oxidative damage and inflammation, and reduced NAD+ levels in the brain, which is further exacerbated by alcohol intake.