Abstract
BackgroundOxidative stress enhances lipid peroxidation (LPO), which both are implicated in the promotion and progression stages of carcinogenesis, in particular under conditions of chronic inflammation and infections. Exocyclic etheno-DNA adducts, which are formed by LPO-products such as 4-hydroxy –2-nonenal, are strongly pro-mutagenic DNA lesions.MethodsThe development of ultra-sensitive detection methods for etheno-adducts in human tissues, white blood cells( WBC) and urine has provided evidence that these adducts are elevated in affected organs of cancer-prone patients, probably acting as a driving force to malignancy.ResultsTwo recent studies that yielded some new insights into disease causation are briefly reviewed:DNA-damage in WBC of mother-newborn child pairs, and lipid peroxidation derived DNA damage in patients with cancer-prone liver diseases. Our results indicate that biomonitoring of etheno-DNA adducts in humans are promising tools (i) to better understand disease aetiopathogenesis, allowing hazard identification(ii) to monitor disease progression and (iii) to verify the efficacy of chemopreventive and therapeutic interventions .Such clinical trials are warranted.
Highlights
Oxidative stress enhances lipid peroxidation (LPO), which both are implicated in the promotion and progression stages of carcinogenesis, in particular under conditions of chronic inflammation and infections
Oxidative stress enhances lipid peroxidation (LPO), which both are implicated in the promotion and progression of chronic degenerative diseases (CDD), including carcinogenesis, in particular under conditions of chronic inflammation [1]
Typical signature of exocyclic DNA damage measured in a cohort of mother-newborn child pairs DNA damage is commonly thought to be involved in CDD causation, and its impact is detrimental during fetal development
Summary
Oxidative stress enhances lipid peroxidation (LPO), which both are implicated in the promotion and progression stages of carcinogenesis, in particular under conditions of chronic inflammation and infections. Exocyclic etheno-DNA adducts, which are formed by LPO-products such as 4-hydroxy –2-nonenal, are strongly promutagenic DNA lesions. Oxidative stress enhances lipid peroxidation (LPO), which both are implicated in the promotion and progression of chronic degenerative diseases (CDD) , including carcinogenesis, in particular under conditions of chronic inflammation [1]. The resulting oxidative stress is currently implicated in over 100 human and animal CDD.Exocyclic ethenoDNA adducts, which are formed by LPO- products such as 4-hydroxy-2-nonenal (HNE), are strongly miscoding, causing specific point mutations. The recent study in a Danish cohort of mother- newborn child pairs is separately dealt with
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