[Atrioventricular block and left ventricular wall mobility disorder in a 44-year-old female patient : A case report of a rarity with pitfalls].

Eosinophilic myocarditis is a rare condition with good treatment options, which can be difficult to diagnose. The clinical presentation can vary from asymptomatic to life-threatening forms. This article describes the case of a 44-year-old woman who suffered from vertigo, chest pain and dyspnea.

Oxidative damage elicited by imbalance of free radical scavenging enzymes is associated with large-scale mtDNA deletions in aging human skin.

Mitochondrial DNA (mtDNA) mutations and impaired respiratory function have been demonstrated in various tissues of aged individuals. We hypothesized that age-dependent increase of ROS and free radicals production in mitochondria is associated with the accumulation of large-scale mtDNA deletions. In this study, we first confirmed that the proportion of mtDNA with the 4977 bp deletion in human skin tissues increases with age.

Concurrent increase of oxidative DNA damage and lipid peroxidation together with mitochondrial DNA mutation in human lung tissues during aging--smoking enhances oxidative stress on the aged tissues.

Although mutation of mitochondrial DNA (mtDNA) in human tissues has been established to associate with intrinsic aging, the impact of environmental factors on the formation and accumulation of mtDNA mutations and oxidative DNA damage in human tissues is poorly understood. We have investigated the levels of mtDNA with the 4977-bp deletion and A3243G point mutation, oxidative DNA damage (indicated by the formation of 8-hydroxy-2'-deoxyguanosine, 8-OH-dG), and lipid peroxides in lung tissues from smokers and nonsmokers of subjects of different ages. The results showed concurrent age-dependent increase of the 4977-bp deleted mtDNA (P < 0.

Aging- and smoking-associated alteration in the relative content of mitochondrial DNA in human lung.

mtDNA mutations and oxidative DNA damage has been observed to accumulate in the lung and other tissues in human aging. Thus, it is of interest to know whether the content of mtDNA is changed in aging tissues of the human. Using a competitive PCR method, we determined the relative content of mtDNA in the lung tissues of 49 subjects aged 16-85 years.

Smoking-associated mitochondrial DNA mutations and lipid peroxidation in human lung tissues.

To investigate the effect of cigarette smoking on mitochondrial DNA (mtDNA) mutation and lipid peroxidation in lung tissues, 152 samples from lung resections were collected. A novel deletion of 4,839 bp of mtDNA was found in 80 (52.6%) of the 152 lung samples.