Cigarette smoking induces an increase in oxidative DNA damage, 8- hydroxydeoxyguanosine, in a central site of the human lung

Abstract

To evaluate the effect of cigarette smoking on oxidative stress in lung tissues, we compared the levels of a type of oxidative DNA damage, 8-hydroxydeoxyguanosine (8-OH-dG), in tissue obtained from the central sites of lungs from 14 current smokers, seven ex-smokers and nine non-smokers. The mean level of 8-OH-dG in the lung tissues from smokers was 1.43-fold higher than that of the non-smokers (the difference was statistically significant, P = 0.0262). A positive correlation between the 8-OH-dG levels in normal lung tissues and the Brinkman index was obtained from smokers and ex-smokers (r = 0.525; P = 0.0134). A positive correlation was also obtained for the 8-OH-dG levels in normal lung tissues and the number of cigarettes smoked per day (r = 0.436; P = 0.0132). These results suggest that oxidative DNA damage is induced in lung DNA by cigarette smoking.

Determination of urinary oxidative DNA damage marker 8-hydroxy-2′-deoxyguanosine and the association with cigarette smoking

“…This result is in agreement with others in the literature [16,39], indicating that cigarette smoking induces oxidative damage to DNA, although the effect was not observed in all smokers.…”

“…Loft et al [9] reported smokers excreted 50% more 8OHdG than non-smokers in 24 h urine, indicating a 50% increased rate of oxidative DNA damage from smoking. Asami et al [16] found a positive correlation between the number of cigarette smoked per day and the 8OHdG levels in normal lung tissues. But there are overall very few data on oxidative DNA damage in smokers.…”

“…Due to its mutagenic potential, 8OHdG has been widely suggested as a biomarker for various cancers [12][13][14]. The concentration of 8OHdG is also evaluated in smokers and non-smokers [9,15,16] since cigarette smoke contains a large amount of oxygen radical forming substances, such as catechol and hydroquinone that may enhance lung carcinogenesis by free radical-mediated reactions. Loft et al [9] reported smokers excreted 50% more 8OHdG than non-smokers in 24 h urine, indicating a 50% increased rate of oxidative DNA damage from smoking.…”

“…HPLC-ECD is the most common method for its high sensitivity and good selectivity. However, using HPLC for 8OHdG often employed complicated and time-consuming double or triple column switching [16,18,22] and two or three-step solid phase extraction (SPE) [16,18]. Capillary electrophoresis (CE) has been interested in life sciences due to its high efficiency, high speed, and small sample size requirement [23][24][25][26][27].…”

Dissociation of DNA damage and mitochondrial injury caused by hydrogen peroxide in SV-40 transformed lung epithelial cells

“…These different reactive species might be responsible for much of the tissue injuries and disease states associated with inflammation. Increased oxidative DNA damage, such as 8-hydroxyguanine formation in human lung tissue [5], is found in smokers compared with non-smokers. Oxidative stress may play an important role in the pathogenesis of smoking-associated diseases, such as chronic obstructive pulmonary diseases (COPD) [6,7], asthma [8], and carcinogenesis [9-11].…”