Changes in and the relationships between alpha-klotho, oxidative stress, and systemic inflammation in cigarette smokers.

Background: Although smoking is known to accelerate aging, the mechanisms by which this occurs have not been fully clarified. Serum-soluble α-Klotho (sαKl), antiaging, anti-inflammatory, and developing resistance to oxidative stress properties are known. Aim: This study aimed to determine the relationship between cigarette smoking, sαKl (antiaging hormone), inflammation, and oxidative stress. Materials and Methods: Participants included in the study were divided into smoking and nonsmoking groups. sαKl, high-sensitivity C-reactive protein (hsCRP), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were assessed and compared in the study participants. Results: There were one hundred and forty-six study participants comprising 47 (32.2%) females and 99 (67.8%) males. There were 79 (54.1%) in the nonsmoking group and 67 (45.9%) in the smoking group. A significant difference was found between the groups in respect of TAS (P < 0.001), OSI (P = 0.017), sαKl (P = 0.013), and hsCRP (P = 0.024) values. A significant negative correlation was found between the sαKl values of the smoking group and the years of smoking (r = -0.271, P = 0.038) and pack-years (r = -0.299, P = 0.021). Among the smoking group, a lower median sαKl value of <3.84 pg/ml was significantly associated with years of smoking (P = 0.028) and pack-years (P = 0.012). Conclusions: This study found that sαKl, OSI, and hsCRP were elevated in those who smoke cigarette. Large prospective studies are needed to further elucidate this area of research.

Effects of smoking on thiol/disulfide homeostasis.

OBJECTIVE: Cigarette smoking is an important risk factor for many diseases. This study aimed to evaluate whether cigarette smoking is associated with changes in the thiol/disulfide homeostasis (TDH), a novel biomarker of systemic oxidative stress. PATIENTS AND METHODS: Eighty-four smokers and 86 non-smoking healthy volunteers were enrolled. Serum native thiol, disulfide and total thiol levels, disulfide/native thiol, disulfide/total thiol, and native thiol/total thiol ratios were analyzed using a new colorimetric method. Carbon monoxide (CO) levels were measured by a piCO smokerlyzer instrument. RESULTS: The native, total, and native/total thiol levels of smoking patients were significantly lower (p<0.001 for each), and disulfide, disulfide/native thiol, and disulfide/total thiol levels were significantly higher in smokers than the healthy controls (p<0.001 for each). The CO levels of all study participants were negatively correlated with native thiol (r= -0.627, p<0.001), total thiol (r= -0.569, p<0.001), native thiol/total thiol (r= -0.515, p<0.001), and positively correlated with disulfide (r=0.398, p<0.001), disulfide/native thiol (r=0.515, p<0.001) and disulfide/total thiol (r=0.515, p<0.001) levels. CONCLUSIONS: To our knowledge, this investigation is the first in the literature that investigated TDH in cigarette smokers. Our results show that cigarette smoking may lead to oxidative stress and TDH shifts through disulfide side compared to the healthy group. Further studies with larger sample size are needed to confirm our results for showing the changes in TDH to contribute to the clinical practice.