Abstract
The daily consumption of tobacco products leads to a boost in free radical production in tissues, promoting the risk for malignancies, metabolic alterations and chronic-inflammatory diseases. This study aimed to broaden the knowledge of the status of the antioxidative (AO) system in the skin, compared to the blood, of healthy appearing smokers. Both, the basic status compared to non-smokers and the short-term impact of controlled cigarette consumption in smokers were analyzed. Our study showed that the basic level of the AO system of smokers significantly differed from that of non-smokers. As determined by resonant Raman spectroscopy (RRS), the levels of exogenous AOs were decreased in both, the skin, in vivo (β-carotene and lycopene), and blood plasma (β-carotene only). In contrast, the levels of glutathione (GSH), the prototypical endogenous AO, which were analyzed by fluorimetric assays in cutaneous tape strips and blood plasma, were increased in the skin, although unchanged in the blood of smokers. Elevated cutaneous GSH levels were reflected by an elevated overall radical scavenging activity in the skin, as quantified by non-invasive electron paramagnetic resonance (EPR) spectroscopy. Analysis of the expression of selected stress-associated genes in blood immune cells by quantitative RT-PCR in subgroups of non-smokers and smokers additionally demonstrated the downregulation of AKR1C2 in smokers, and its negative correlation with blood plasma levels of the protective immune mediator interleukin-22, assessed by the ELISA technique. Controlled cigarette consumption did not alter exogenous or endogenous AOs in the skin of smokers, but decreased lycopene levels in blood plasma. Moreover, there was a decline in blood IL-22 levels, while no relevant response of blood cell gene expressions was found after the considered short time. Our data therefore demonstrate a strengthened endogenous AO status in the skin of smokers, which may indicate a long-term adaptation to chronic oxidative stress in this specific organ. While this effect was not clearly visible in the blood, this compartment seems to be useful as an immediate indicator of the body’s AO consumption. Moreover, decreased levels of AKR1C2, which we show for the first time to be expressed in immune cells, may be a candidate marker for long-term smoking. In addition, this study demonstrates that the rate constant of a spin probe decline determined by EPR spectroscopy mainly represents the endogenous AO status of a tissue.
Highlights
Physical and mental stress, and certain habits such as regular cigarette smoking, promote the generation of free radicals, like reactive oxygen species (ROS) in our cells [1,2]
In order to determine the basic AO status in the skin for nSm, mSm and severe smokers (sSm), different non-invasive spectroscopic approaches and molecular biological methods were performed: the tissue radical scavenging capacity was assessed by the absolute rate constant of the decay of the spin probe TEMPO, monitored by electron paramagnetic resonance (EPR)
The GSH concentration was quantified in the upper skin layer, using a fluorimetric assay sampled by tape stripping
Summary
Certain habits such as regular cigarette smoking, promote the generation of free radicals, like reactive oxygen species (ROS) in our cells [1,2]. The habit “smoking” is one of the main causes of oxidative stress development in the body. Cigarettes contain over 600 different ingredients, creating more than 7000 chemicals when burned, and inducing up to 1015 –1017 free radicals in the aerosol per puff during cigarette smoking [4]. It is not surprising that the consumption of cigarettes and other tobacco products is associated with physiological disorders, such as pulmonary diseases, cardiovascular dysfunction, reproductive and developmental effects and insulin resistance [5]. ROS are significantly involved in the development of inflammatory skin diseases, skin cancer and premature skin aging [6,7]
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