Increased production of hydrogen peroxide by peripheral blood monocytes associated with smoking exposure intensity in smokers

Abstract

BackgroundSmoking is known to be associated with oxidative stress; however, it has not been elucidated whether the oxidative response is influenced by the intensity of smoking exposure.ObjectivesEvaluate the effect of smoking exposure on the secretion of hydrogen peroxide (H2O2) by the peripheral blood monocytes of smokers.MethodsA total of 25 smokers (50.3±8.8 years, 48% male) underwent the following evaluations: spirometry, pulse oximetry, body composition and total peripheral blood count. Peripheral blood monocyte (PBM) cultures were isolated and maintained, and IL-6 and TNF-α were measured in the plasma and in the supernatants of spontaneous and stimulated cultures. H2O2 was evaluated in the supernatants of the PBM cultures, and a subset of the PBM culture supernatants was stimulated with phorbol myristate acetate (PMA). We also evaluated 38 healthy controls (49.1±8.2 years, 42% male).ResultsThe spontaneous and stimulated monocytes’ secretion of H2O2 were statistically higher in the smokers than in the healthy controls (p<0.001). The H2O2 secretions were statistically significant higher after stimulation with PMA in both groups (p<0.001). In the multiple regression analysis, we identified a positive, statistically significant association between pack-years of smoking and the spontaneous secretion of H2O2 by PBM culture, adjusted for potential confounding variables. The association between PBM culture secretion of H2O2 and the production of TNF-α and IL-6 was not significant.ConclusionWe identified a positive association between higher production of H2O2 in smokers and higher smoking exposure during life. The influence of pack-years smoking may be a key modifiable factor in oxidative stress associated to smoking.

Effects of Cigarette Smoke Condensate on Oxidative Stress, Apoptotic Cell Death, and HIV Replication in Human Monocytic Cells

“…In addition to its inherent carcinogenicity, cigarette smoke is a well-known inducer of oxidative stress. In monocytes/macrophages, which are known cellular target and reservoir for HIV infection [ 11 , 12 ], exposure to cigarette smoke has been shown to disrupt the redox homeostasis [ 13 ], downregulate the expression of antioxidant genes [ 14 , 15 ], and enhance the pro-inflammatory responses [ 16 , 17 ]. Based on the significant role of oxidative stress in mediating HIV pathogenesis [ 18 , 19 ], it is rationalized that exposure of myeloid lineage cells to cigarette constituents would result in enhanced oxidative stress and subsequent induction of cellular toxicity through apoptotic pathway as well as HIV replication in monocytic cells.…”

E‐Cigarette Vapor Induces an Apoptotic Response in Human Gingival Epithelial Cells Through the Caspase‐3 Pathway

“…Cigarette smoke is a well‐known inducer of oxidative stress. Exposure of human cells, such as monocytes and macrophages, to cigarette smoke has been shown to disrupt redox homeostasis (Tanni et al, ), downregulate antioxidant gene expression (Goven et al, ), and enhance pro‐inflammatory responses (Lerner et al, ). Furthermore, the deleterious effect of cigarette smoke on gingival cells has been reported in deregulating gingival fibroblast cell cycle progression by increasing the G 0 /G 1 phase and decreasing the S and G 2 /M phases (Alamri et al, ).…”

Tissue Protein Carbonylation in Aging: A Strategic Analysis of Age-Related Protein Modification

“…, alkoxyl (RO), hydroperoxyl (HO [8]. Protein carbonyl content is actually the most general indicator and by far the most commonly used marker of protein oxidation [1,2,9] and accumulation of protein carbonyls has been observed in several human diseases including Alzheimer's disease (AD), diabetes mellitus, inflammatory bowel disease (IBD), and arthritis [9].…”