Serum catalase, thiol and myeloperoxidase levels in children passively exposed to cigarette smoke

Abstract

Background: Free radicals found in cigarette smoke can harm all tissues and cellular structures in the human body. Passive smoking increases free radical production, leads to the depletion of antioxidants and increases oxidative stress which causes lipid peroxidation. Many studies have been conducted to determine the effects of passive smoking on antioxidant enzymes and lipid levels in adults, but pediatric studies on this topic are few. In our study, we compared the levels of antioxidants, oxidants, total and LDL cholesterol in children exposed to passive cigarette smoking with a healthy control group that was not exposed to passive smoking. Methods: A total of 41 children (4-17 years of age, 24 girls and 17 boys) exposed to passive smoking and 18 healthy girls and 12 healthy boys were included in this study. Secondhand smoking was confirmed via measurement of the cotinine/creatinine ratio. Various sociodemographic characteristics of patients were recorded. The levels of catalase, thiol, myeloperoxidase were measured to determine the antioxidant and oxidant levels in children, while the levels of total cholesterol and LDL cholesterol were measured to determine the alterations in lipid profile. Results: The groups were similar in regard to demographic characteristics. Myeloperoxidase levels were significantly higher in the passive cigarette smoking group compared to the non-exposure group; however, catalase and thiol levels were similar. In regard to lipid profile, the levels of total cholesterol and LDL cholesterol were also similar in those with and without exposure to passive smoking. Conclusions: Our findings suggest that the effects of passive smoking initially influence oxidants (MPO), but not antioxidants (thiol and catalase). However, it is apparent that passive smoking adversely affects oxidative balance in children and this may lead to the development of various diseases which could cause significant morbidity and mortality.

Effect of smoking on the redox status of knee osteoarthritis: A preliminary study

“…These findings could be explained since smoking has been shown to increase the activity of the enzyme, which is involved in the generation of ROS, which favor the process of cartilage loss. 42,43 In addition, no studies have evaluated the effect of tobacco on MPO activity in patients with OA; therefore, our results are the first to suggest that smoking favors greater MPO activity, possibly through the activation of phagocytic cells, especially polymorphonuclear (PMN) cells, enhancing joint damage because MPO in the presence of chlorides is capable of generating HOCL and chlorine molecules, which are highly reactive and capable of oxidizing type II collagen, one of the main ECM proteins, increasing the susceptibility of type II collagen to proteolytic degradation. 7 In this study, ROS was only assessed in SF because the amount of plasma sample obtained was insufficient to perform all assays.…”

White Matter Lesions in Migraine

“…Moreover, during a migraine attack, serum concentrations of C-reactive protein, von Willebrand factor, IL-1b, IL-6, IL-8, and tumor necrosis factor-a increase further. 70 There is evidence for intracranial plasma extravasation ipsilateral to the side of headache, with the demonstration of technetium-99m human serum albumin tracer extravasation in the area of reported pain, 71 and gadolinium enhancement in close vicinity to the middle meningeal artery following a series of migraine attacks has been reported. 72 Neuroinflammation has been studied more extensively in multiple sclerosis.…”

Advanced brain MRI may help understand the link between migraine and multiple sclerosis

“…Furthermore, certain microglial inflammasome, NLRP3, mediate the release of IL-1β and thereby contribute to central sensitization [ 89 ]. SD as the electrophysiologic event underlying migraine attacks has been demonstrated to further temporarily upregulate pro-inflammatory cytokines such as IL-6, IL-1β and TNF-α during migraine attacks [ 90 ]. A transient increase in the proinflammatory cytokine ICAM-1 and chemokine levels has been confirmed in the jugular blood of migraine patients during attacks [ 91 ] and intracranial inflammatory plasma extravasation ipsilateral to the side of headache has been demonstrated with Tc-99 m human serum albumin tracer extravasation in the area of pain [ 92 ] as well as gadolinium enhancement close to the middle meningeal artery [ 93 ].…”