Abstract
In lung cancer (LC), alterations in redox balance are extensively observed and are a consequence of disease as well as co-occurrent with smoking. We previously demonstrated that metabolic disturbances such as trace element status and carbohydrate metabolism alterations are linked with redox status. The aim of this study was to evaluate relationships between the serum parameters of lipid metabolism and redox balance in LC patients. Serum parameters of lipid metabolism, i.e. total cholesterol (T-C), HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), triglycerides (TG), T-C:HDL-C ratio, non-HDL-C, apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B) and Apo-B:Apo-A1 ratio, as well as systemic redox status, i.e. total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), vitamin E (VE), vitamin C (VC), malonyldialdehyde (MDA), conjugated dienes (CD), and 4-hydroxynonenal (4-HNE) were determined in 92 LC patients and 82 control subjects (CS). LC women had significantly lower T-C and LDL-C, and higher TG, while HDL-C, Apo-A1 and Apo-B were significantly decreased in LC patients regardless of sex, when compared to CS. LC men had alterations in the systemic total redox balance such as lower TAS and higher OSI than CS men. LC women had lower VC, but VE was decreased in LC patients, regardless of sex. We observed higher lipid peroxidation in LC patients expressed via higher 4-HNE and CD. Systemic redox disturbances were associated with serum lipid alterations: TOS and OSI were positively correlated with T-C:HDL-C ratio and Apo-B:Apo-A1 ratio and negatively with HDL-C. The parameters of lipid peroxidation CD and MDA were significantly associated with variables reflecting lipid disturbances. The observed correlations were strengthened by general overweight/obesity, abdominal obesity, hypertriglyceridemia and non-smoking status. In conclusion, parameters related to lipid alterations are associated with oxidative stress in LC patients. The largest contribution from lipid parameters was revealed for T-C:HDL-C ratio, HDL-C and Apo-B:Apo-A1 ratio, while the largest contribution from redox status was revealed for OSI and VE. Overweight, obesity, hypertriglyceridemia and non-smoking status intensified these relationships.
Highlights
Disturbances in anti-/prooxidant balance resulting in oxidative stress have been recognized and intensively studied over the last several decades as one of the main factors contributing to chronic inflammation
Based on the above-presented information, that alterations in lipid metabolism may influence systemic redox status, and the lack of such studies in different cancer populations, including lung cancer, we aimed to evaluate relationships between serum markers of lipid metabolism and parameters related to redox balance in lung cancer patients
Patients were heterogeneous in terms of histological type of lung cancer and clinical stage of disease, there were no differences between lung cancer women and men
Summary
Disturbances in anti-/prooxidant balance resulting in oxidative stress have been recognized and intensively studied over the last several decades as one of the main factors contributing to chronic inflammation. The most common malignancy worldwide, chronic lung inflammation is proposed as one of the main endogenic risk factors, regardless of smoking status. The link between cigarette smoking and redox imbalance in lung cancer has been extensively studied and is widely known, factors other than tobacco smoke may contribute to systemic oxidative stress in lung cancer patients, since prevalence of the disease is systematically increasing among non-smokers [5]. Alterations of lipid metabolism in lung cancer patients have been demonstrated in several cohort and experimental studies and have even been considered as potential risk factors [7,8,9,10]. Some components of lipid metabolism, e.g. HDL-C, may present direct antioxidant activity [11], while the level of modification of others, e.g. LDL-C and TG, may indirectly protect from oxidative stress and inflammation [11,12,13]
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