Abstract
Drinking alcohol and smoking cigarettes results in the formation of reactive aldehydes in the lung, which are capable of forming adducts with several proteins and DNA. Acetaldehyde and malondialdehyde are the major aldehydes generated in high levels in the lung of subjects with alcohol use disorder who smoke cigarettes. In addition to the above aldehydes, several other aldehydes like 4-hydroxynonenal, formaldehyde and acrolein are also detected in the lung due to exposure to toxic gases, vapors and chemicals. These aldehydes react with nucleophilic targets in cells such as DNA, lipids and proteins to form both stable and unstable adducts. This adduction may disturb cellular functions as well as damage proteins, nucleic acids and lipids. Among several adducts formed in the lung, malondialdehyde DNA (MDA-DNA) adduct and hybrid malondialdehyde-acetaldehyde (MAA) protein adducts have been shown to initiate several pathological conditions in the lung. MDA-DNA adducts are pre-mutagenic in mammalian cells and induce frame shift and base-pair substitution mutations, whereas MAA protein adducts have been shown to induce inflammation and inhibit wound healing. This review provides an insight into different reactive aldehyde adducts and their role in the pathogenesis of lung disease.
Highlights
The lung is a highly specialized organ charged with the principal role of O2/CO2 exchange between atmosphere and bloodstream [1]
Chronic alcohol abuse predisposes the host to pneumonia and acute respiratory distress syndrome (ARDS), very few studies have focused on the role of alcohol metabolism in alcohol-induced toxicity and its consequences in the lung
Many studies have been directed toward cigarette smoke-induced oxidative stress, but it has been shown that alcohol increases lipid peroxidation (LPO) leading to the generation of reactive aldehydes such as acetaldehyde and MDA
Summary
The lung is a highly specialized organ charged with the principal role of O2/CO2 exchange between atmosphere and bloodstream [1]. The enormous surface area of the airways and continuous exposure to external air makes the lung vulnerable to numerous inhaled toxicants, gases, pathogens and chemicals [2] All of these exposures make the lung susceptible to varying degrees of physical, chemical, and biological insults [3]. To combat these insults and to defend against inhaled pathogens and other toxicants, the lung employs a defense mechanism including exhalation, cough reflex, ciliary beat, and mucus clearance [4], as well as a highly complex innate immune system including airway epithelial cells [5] and resident and recruited leukocytes [2]. Oxidative stress associated with increased production of ROS in the lung due to various toxic inhalants may predispose individuals to lung diseases such as chronic obstructive pulmonary disease (COPD) [10]
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