Abstract

Cigarette smoke exposure is strongly related to premature mortality and morbidity worldwide, being a risk factor of numerous pathologies. In fact, smoking is widely recognized as one of the most relevant risk factors of several inflammatory conditions and non-communicable diseases, including different lung cancers and other malignant pathologies, as well as coronary heart disease, stroke, and chronic obstructive pulmonary disease. Cigarette smoke consists in a complex matrix of thousands of different chemical compounds and substances, which by different mechanisms generate damage in biochemical * Camilo Sotomayor, Ignacio Cortés, Matías Libuy et al. 2 pathways and biological molecules both directly and indirectly. Most of these substances have carcinogenic, oxidative and pro-inflammatory effects as well as a combination of them. Specifically, reactive oxygen species (ROS) and reactive nitrogen species (RNS), reactive carbonyl compounds, and other molecules may generate oxidative injury in almost all kinds of biomolecules, compromising their function and/or structure. As a result, cigarette smoking generates oxidative stress, chronic inflammation and structural and functional alterations of the cell, leading to unspecific cell damage such as malignant cell proliferation, apoptosis and angiogenesis. These mechanisms, among others, are the cellular basis of all smoking related diseases.