Correlation Analysis of Alveolar Macrophage Cytochemical Parameters in Smoking and Pulmonary Oncology

Abstract

Cytochemical examination of alveolar macrophages (AM) obtained by bronchoalveolar lavage (BAL) was performed in healthy volunteers (11 non-smokers and 11 smokers) and in 9 patients with squamous lung carcinoma (all of them smokers or ex-smokers) in order to analyze its peculiarities related to the smoking habit and to lung malignancy. Assessment of non-specific esterases: alpha-naphthyl acetate esterase (ANAE) and butyrate esterase (BUT), chloroacetate esterase (CHL), acid phosphatase (AcP), intracellular glycogen (PAS reaction), lipids (Sudan black B reaction-SBB) and iron (Perl's reaction) was performed by a semiquantitative cytochemical method (1). A significant correlation was obtained between BUT and stage of squamous lung carcinoma (varying between I and IV) (r = 0.52, p < 0.05). There was a correlation between BUT and Perl's in healthy controls (r = 0.76, p < 0.05). The same type of correlation was observed in control smokers (r = 0.64, p < 0.05), in addition to a correlation between CHL and AcP (r = 0.69, p < 0.05). There was no significant BUT/Perl's correlation in patients with squamous cell lung carcinoma (r = 0.23, p > 0.05), but significant AcP/CHL correlation as was observed in control smokers (r = 0.73, p < 0.05), and a "new" type of correlation was shown to exist between ANAE and SBB (r = 0.77, p < 0.05). In spite of the unresolved nature of lung cancer, correlation analysis of cytochemical parameters in AM might have an important part in the analysis of their relative contribution to the development of smoking-related disorders and lung malignancies.

Cigarette Smoke Particle-Induced Lung Injury and Iron Homeostasis

“…[19][20][21][22] Subsequently, cell exposure to CSP, with its included HULIS, results in an internalization and successive complexation and sequestration of host iron at the particle surface. 12,[23][24][25][26][27][28][29] Compounds which complex iron can provide a template for additional condensation of ironhydroxides and a formation of oxide-centered nanoparticles follows. 30 Iron homeostasis in the cell is disrupted.…”