The Combination of Cigarette Smoking and Alcohol Consumption Synergistically Increases Reactive Carbonyl Species in Human Male Plasma.

Kanae Mure,Minae Mure,Toshiyuki Sakai,Mano Horinaka,Michihiro Mutoh,Hideki Ishikawa,Keiji Wakabayashi,Susumu Tomono

doi:10.3390/ijms22169043

Abstract

Cigarette smoking and alcohol consumption are major risk factors for lifestyle-related diseases. Although it has been reported that the combination of these habits worsens risks, the underlying mechanism remains elusive. Reactive carbonyl species (RCS) cause chemical modifications of biological molecules, leading to alterations in cellular signaling pathways, and total RCS levels have been used as a lipid peroxidation marker linked to lifestyle-related diseases. In this study, at least 41 types of RCS were identified in the lipophilic fraction of plasma samples from 40 subjects using liquid chromatography/electrospray ionization tandem mass spectrometry (LC/ESI-MS/MS). Higher levels of 10 alkanals, 5 trans-2-alkenals, 1 cis-4-alkenal, and 3 alkadienals were detected in the smoking/drinking group (N = 10) as compared to those with either habit (N = 10 each) or without both habits (N = 10) in the analysis of covariances adjusted for age and BMI. The levels of 3 alkanals, 1 trans-2-alkenal, 1 alkadienal, and 1 4-hydroxy-2-alkenal in the smoking/drinking group were significantly higher than those in the no-smoking/drinking and no-smoking/no-drinking groups. These results strongly indicate that the combination of cigarette smoking and alcohol drinking synergistically increases the level and variety of RCS in the circulating blood, and may further jeopardize cellular function.

Highlights

Smoking and alcohol consumption have been reported as major risk factors for cancers, cardiovascular diseases (CVD), and other lifestyle-related diseases
We successfully identified a wide range of lipophilic reactive carbonyl species (RCS) in chloroform/methanol extractable fractions of human plasma samples by dansyl hidrazinederivatization followed by LC/ESI-MS/MS analysis in a selected reaction mode that we developed previously
There is no surprise that higher levels of RCS were detected in the smoking/no-drinking group as compared to the no-smoking/no-drinking group in this study

Summary

Introduction

Smoking and alcohol consumption have been reported as major risk factors for cancers, cardiovascular diseases (CVD), and other lifestyle-related diseases. Health Organization (WHO), tobacco use, including cigarette smoking, causes more than 7 million deaths worldwide each year [1]. WHO estimates alcohol consumption contributes to 3 million deaths each year globally as well as to the disabilities and the poor health of millions of people worldwide [2]. It has been reported that the combination of smoking and alcohol drinking worsens the development and progression of various cancers and CVD [3,4,5]; the underlying mechanism remains elusive. Cigarette smoke contains highly reactive free radicals which promote reactive oxygen species (ROS) production [7,8]. Various types of RCS have been detected in cigarette mainstream smoke, alcoholic beverages, and human biological samples (Table S1) [10,11,12,13,14,15,16,17,18]

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