Foreword

Nicotine and tar are well-known ingredients in cigarette smoke. Nicotine creates a physical and psychological dependence, and tar is a black mixture of hydrocarbons and free carbon in the particle phase of cigarette smoke. Tar includes harmful mutagenic and carcinogenic agents. In this review, we focus on ingredients in the gas phase of cigarette smoke, excluding nicotine and tar. In particular, the α,β-unsaturated carbonyl compounds acrolein (ACR) and methyl vinyl ketone (MVK) are focused on as components in cigarette smoke affecting human health.

The first review is “A Standardized Method for the Preparation of a Gas Phase Extract of Cigarette Smoke” by H. Higashi et al. Gas phase extracts of cigarette smoke (CSE) are widely used in smoking research instead of complete cigarette smoke. However, no standard method for preparing CSE has yet been established, making it difficult to obtain reliable, comparable data from diverse preparation procedures. H. Higashi et al. have recently succeeded in establishing a standard method for CSE preparation utilizing the tar weight trapped on the Cambridge filter in an apparatus for the preparation of CSE.

“Mass Spectrometric Approaches to the Identification of Potential Ingredients in Cigarette Smoke Causing Cytotoxicity” are reviewed by the group of Horiyama. Initially, they focused on L-tyrosine (Tyr), a chemically active amino acid with a highly reactive hydroxyl group, as one of peptides or proteins modified by ingredients in cigarette smoke. They identified the various Tyr derivatives formed by the reaction of CSE with Tyr using a sensitive liquid chromatography/mass spectrometry (LC/MS) and LC/MS/MS method and found that Tyr easily reacts with MVK in CSE. Most recently, they have shown that MVK reacts with glutathione (GSH) in cells to form the GSH–MVK adduct, and thus a possible factor for CSE-induced cytotoxicity is a decrease in intracellular GSH levels.

The third review is by Horinouchi et al. on “Carbonyl Compounds in the Gas Phase of Cigarette Mainstream Smoke and Their Pharmacological Properties,” focusing on the effects of CSE on intracellular signal transduction pathways. They clarified that ACR and MVK induce protein kinase C (PKC)-dependent activation of reduced nicotinamide adenine dinucleotide phosphate oxidase (NOX) and subsequent generation of reactive oxygen species via NOX, causing plasma membrane damage and cell apoptosis. Furthermore, ACR and MVK trigger the carbonylation of PKCα, an irreversible oxidative modification.

Finally, “Recent Progress in Analytical Methods for Determination of Urinary 3-Hydroxypropylmercapturic Acid, a Major Metabolite of Acrolein” is the title of the review by K. Higashi et al. 3-Hydroxypropylmercapturic acid (3-HPMA), a major metabolite of ACR in human urine used as a noninvasive biomarker of cigarette smoke, was their research focus. First, they compared urinary 3-HPMA levels in smokers and nonsmokers. As expected, smokers showed higher median 3-HPMA levels than nonsmokers. They next measured urinary 3-HPMA levels in patients with brain infarction. Unexpectedly, the urinary levels from stroke patients were lower than in controls. Moreover, brain infarction size was inversely correlated with the urinary 3-HPMA level. Therefore, 3-HPMA may be a candidate biomarker for diagnosing brain infarction.

These updated review articles are intriguing and will lead to further progress in this research field. The editor of this Current Topics series appreciates all the authors for their notable contributions. The authors gratefully acknowledge support from a grant by the Smoking Research Foundation.