Effects of Cigarette Smoke on TSPO-related Mitochondrial Processes.

Moshe Gavish,Abraham Weizman,Rafael Nagler,Nidal Zeineh,Martin Gabay

doi:10.3390/cells8070694

Abstract

The 18 kDa translocator protein (TSPO) is an initiator of the mitochondrial apoptosis cascade. Cigarette smoke (CS) exposure provokes alterations in TSPO expression as well as upregulation of its related functions such as mitochondrial membrane potential (ΔψM) and reactive oxygen species generation, which are associated with cell death. In the current study, H1299 lung cancer cell line exposed to CS for various time periods (30 mins, 60 mins and 120 mins) and TSPO expression and cell death processes were studied. CS exposure for 30 mins resulted in a non-significant increase in TSPO expression by 24% (p > 0.05 vs. control). CS exposure for 60 mins and 120 mins resulted in a significant increase by 43% (p < 0.05 vs. control) and by 47% (p < 0.01 vs. control), respectively. Furthermore, TSPO-related mitochondrial functions were upregulated at the 120 mins time point following CS exposure. TSPO expression is upregulated by CS, suggesting that TSPO plays a role in cell death processes induced by CS exposure. Alterations in TSPO-related cell death processes suggest that TSPO may be involved in the tissue damage caused by CS.

Highlights

Tobacco smoke, cigarette smoke (CS), is a major concern regarding human health, and is considered to be the second most common cause of death worldwide, which is rapidly expanding, imposing a worldwide menace to human health [1,2,3]
translocator protein (TSPO) expression is upregulated by CS, suggesting that TSPO plays a role in cell death processes induced by CS exposure
Following 30 mins of CS exposure, TSPO expression in the CS group increased by 24%, as compared to the control group, without statistical significance

Summary

Introduction

Cigarette smoke (CS), is a major concern regarding human health, and is considered to be the second most common cause of death worldwide, which is rapidly expanding, imposing a worldwide menace to human health [1,2,3]. CS contains approximately 250 toxic compounds [5], and causes approximately 6 million death cases per year worldwide. It is predicted that tobacco use will lead to more than 8 million death cases per year by the year 2030 [1]. CS appears to affect various organ systems, and mainly leads to diseases of the respiratory tract such as chronic obstructive pulmonary diseases (COPD) and cancer, lung, laryngeal and tongue cancers [7,8]. The mechanisms responsible for the CS-induced tissue damage are unclear

Methods

Results

Conclusion