Exposure to aerosol extract from heated tobacco products causes a drastic decrease of glutathione and protein carbonylation in human lung epithelial cells

Nishimoto-Kusunose, Shoichi; Sawa, Marie; Inaba, Yohei; Ushiyama, Akira; Ishii, Kazuyuki; Hattori, Kenji; Ogasawara, Yuki

doi:10.1016/j.bbrc.2021.12.004

Cited by 8 publications

(7 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As a result of the interaction of acrolein with GSH, GSH-acrolein adducts are formed, the cellular GSH pool is inactivated, and the tripeptide is unable to neutralize ROS. These findings might be a biochemical mechanism of acrolein-induced toxicity that has been found in patients with COPD [ 91 , 92 , 93 ]. In vitro studies on a human airway tissue model showed an acrolein dose- and length-dependent depletion of GSH and a consequently disrupted redox balance [ 14 ].…”

Section: Acrolein Is One Of the Main Risk Factors For Chronic Obstruc...mentioning

confidence: 90%

The Tobacco Smoke Component, Acrolein, as a Major Culprit in Lung Diseases and Respiratory Cancers: Molecular Mechanisms of Acrolein Cytotoxic Activity

Hikisz

Jacenik

2023

Cells

View full text Add to dashboard Cite

Acrolein, a highly reactive unsaturated aldehyde, is a ubiquitous environmental pollutant that seriously threatens human health and life. Due to its high reactivity, cytotoxicity and genotoxicity, acrolein is involved in the development of several diseases, including multiple sclerosis, neurodegenerative diseases such as Alzheimer’s disease, cardiovascular and respiratory diseases, diabetes mellitus and even the development of cancer. Traditional tobacco smokers and e-cigarette users are particularly exposed to the harmful effects of acrolein. High concentrations of acrolein have been found in both mainstream and side-stream tobacco smoke. Acrolein is considered one of cigarette smoke’s most toxic and harmful components. Chronic exposure to acrolein through cigarette smoke has been linked to the development of asthma, acute lung injury, chronic obstructive pulmonary disease (COPD) and even respiratory cancers. This review addresses the current state of knowledge on the pathological molecular mechanisms of acrolein in the induction, course and development of lung diseases and cancers in smokers.

show abstract

Section: Acrolein Is One Of the Main Risk Factors For Chronic Obstruc...mentioning

confidence: 90%

The Tobacco Smoke Component, Acrolein, as a Major Culprit in Lung Diseases and Respiratory Cancers: Molecular Mechanisms of Acrolein Cytotoxic Activity

Hikisz

Jacenik

2023

Cells

View full text Add to dashboard Cite

show abstract

“…In our previous in vitro study, we found that GSH was rapidly decreased in lung epithelial cells upon exposure to the aerosol extract of HTPs [ 13 ]. Moreover, a recent in vivo study, using our developed apparatus for aerosol exposure in animals, revealed that the reduced form of GSH decreased in mouse lung macrophages [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

“…Thus, we focused on the acute stress responses induced by IQOS aerosols, and the related factors were comparatively analyzed in the present study. GSH levels transiently decrease during reaction with xenobiotics to form conjugates, or the reduced form of GSH is oxidized to GSSG by reaction with reactive oxygen species in the cell [ 13 , 15 ]; however, the biosynthetic system and redox system of GSH are rapidly activated in response to the decrease in the reduced form of GSH [ 22 , 23 ]. The Nrf2 pathway is a well-known transcription factor involved in GSH synthesis [ 24 , 25 ].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Exposure to Heated Tobacco Products Aerosol Causes Acute Stress Responses in the Lung of Mouse

et al. 2022

View full text Add to dashboard Cite

In the present study, we evaluated the acute response of mice exposed to IQOS aerosol, a brand-name heated tobacco product (HTP), in the lung tissue. First, the thiobarbituric acid-reactive substances (TBA-RS) value was measured as an index to assess oxidative stress, and a significant increase was observed after exposure, followed by a significant increase in the total lung GSH concentration. The stress responses induced by IQOS aerosols was then analyzed by focusing on the changes in Nrf2 and ATF4, which are transcription factors that induce the expression of genes involved in GSH biosynthesis or metabolism. Although Nrf2 activation was not observed, significant accumulation of ATF4 in the nuclear fraction was noted three hours after exposure to IQOS aerosols. Upon an examination of changes in factors in the GSH biosynthetic system, a significant increase in cystine concentration in the lung tissue was measured, and an increase in xCT expression level was observed in the cell membrane fraction three–six hours after IQOS exposure. Furthermore, characteristic changes in HO-1, a stress-response protein regulated by ATF4, was discovered six hours after IQOS exposure. Moreover, analysis of the upstream ATF4 regulatory system revealed that phosphorylation of eIF2α was enhanced in the lung cytoplasmic fraction three hours after exposure to IQOS aerosols. These findings suggest that ER stress might be induced as an early response to IQOS aerosol exposure, accompanied by the activation of the eIF2α-ATF4 axis. These intracellular changes have also been reported after exposure to combustible cigarette smoke. Thus, the acute response found in the lungs of mice in the present study demonstrate that the inhalation of aerosols from IQOS elicits a biological response similar to that of combustible cigarette smoke. In conclusion, our results provide evidence that the biological effects of HTPs, such as IQOS, cannot be ignored in the lungs.

show abstract

“…Four articles were identified that utilized fractionated sampling liquid extracts to compare the in vitro effects of HTPs with cigarettes on respiratory tract cell lines [79][80][81][82]. In the first study, the gas-vapor phase of mainstream smoke from three 3R4F Kentucky reference cigarettes and of aerosol from six IQOS HTP consumables was bubbled into PBS to produce extracts [79]. Cytotoxicity was determined in A549 human lung epithelial cells after a 48-hour incubation period with the extracts.…”

Section: Cell Lines Modeling the Respiratory Tractmentioning

confidence: 99%

The Product Science of Electrically Heated Tobacco Products: An Updated Narrative Review of the Scientific Literature

Cordery,

Thompson,

Stevenson

et al. 2024

Cureus

View full text Add to dashboard Cite

Heated tobacco products represent a novel category of tobacco products in which a tobacco consumable is heated to a temperature that releases nicotine from the tobacco leaf but not to a temperature sufficient to cause combustion. Heated tobacco products may therefore have the potential to be a less harmful alternative for adult smokers who would otherwise continue to smoke cigarettes, as their use should result in exposure to substantially fewer and lower levels of toxicants. This update represents a two-year extension to our previous narrative review, which covered peer-reviewed journal articles published up to August 31, 2021. The scientific evidence published between 2021 and 2023 continues to indicate that aerosols produced from heated tobacco products contain fewer and substantially lower levels of harmful and potentially harmful constituents and that these observed reductions consistently translate to reduced biological effects in both in vitro and in vivo toxicological studies. Biomarker and clinical data from studies in which product use is controlled within a clinical setting continue to suggest changes in levels of biomarkers of exposure, biomarkers of potential harm, and clinical endpoints indicating the potential for reduced harm with switching to exclusive use of heated tobacco products in adult smokers. Overall, the available peer-reviewed scientific evidence continues to indicate that heated tobacco products offer promise as a potentially less harmful alternative to cigarettes, and as such, the conclusions of our original narrative review remain valid.

show abstract

Exposure to aerosol extract from heated tobacco products causes a drastic decrease of glutathione and protein carbonylation in human lung epithelial cells

Cited by 8 publications

References 25 publications

The Tobacco Smoke Component, Acrolein, as a Major Culprit in Lung Diseases and Respiratory Cancers: Molecular Mechanisms of Acrolein Cytotoxic Activity

The Tobacco Smoke Component, Acrolein, as a Major Culprit in Lung Diseases and Respiratory Cancers: Molecular Mechanisms of Acrolein Cytotoxic Activity

Exposure to Heated Tobacco Products Aerosol Causes Acute Stress Responses in the Lung of Mouse

The Product Science of Electrically Heated Tobacco Products: An Updated Narrative Review of the Scientific Literature

Contact Info

Product

Resources

About