May 10, 2021 12:15 AM PDT
Harmful chemicals of heat not burn product
Harmful and potential harmful chemicals (HPHCs) and oxidative stress of macrophages are major factors responsible for smoking-caused chronic respiratory diseases. However, comparisons of HPHCs among heat not burn (HnB) product and ultra-light cigarette and their induced oxidative stress of macrophages have not been investigated.To get more news about [url=https://www.hitaste.net/]Hitaste P8[/url], you can visit hitaste.net official website.
Aim
The study detected HPHCs deliveries from HnB and ultra-light and measured their induced oxidative stress of macrophages cultured at air-liquid interface (ALI).
Methods
Total particulate matter, tar and 28 chemicals delivered from HnB, ultra-light and 3R4F cigarettes were determined. Mouse mononuclear macrophages at ALI were exposed to the aerosol of three tobacco products. Cell viability was measured by MTT assay. Reduced glutathione was detected by colorimetry method. Reactive oxygen species (ROS) was determined by fluorescence method.
Results
The results showed levels of 26 common HPHCs from both HnB product and ultra-light cigarette were less than that from 3R4F cigarette. HnB product delivered formaldehyde, acetaldehyde, propanal, butyraldehyde and crotonaldehyde more than ultra-light cigarette. The levels of 21 HPHCs were lower in the HnB product compared to the ultra-light cigarette. At the same exposure dose and time, the order of cell viability induced by aerosol of that was HnB > ultra-light > 3R4F, the order of content of intracellular reduced glutathione induced by aerosol of that was HnB > ultra-light > 3R4F. It showed no significant difference of ROS level between ultra-light and HnB in each designed exposure dose. HnB induced more ROS than ultra-light cigarette in each designed exposure time.
Harmful chemicals of heat not burn product
Harmful and potential harmful chemicals (HPHCs) and oxidative stress of macrophages are major factors responsible for smoking-caused chronic respiratory diseases. However, comparisons of HPHCs among heat not burn (HnB) product and ultra-light cigarette and their induced oxidative stress of macrophages have not been investigated.To get more news about [url=https://www.hitaste.net/]Hitaste P8[/url], you can visit hitaste.net official website.
Aim
The study detected HPHCs deliveries from HnB and ultra-light and measured their induced oxidative stress of macrophages cultured at air-liquid interface (ALI).
Methods
Total particulate matter, tar and 28 chemicals delivered from HnB, ultra-light and 3R4F cigarettes were determined. Mouse mononuclear macrophages at ALI were exposed to the aerosol of three tobacco products. Cell viability was measured by MTT assay. Reduced glutathione was detected by colorimetry method. Reactive oxygen species (ROS) was determined by fluorescence method.
Results
The results showed levels of 26 common HPHCs from both HnB product and ultra-light cigarette were less than that from 3R4F cigarette. HnB product delivered formaldehyde, acetaldehyde, propanal, butyraldehyde and crotonaldehyde more than ultra-light cigarette. The levels of 21 HPHCs were lower in the HnB product compared to the ultra-light cigarette. At the same exposure dose and time, the order of cell viability induced by aerosol of that was HnB > ultra-light > 3R4F, the order of content of intracellular reduced glutathione induced by aerosol of that was HnB > ultra-light > 3R4F. It showed no significant difference of ROS level between ultra-light and HnB in each designed exposure dose. HnB induced more ROS than ultra-light cigarette in each designed exposure time.