Effects of Ambroxol on Spontaneous or Stimulated Generation of Reactive Oxygen Species by Bronchoalveolar Lavage Cells Harvested from Patients With or Without Chronic Obstructive Pulmonary Diseases

Pharmacology ◽  
1999 ◽  
Vol 59 (3) ◽  
pp. 135-141 ◽  
Author(s):  
Shinji Teramoto ◽  
Masashi Suzuki ◽  
Eijiro Ohga ◽  
Takeo Ishii ◽  
Hirotoshi Matsui ◽  
...  
2020 ◽  
Vol 23 (1) ◽  
pp. 57-64
Author(s):  
M. A. Shirshakova ◽  
Elena A. Morozova

A smokers lips are more likely to change because of exposure to reactive oxygen species that contain oxygen in large quantities in tobacco smoke. Oxidative stress is a crucial factor in the development of smoking-related diseases, such as oral cancer, lung cancer, and chronic obstructive pulmonary diseases. The damaging effect occurs because of the imbalance between the generation of reactive oxygen species and their detoxification. Markers of oxidative stress include parameters of lipid peroxidation, the activity of glutathione and antioxidant enzymes, and oxidative DNA damage. The destruction of hyaluronic acid (HA), the only drug used to correct lip changes, in smokers is accelerated by its participation in reactions with active oxygen forms, and not just by pathemization because of enzymatic cleavage by hyaluronidase. Mannitol has strong antioxidant properties, which makes it an ideal auxiliary substance in the composition of fillers based on HA. The role of reactive oxygen species in the aging process and their effects on both endogenous HA and HA-based drugs developed for esthetic use are discussed. A review of drugs, based on mannitol with hyaluronic fillers, is provided. The inclusion of mannitol in hyaluronic fillers is an effective and safe way to improve both short-term and long-term esthetic effects of the HA injection.


2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Mads Emil Bjørn ◽  
Hans Carl Hasselbalch

Reactive oxygen species (ROS) have been implicated in a wide variety of disorders ranging between traumatic, infectious, inflammatory, and malignant diseases. ROS are involved in inflammation-induced oxidative damage to cellular components including regulatory proteins and DNA. Furthermore, ROS have a major role in carcinogenesis and disease progression in the myeloproliferative neoplasms (MPNs), where the malignant clone itself produces excess of ROS thereby creating a vicious self-perpetuating circle in which ROS activate proinflammatory pathways (NF-κB) which in turn create more ROS. Targeting ROS may be a therapeutic option, which could possibly prevent genomic instability and ultimately myelofibrotic and leukemic transformation. In regard to the potent efficacy of the ROS-scavenger N-acetyl-cysteine (NAC) in decreasing ROS levels, it is intriguing to consider if NAC treatment might benefit patients with MPN. The encouraging results from studies in cystic fibrosis, systemic lupus erythematosus, and chronic obstructive pulmonary disease warrant such studies. In addition, the antioxidative potential of the widely used agents, interferon-alpha2, statins, and JAK inhibitors, should be investigated as well. A combinatorial approach using old agents with anticancer properties together with novel JAK1/2 inhibitors may open a new era for patients with MPNs, the outlook not only being “minimal residual disease” and potential cure but also a marked improvement in inflammation-mediated comorbidities.


2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Yang Sun ◽  
Sachiko Ito ◽  
Naomi Nishio ◽  
Yuriko Tanaka ◽  
Nana Chen ◽  
...  

Chronic obstructive pulmonary disease (COPD) is characterized by lung destruction and inflammation. As a major compound of cigarette smoke, acrolein plays a critical role in the induction of respiratory diseases. GADD34 is known as a growth arrest and DNA damage-related gene, which can be overexpressed in adverse environmental conditions. Here we investigated the effects of GADD34 on acrolein-induced lung injury. The intranasal exposure of acrolein induced the expression of GADD34, developing the pulmonary damage with inflammation and increase of reactive oxygen species (ROS). Conversely, the integrality of pulmonary structure was preserved and the generation of ROS was reduced in GADD34-knockout mice. Acrolein-induced phosphorylation of eIF2αin GADD34-knockout epithelial cells by shRNA protected cell death by reducing misfolded protein-caused oxidative stress. These data indicate that GADD34 participates in the development of acrolein-induced lung injury.


Respiration ◽  
1995 ◽  
Vol 62 (3) ◽  
pp. 125-129 ◽  
Author(s):  
Wei Dong Song ◽  
An Cheng Zhang ◽  
Yu Ying Pang ◽  
Li Hua Liu ◽  
Jing Yun Zhao ◽  
...  

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