The compound trans-4-hydroxy-2-nonenal (hne) is thought to lead to infections o the lung when cigarettes are smoked
Answers
Lipid peroxide (LPO) is a cellular process that is usually under normal physical conditions. Under extreme oxidative stress, the level of LPO becomes very important, and the growing body of evidence has shown that excessive LPO can be involved in carcinogenesis. Trans-4-Hydroxy-2 -Nonal (4-HNE) is a major product of LPO, and its level becomes relatively high in cells under oxidative stress. 4-HNE is capable of easily reacting with various cellular components including DNA and proteins. We had previously found that 4-HNE-DNA behavior is a powerful mutation in human cells and it has been made individually in the coding 249 of a mutant hotspot, p53 gene in human cancer. In order to understand the role of 4-HNE in cancer, we addressed the question whether 4-HNE affects DNA repair in human cells. We found that Benzo [A] piryn-dial epoxide and repair capability for UV light-induced DNA damage were compromised in human cell extracts treated with human cells or 4-HNE, mainly with cellular repair proteins. 4-HNE is through negotiation. . We also found that 4-HNE cells make Benzo [A] pyrein dial apoxide- and very sensitive to UV-induced murder. These results strongly suggest that this LPO metabolite also damages the DNA repair system not only in DNA but also in human cells. We propose that these two harmful effects of LPO may be contributory in human cancerous organisms.
Lipid peroxide (LPO) is a common cellular process that cells are under oxidative stress, which are aware of genobiotics, and are subject to bacterial or viral infections . The rising body of evidence has shown that excessive LPO can play a key role in various human diseases, including cancer. To find out that people with a defective HFE gene have an excessive amount of iron accumulation in their liver, resulting in excessive oxidative stress and high level of LPO, it is evidence that LPO is involved in human cancerous. If preventive measures are not taken, then these individuals develop hemochromatosis and ultimately develop liver cancer . In animal models, it has also been found that a high level of LPO is tightly connected to carcinogenesis
Answer:
The respiratory system extends from the nose and upper airway to the alveolar surface of the lungs, where gas exchange occurs. Inhaled tobacco smoke moves from the mouth through the upper airway, ultimately reaching the alveoli. As the smoke moves more deeply into the respiratory tract, more soluble gases are adsorbed and particles are deposited in the airways and alveoli. The substantial doses of carcinogens and toxins delivered to these sites place smokers at risk for malignant and nonmalignant diseases involving all components of the respiratory tract including the mouth.
Consider, for example, the lungs of a 60-year-old person with a 40-pack-year1 smoking history starting at age 20 years. By age 60 years, this person will have inhaled the smoke from approximately 290,000 cigarettes and will bear a substantial risk for chronic obstructive pulmonary disease (COPD) and lung cancer. The dose of inhaled toxic particles and gases received from each of these cigarettes varies depending on the nature of the tobacco, the volume and number of puffs of smoke drawn from the cigarette, the amount of air drawn in through ventilation holes as the smoke is inhaled, and local characteristics within the lung that determine the diffusion of toxic gases and the deposition of particles. Because of this repetitive and sustained injurious stimulus, the repair and remodel process that heals the damaged lung tissue takes place at the same time the lung’s defenses continue to deal with this unrelenting inhalation injury.