Lining-cell damage, lung

The problem is that it breaks down into elements that are solid. These solids include polonium-214, polonium-218, and lead-214. These elements are more of a threat to your health. If you inhale them, they may stick to the lining of your lungs. While there, they give off radiation. The radiation can kill or damage cells. The final result of radon escaping into a building can be a variety of respiratory problems. Respiratory problems are... 

There are over 40 different cell types in the respiratory system, and those particularly susceptible are the lining cells of trachea and bronchi, endothelial cells and the interstitial cells (fibroblasts and fibrocytes). Some toxic substances such as sulphur dioxide, nitrogen dioxide and ozone cause acute, direct damage to lung tissue, whereas others, such as nickel carbonyl may lead to the formation of tumours. 

Fig. 41.2 Cellular location and schematic representation of the apoptotic pathways activated by Berberine in tumor cells. Upper panels, berberine accumulates in the nucleus of A549 lung carcinoma cell line. Cells were incubated with berberine (50 pM) for the indicated times and, subsequently, nuclei were stained with the fluorescent dye DRAQ5. Images were taken in a Leica TCS SP2 confocal microscope. Pictures correspond to the central section in a confocal z-stack acquired sequentially. Green berberine Red DRAQ5 Grey DIC image. Lower panel, berberine activates in vitro the intrinsic cell death pathway. Berberine-induced apoptosis is initiated after DNA damage by cell cycle arrest in GO/Gl mediated by the ATM/p53 pathway. In addition, berberine is able to block cell cycle in G2M by activation the ATM/Chkl p53-independent pathway in some tumor cell types. Activation of these pathways leads to transcription (TF) of...

Usnic acid triggered the oxidative stress and disruption of the normal metabolic processes of breast cancer cell line MCF7 and lung cancer cell line HI 299 (null for p53) however, it was not involved in DNA damage. It was suggested that the property of usnic acid as a non-genotoxic anticancer agent that works in a p53-independent manner makes it a potential candidate for novel cancer therapy (Mayer et al. 2005). 

Kistler GS, Caldwell PR, Weibel ER. Development of fine structural damage to alveolar and capillary lining cells in oxygen-poisoned rat lungs. J Cell Biol 1967 32(3) 605-628. 

Shellard SA, Fichtinger-Schepman AMJ, Lazo JS, Hill BT. Evidence of differential cisplatin DNA adduct formation, removal and tolerance of DNA damage in three human lung carcinoma cell lines. Anti-Cancer Drugs 1993 4 491-500. 

Genotoxicity studies with A-hydroxyacetamide, a possible metabolite of acetamide, have shown that this agent is weakly mutagenic in Salmonella typhimurium and induces DNA damage in a rat hepatoma cell line. However, it did not bind covalently to DNA in vitro and did not induce morphological transformation of Syrian hamster embryo cells in vitro or inhibit gap-junctional intercellular communication in Chinese hamster lung V79 cells. 

Normally, epithelial cells that line the inner surface of the lungs secrete a substance that traps and kills bacteria, and the cilia on the epithelial cells constantly sweep away the resulting debris. When CFTR is defective or missing, this process is less efficient, and frequent infections by bacteria such as S. aureus and P. aeruginosa progressively damage the lungs and reduce respiratory efficiency. 

The camptothecins are natural products that are derived from the Camptotheca acuminata tree, and they inhibit the activity of topoisomerase I, the key enzyme responsible for cutting and religating single DNA strands. Inhibition of the enzyme results in DNA damage. Topotecan is indicated in the treatment of patients with advanced ovarian cancer who have failed platinum-based chemotherapy and is also approved as second-line therapy of small cell lung cancer. The main route of elimination is renal excretion, and for this reason caution must be exercised in patients with abnormal renal function, with dosage reduction being required. 

It appears that the primary targets of the toxic oil were the cells lining the lungs which became damaged, leading to problems in the respiratory system such as the accumulation of fluid in the lungs. The initial phase lasted for one to two months and accounted for many of the deaths. 

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