Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
Polish version English version Language
enabled [disable] Abstract
Number of results

Results found: 3

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
1
Content available remote

Carotenoids and lung cancer: biochemical aspects

100%
Salerno C., Crifò C., Siems W.
Open Chemistry
|
2011
|
vol. 9
|
issue 1
1-6
EN
Carotenoids are part of the human diet and a regular low-dose intake of these compounds from natural sources is normally preferred. Carotenoid supplementation in various diseases, including cancer, was described to be useful, but evidence has been obtained that high-dose supplementation of β-carotene may be unsafe, especially to smokers and asbestos-exposed workers, because of a stastically detected increased cancer risk. The negative effect might be mediated by carotenoid breakdown products having a high reactivity towards biomolecules. It has been suggested that these compounds originate from nonenzymatic cleavage of carotenoids by oxidants liberated in large amounts by neutrophils that accumulate in various inflammatory diseases and, in particular, in pulmonary disorders characterized by profound abnormalities in inflammatory pathways, such as those triggered by tobacco smoking. Carotenoid breakdown products, in turn, may affect neutrophil response in different ways that depend on the concentration that is reached by these products in the medium. In vitro studies show that nanomolar and micromolar concentrations of carotenoid derivatives stimulate superoxide production by neutrophils activated by phorbol myristate acetate (PMA), while a slight inhibition is noticed with cells activated by the chemotactic tripeptide N-formyl-Met-Leu-Phe (f-MLP). At higher concentrations, carotenoid breakdown products inhibit superoxide production in the presence of both PMA and f-MLP. [...]
2
Content available remote

Pain and mobility improvement and MDA plasma levels in degenerative osteoarthritis, low back pain, and rheumatoid arthritis after infrared A-irradiation

76%
Siems W., Bresgen N., Brenke R., Siems R., Kitzing M., Harting H., Eckl P. M.
|
2010
|
vol. 57
|
issue 3
313-319
EN
Infrared (IR)-A irradiation can be useful in back and musculoskeletal pain therapy. In this study joint and vertebral column pain and mobility were measured during two weeks of IR-A irradiation treatment of patients suffering from degenerative osteoarthritis of hip and knee, low back pain, or rheumatoid arthritis. Additionally, before and after IR-A treatment MDA serum levels were measured to check if MDA variations accompany changes in pain intensity and mobility. Two-hundred and seven patients were divided into verum groups getting IR-irradiation, placebo groups getting visible, but not IR irradiation, and groups getting no irradiation. In osteoarthritis significant pain reduction according to Visual Analogue Scale and mobility improvements occurred in the verum group. Even though beneficial mean value changes occurred in the placebo group, the improvements in the placebo and No Irradiation groups were without statistical significance. In low back pain, pain and mobility improvements (by 35-40%) in the verum group were found, too. A delayed (2nd week) mobility improvement in rheumatoid arthritis was seen. However, pain relief was seen immediately. In patients suffering from low back pain or rheumatoid arthritis, the pain and mobility improvements were accompanied by significant changes of MDA serum levels. However, MDA appears not a sensitive biofactor for changes of the pain intensity in degenerative osteoarthritis. Nevertheless, unaffected or lowered MDA levels during intensive IR-A therapy argue against previous reports on free radical formation upon infrared. In conclusion, rapid beneficial effects of IR-A towards musculoskeletal pain and joint mobility loss were demonstrated.
3
Content available remote

Cytotoxicity of β-carotene cleavage products and its prevention by antioxidants

76%
Alija A. J., Bresgen N., Bojaxhi E., Vogl C., Siems W., Eckl P. M.
|
2010
|
vol. 57
|
issue 2
217-221
EN
When we investigated the genotoxicity of β-carotene cleavage products (CPs) in primary rat hepatocytes stimulated to proliferate, we observed dose-dependent increases of chromosomal aberrations, sister chromatid exchanges and micronuclei. In contrast to other genotoxic substances, however, this increased genotoxicity was not accompanied by increased cytotoxicity. As a consequence we observed metaphases showing massive chromosomal damage, indicating inhibition of apoptosis by CPs enabling these cells to proceed in the cell cycle. Since proliferative stimulation by growth factors may support this effect, the in vitro toxicological effects of CPs were studied on proliferatively quiescent primary rat hepatocytes. A significant increase of both apoptosis and necrosis was found. Supplementation with antioxidants did not significantly lower the level of apoptosis, while the level of necrosis was significantly reduced by Trolox and N-acetylcysteine at all concentrations tested as well as ascorbic acid (50 µM) and a combination of Trolox (50 µM) and ascorbic acid (50 µM). These observations indicate that a) the cytotoxic potential in combination with the genotoxic potential of CPs may promote the initiation of cells due to compensatory cell division in exposed tissues and may aggravate inflammatory processes under chronic exposure, and b) the applied antioxidants may protect from cytotoxicity primarily via the detoxification of aldehydic β-carotene cleavage products.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.