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Bystander cell death and stress response is inhibited by the radical scavenger α(1)-microglobulin in irradiated cell cultures.

Gram, Magnus LU ; Nilsson, Charlotta LU ; Rutardottir, Sigurbjörg LU ; Paczesny, Jan; Pallon, Jan LU and Åkerström, Bo LU (2010) In Radiation Research 174(5). p.590-600
Abstract
Alpha-particle irradiation of cells damages not only the irradiated cells but also nontargeted bystander cells. It has been proposed that the bystander effect is caused by oxidants and free radicals generated by the radiation. Recent studies have shown that α(1)-microglobulin protects against cell damage caused by oxidants and free radicals. Using a novel experimental system that allows irradiation of 0.02% of a human hepatoma monolayer, leaving 99.98% as bystander cells, we investigated the influence of oxidative stress and the cell-protective effects of α(1)-microglobulin during α-particle irradiation. The results showed an increase in cell death in both irradiated cells and bystander cells. A significant increase in apoptosis, oxidation... (More)
Alpha-particle irradiation of cells damages not only the irradiated cells but also nontargeted bystander cells. It has been proposed that the bystander effect is caused by oxidants and free radicals generated by the radiation. Recent studies have shown that α(1)-microglobulin protects against cell damage caused by oxidants and free radicals. Using a novel experimental system that allows irradiation of 0.02% of a human hepatoma monolayer, leaving 99.98% as bystander cells, we investigated the influence of oxidative stress and the cell-protective effects of α(1)-microglobulin during α-particle irradiation. The results showed an increase in cell death in both irradiated cells and bystander cells. A significant increase in apoptosis, oxidation markers and expression of the stress response genes heme oxygenase 1, superoxide dismutase, catalase, glutathione peroxidase 1, p21 and p53 were observed. Addition of α(1)-microglobulin reduced the amount of dead cells and inhibited apoptosis, formation of oxidation markers, and up-regulation of stress response genes. The results emphasize the role of oxidative stress in promoting bystander effects. Furthermore, the results suggest that α(1)-microglobulin protects nonirradiated cells by eliminating oxidants and free radicals generated by radiation and imply that α(1)-microglobulin can be used in radiation therapy of tumors to minimize damage to surrounding tissues. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Radiation Research
volume
174
issue
5
pages
590 - 600
publisher
Radiation Research Society
external identifiers
  • wos:000283829800007
  • pmid:20954860
  • scopus:77958103209
ISSN
0033-7587
DOI
10.1667/RR2213.1
language
English
LU publication?
yes
id
8c135f11-a871-4e93-ad50-722e7d71d148 (old id 1711040)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20954860?dopt=Abstract
date added to LUP
2010-11-05 15:39:48
date last changed
2018-07-08 03:40:17
@article{8c135f11-a871-4e93-ad50-722e7d71d148,
  abstract     = {Alpha-particle irradiation of cells damages not only the irradiated cells but also nontargeted bystander cells. It has been proposed that the bystander effect is caused by oxidants and free radicals generated by the radiation. Recent studies have shown that α(1)-microglobulin protects against cell damage caused by oxidants and free radicals. Using a novel experimental system that allows irradiation of 0.02% of a human hepatoma monolayer, leaving 99.98% as bystander cells, we investigated the influence of oxidative stress and the cell-protective effects of α(1)-microglobulin during α-particle irradiation. The results showed an increase in cell death in both irradiated cells and bystander cells. A significant increase in apoptosis, oxidation markers and expression of the stress response genes heme oxygenase 1, superoxide dismutase, catalase, glutathione peroxidase 1, p21 and p53 were observed. Addition of α(1)-microglobulin reduced the amount of dead cells and inhibited apoptosis, formation of oxidation markers, and up-regulation of stress response genes. The results emphasize the role of oxidative stress in promoting bystander effects. Furthermore, the results suggest that α(1)-microglobulin protects nonirradiated cells by eliminating oxidants and free radicals generated by radiation and imply that α(1)-microglobulin can be used in radiation therapy of tumors to minimize damage to surrounding tissues.},
  author       = {Gram, Magnus and Nilsson, Charlotta and Rutardottir, Sigurbjörg and Paczesny, Jan and Pallon, Jan and Åkerström, Bo},
  issn         = {0033-7587},
  language     = {eng},
  number       = {5},
  pages        = {590--600},
  publisher    = {Radiation Research Society},
  series       = {Radiation Research},
  title        = {Bystander cell death and stress response is inhibited by the radical scavenger α(1)-microglobulin in irradiated cell cultures.},
  url          = {http://dx.doi.org/10.1667/RR2213.1},
  volume       = {174},
  year         = {2010},
}