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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 (author)
Lund University,Lunds universitet,Infektionsmedicin,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Infection Medicine (BMC),Section III,Department of Clinical Sciences, Lund,Faculty of Medicine
Nilsson, Charlotta (author)
Lund University,Lunds universitet,Kärnfysik,Fysiska institutionen,Institutioner vid LTH,Lunds Tekniska Högskola,Nuclear physics,Department of Physics,Departments at LTH,Faculty of Engineering, LTH
Rutardottir, Sigurbjörg (author)
Lund University,Lunds universitet,Infektionsmedicin,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Infection Medicine (BMC),Section III,Department of Clinical Sciences, Lund,Faculty of Medicine
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Paczesny, Jan (author)
Pallon, Jan (author)
Lund University,Lunds universitet,Kärnfysik,Fysiska institutionen,Institutioner vid LTH,Lunds Tekniska Högskola,Nuclear physics,Department of Physics,Departments at LTH,Faculty of Engineering, LTH
Åkerström, Bo (author)
Lund University,Lunds universitet,Infektionsmedicin,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Infection Medicine (BMC),Section III,Department of Clinical Sciences, Lund,Faculty of Medicine
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 (creator_code:org_t)
2010
2010
English.
In: Radiation Research. - 0033-7587. ; 174:5, s. 590-600
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Infektionsmedicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Infectious Medicine (hsv//eng)

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