TY - JOUR
T1 - Superoxide removal and radiation protection in bacteria
AU - Ewing, David
AU - Jones, Steven R.
N1 - Funding Information:
1 This work is supported by Grant CA-30921, awarded by the National Cancer Institute, DHHS. ’ To whom correspondence should be addressed. a Present address: Department of Medicine, Johns Hopkins Hospital, Baltimore, MD 21205.
PY - 1987/4
Y1 - 1987/4
N2 - Previous work with procaryotic cells has identified one kind of lethal damage from ionizing radiation which occurs only within a specific range of low O2 concentrations, about 10-6 to 10-4 m. Within this range, protection can occur in three ways: (a) through the enzymatic decomposition of hydrogen peroxide (H2O2) by added catalase, (b) through the enzymatic degradation of superoxide anion radicals (.O2 -) by added superoxide dismutase (SOD), and (c) through scavenging hydroxyl radicals (.OH) by various additives. These results indicate that three radiolytic products, H2O2, .OH, and .O2 - (and/or the conjugate acid, the perhydroxyl radical, .HO2) are involved in this single kind of radiation-induced damage. Although the radiolytic productions of H2O2 and .O2 - are strongly enhanced in higher O2 concentrations, neither enzyme protects when these air-equilibrated bacteria are irradiated. These experiments address this apparent contradiction and focus on the specific issue of why the addition of SOD protects at low but not at high O2 concentrations. We propose that, at a given O2 concentration, .O2 - (and/or .HO2) may either react (with some cellular component?) to cause damage or react (with itself) to form hydrogen peroxide (H2O2). The specific O2 concentration during irradiation would determine the relative rates of these competing reactions and therefore the O2 concentration itself would establish whether or not we will observe damage from .O2 -.
AB - Previous work with procaryotic cells has identified one kind of lethal damage from ionizing radiation which occurs only within a specific range of low O2 concentrations, about 10-6 to 10-4 m. Within this range, protection can occur in three ways: (a) through the enzymatic decomposition of hydrogen peroxide (H2O2) by added catalase, (b) through the enzymatic degradation of superoxide anion radicals (.O2 -) by added superoxide dismutase (SOD), and (c) through scavenging hydroxyl radicals (.OH) by various additives. These results indicate that three radiolytic products, H2O2, .OH, and .O2 - (and/or the conjugate acid, the perhydroxyl radical, .HO2) are involved in this single kind of radiation-induced damage. Although the radiolytic productions of H2O2 and .O2 - are strongly enhanced in higher O2 concentrations, neither enzyme protects when these air-equilibrated bacteria are irradiated. These experiments address this apparent contradiction and focus on the specific issue of why the addition of SOD protects at low but not at high O2 concentrations. We propose that, at a given O2 concentration, .O2 - (and/or .HO2) may either react (with some cellular component?) to cause damage or react (with itself) to form hydrogen peroxide (H2O2). The specific O2 concentration during irradiation would determine the relative rates of these competing reactions and therefore the O2 concentration itself would establish whether or not we will observe damage from .O2 -.
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U2 - 10.1016/0003-9861(87)90080-4
DO - 10.1016/0003-9861(87)90080-4
M3 - Article
C2 - 3034162
AN - SCOPUS:0023275093
SN - 0003-9861
VL - 254
SP - 53
EP - 62
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
IS - 1
ER -