TY - JOUR
T1 - Superoxide dismutase and catalase activities in Ataxia telangiectasia and normal fibroblast cell extracts
AU - Sheridan, Richard B.
AU - Huang, P. C.
N1 - Funding Information:
This study was supported by grants from the National Foundation/March of Dimes (CRBS-300) and NIH (R01 ES 01596, P01 ES 00454). We thank Dr. Alan Lehmann for his gift of AT4BI and AT5BI.
PY - 1979/7
Y1 - 1979/7
N2 - Superoxide dismutase (EC 1.15.1.1) and catalase (EC 1.11.1.6) are important enzymes involved in protection of the cell from harmful effects of oxidative degradation. The respective substrates for these enzymes, superoxide anion and hydrogen peroxide, can be generated within the cell either by normal metabolism or by ionizing radiation. The hypothesis that the inherent radiosensitivity associated with the human autosomal recessive disease Ataxia telangiectasia is due to decreased levels of SOD and/or catalase was tested. The results suggest that fibroblast cells derived from ataxia patients are normal with respect to these two enzymes.
AB - Superoxide dismutase (EC 1.15.1.1) and catalase (EC 1.11.1.6) are important enzymes involved in protection of the cell from harmful effects of oxidative degradation. The respective substrates for these enzymes, superoxide anion and hydrogen peroxide, can be generated within the cell either by normal metabolism or by ionizing radiation. The hypothesis that the inherent radiosensitivity associated with the human autosomal recessive disease Ataxia telangiectasia is due to decreased levels of SOD and/or catalase was tested. The results suggest that fibroblast cells derived from ataxia patients are normal with respect to these two enzymes.
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U2 - 10.1016/0027-5107(79)90141-6
DO - 10.1016/0027-5107(79)90141-6
M3 - Article
C2 - 481442
AN - SCOPUS:0018428372
SN - 0027-5107
VL - 61
SP - 381
EP - 386
JO - Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
JF - Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
IS - 2
ER -