Titlebook: Anticarcinogenesis and Radiation Protection; Peter A. Cerutti,Oddvar F. Nygaard,Michael G. Simi Book 1987 Plenum Press, New York 1987 canc

小平面

Book 1987d free radical chemistry. At the basis of carcinogenesis lie changes in the dynamics of growth and differentiation of specific cell subpopulations in the target tissue. ‘These changes are brought about by selective toxicity and modulation of gene expression that are induced by xenobiotic carcinogens

拘留

biology and free radical chemistry. At the basis of carcinogenesis lie changes in the dynamics of growth and differentiation of specific cell subpopulations in the target tissue. ‘These changes are brought about by selective toxicity and modulation of gene expression that are induced by xenobiotic carcinogens978-1-4615-6464-5978-1-4615-6462-1

壓碎

Peter A. Cerutti,Oddvar F. Nygaard,Michael G. Simi

沒血色

吸引力

Amplification of Tissue Peroxides in Diseasefication by the fatty acid oxygenases of “triggering” levels of hydroperoxide (3) to higher levels that permit pathological rates of eicosanoid synthesis needs careful study. Intracellular levels of to 10.to 10. M lipid hydroperoxide seem likely to be involved in this amplification.

AWRY

Peroxisome Proliferation-Related Oxidative Stress and Hepato-Carcinogenesiserators form a novel class of chemical carcinogens (8), An understanding of the mechanism of induction of peroxisome proliferation and the metabolic events that accompany persistent increase in the number of these organelles is necessary to resolve the question whether these nongenotoxic hepatocarci

組裝

繁重

Mitochondrial DNA Damage during Mitochondrial Lipid Peroxidationg DNA damage to eukaryotic genes by lipid peroxidation is limited and indirect (5,13). In this communication, evidence is reported showing extensive damage to DNA of liver mitochondria occurring concomitantly with mitochondrial lipid peroxidation. Mitochondrial rather than nuclear DNA was studied si

Commonplace

The Expression of Bacterial DNA Alkylation Repair Enzymes in Mer- Human Cellst yet clear which alkylated lesions cause mutation and which cause cell death. Like ., mammalian cells can repair 06alkylG, N3alkylA, N3alkylG, 04alkylT, 02alkylT and 02alkylC lesions (10–21). However, because observations have been made with a variety of cell types the results have not always been

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