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2-Methoxyestradiol induces apoptosis in Ewing sarcoma cells through mitochondrial hydrogen peroxide production.
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The Ewing sarcoma is the second most common bone tumor in children and young adults. Despite the advances in therapy, the 5-year survival rate for patients with metastatic disease is poor, indicating the need for alternative treatments. Here, we report that 2-methoxy-estradiol (2-Me), a natural
NTP Toxicology and Carcinogenesis Studies of Rotenone (CAS No. 83-79-4) in F344/N Rats and B6C3F1 Mice (Feed Studies).
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Toxicology and carcinogenesis studies of rotenone (more than 98% pure), a pesticide, were conducted in B6C3F1 mice and F344/N rats for 14 days, 13 weeks, and 2 years. Results of the Fourteen-Day Studies: In the 14-day studies (dietary rotenone concentrations of 0-600 ppm in the first 14-day studies
Characterization of binding and uptake of 3,3',5-triido-L-thyronine in cultured mouse fibroblasts.
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The binding and internalization of 3,3'-[125I] 5-triiodo-L-thyronine ([125I]T3) was studied in cultured Swiss 3T3-4 mouse fibroblasts. At 0 C, the binding of T3 to cells is saturable, reversible, and stereospecific. These results together with those of earlier fluorescence studies using
Mode of action of the bioreductive alkylating agent, 2,3-bis(chloromethyl)-1,4-naphthoquinone.
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The bioreductive alkylating agent, 2,3-bis(chloromethyl)-1,4-napthoquinone (CMNQ), has been shown to inhibit the growth of Sarcoma 180 ascites cells in vivo. Evidence for the reductive activation of this agent via the mitochondrial respiratory chain was provided by CMNQ-induced oxidation of reduced
A role for nuclear translocation of tripeptidyl-peptidase II in reactive oxygen species-dependent DNA damage responses.
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Responses to DNA damage are influenced by cellular metabolism through the continuous production of reactive oxygen species (ROS), of which most are by-products of mitochondrial respiration. ROS have a strong influence on signaling pathways during responses to DNA damage, by relatively unclear
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