T D Oberley1, W Zhong, L I Szweda, L W Oberley. 1. Pathology and Laboratory Medicine Service, William S. Middleton Memorial Veterans Administration Hospital, Madison, Wisconsin, USA. Terry.Oberley@med.va.gov
Abstract
BACKGROUND: The risk for prostate cancer seems to be reduced by certain antioxidant compounds (vitamins E and A, and selenium). METHODS: Antioxidant enzymes and oxidative damage products were localized in normal prostatic epithelium and malignant glands in primary and metastatic prostatic adenocarcinomas, using well-characterized antibodies and immunoperoxidase techniques. RESULTS: Antioxidant enzymes and four markers of oxidative damage were compared in basal and secretory cells of normal prostatic epithelium and prostate adenocarcinoma cells, and each cell type had unique patterns of enzymes and oxidative damage products. One marker of oxidative damage, a fluorophore derived from 4-hydroxy-2-nonenal-lysine adduction, was found in secretory cells of normal but not malignant epithelium, demonstrating a different oxidative metabolism in normal vs. malignant prostate epithelium. Metastatic lesions from primary prostate cancer had higher levels of manganese superoxide dismutase and nuclear oxidative damage products than did primary tumors. CONCLUSIONS: Antioxidant enzymes and oxidative damage products are modulated in metastatic compared to primary prostate cancer. Copyright 2000 Wiley-Liss, Inc.
BACKGROUND: The risk for prostate cancer seems to be reduced by certain antioxidant compounds (vitamins E and A, and selenium). METHODS: Antioxidant enzymes and oxidative damage products were localized in normal prostatic epithelium and malignant glands in primary and metastatic prostatic adenocarcinomas, using well-characterized antibodies and immunoperoxidase techniques. RESULTS: Antioxidant enzymes and four markers of oxidative damage were compared in basal and secretory cells of normal prostatic epithelium and prostate adenocarcinoma cells, and each cell type had unique patterns of enzymes and oxidative damage products. One marker of oxidative damage, a fluorophore derived from 4-hydroxy-2-nonenal-lysine adduction, was found in secretory cells of normal but not malignant epithelium, demonstrating a different oxidative metabolism in normal vs. malignant prostate epithelium. Metastatic lesions from primary prostate cancer had higher levels of manganese superoxide dismutase and nuclear oxidative damage products than did primary tumors. CONCLUSIONS: Antioxidant enzymes and oxidative damage products are modulated in metastatic compared to primary prostate cancer. Copyright 2000 Wiley-Liss, Inc.
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