CI NADH: ubiquinone oxidoreductase activity is impaired rather than predominant in high-grade malignant fresh prostate tissue. The results document a CII succinate: quinone oxidoreductase (SQR) dominant succinate oxidative flux model in the fresh non-malignant prostate tissue, which is enhanced in malignant tissue. Our objective is to document relative mitochondrial CI and complex II (CII) convergent electron flow to the Q-junction and to identify electron transport system (ETS) alterations in fresh PCa tissue. Thus, few mitochondrial respiratory assessments of freshly procured human PCa tissue have been published on this question. However, confirmatory respiratory analysis on fresh human tissue has been hampered by multiple difficulties.
Several publications have provided indirect evidence based on investigations using pre-clinical models, established cell lines, and fixed or frozen tissue bank samples. The unique metabolic properties of PCa cells have become a hot research area. Molecular mechanisms for this transformation are attributed to declining mitochondrial zinc concentrations. The transformation of prostatic epithelial cells to prostate cancer (PCa) has been characterized as a transition from citrate secretion to citrate oxidation, from which one would anticipate enhanced mitochondrial complex I (CI) respiratory flux.
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