TY - JOUR T1 - Molecular Replacement for Cancer Metabolic and Mitochondrial Dysfunction, Fatigue and the Adverse Effects of Cancer Therapy JF - Cancer Genomics - Proteomics JO - Cancer Genomics Proteomics SP - 159 LP - 168 VL - 3 IS - 3-4 AU - GARTH L. NICOLSON AU - KENNETH A. CONKLIN Y1 - 2006/05/01 UR - http://cgp.iiarjournals.org/content/3/3-4/159.abstract N2 - During cancer treatment drug-induced oxidative stress can limit the effectiveness of therapy and cause a number of side effects such as fatigue, nausea, vomiting and diarrhea, as well as more serious adverse effects including cardiomyopathy, peripheral neuropathy, hepatotoxicity and pulmonary fibrosis. Many of these adverse effects are due to oxidative stress-mediated damage to normal tissues. Antioxidant administration and molecular replacement can mitigate the damage to normal tissues and reduce the adverse effects of cancer therapy without loss of therapeutic potential. For example, loss of efficiency in the electron transport chain caused by membrane peroxidation and reduction in coenzyme Q10 can occur during cytotoxic therapy. Molecular replacement of membrane lipids and enzymatic cofactors administered as nutritional supplements with antioxidants can prevent oxidative membrane damage and reduction of cofactors in normal tissues, restore mitochondrial and other cellular functions and reduce the adverse effects of cancer therapy. Recent clinical trials using cancer and non-cancer patients with chronic fatigue have shown the benefit of Molecular Replacement Therapy plus antioxidants in restoring mitochondrial electron transport function, reducing moderate to severe chronic fatigue and protecting mitochondrial and other cellular structures and enzymes from oxidative or other damage due to cytotoxic therapy. ER -