Molecular Bases of Disease
myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience: A NEW MECHANISM RELEVANT TO THE PATHOGENESIS OF DIABETIC NEPHROPATHY
Diabetic nephropathy (DN) is characterized by perturbations in metabolic/cellular signaling pathways with generation of reactive oxygen species (ROS). The ROS are regarded as a common denominator of various pathways, and they inflict injury on renal glomerular cells. Recent studies indicate that tubular pathobiology also plays a role in the progression of DN. However, the mechanism(s) for how high (25 mm) glucose (HG) ambience induces tubular damage remains enigmatic. myo-Inositol oxygenase (MIOX) is a tubular enzyme that catabolizes myo-inositol to d-glucuronate via the glucuronate-xylulose (G-X) pathway.Antioncogenic and Oncogenic Properties of Nrf2 in Arsenic-induced Carcinogenesis
Background: Arsenic induced cell transformation and carcinogenesis.Results: Arsenic-transformed cells have the property of apoptosis/autophagy resistance.Conclusion: The constitutive activation of Nrf2 in arsenic-transformed cells up-regulates antioxidants, decreases ROS generation, and causes apoptosis resistance and tumorigenesis.Significance: Antioncogenic role of inducible Nrf2 in normal cells and oncogenic role of constitutive activation of Nfr2 in cancer cells may increase our understanding of the mechanism of arsenic carcinogenesis and its prevention.
