| Toxicity |
Interacting Protein |
Mechanism |
Reference |
| Mitochondrial Defects | 3-hydroxy-3-methylglutaryl-coenzyme A reductase (P04035) | Elevation in plasma HMG CoA reductase activity, which induced alteration in intracellular calcium/magnesium ratios and low ubiquinone levels can lead to a mitochondrial dysfunction [ ADR Type 1 ] | Hypothalamic digoxin mediated model for oncogenesis
|
| Mitochondrial Defects | Sodium/potassium-transporting ATPase (P05023) | Membrane Na+-K+ ATPase inhibition due to elevated diGOxin@which induced alteration in intracellular calcium/magnesium ratios and low ubiquinone levels can lead to a mitochondrial dysfunction [ ADR Type 1 ] | Hypothalamic digoxin mediated model for oncogenesis
|
| Myelosuppression | Multidrug resistance protein 1 (P08183) | Myelosuppression [ ADR Type 1 ] | Functional polymorphisms of the human multidrug-resistance gene: multiple sequence variations and correlation of one allele
|
| Oncogenesis | Caspase-3 (P42574) | DiGOxin induced alteration in intracellular calcium/magnesium ratios and low ubiquinone levels can lead to a mitochondrial dysfunction resulting in increased free radical generation and reduced scavenging & caspase-3 activation producing a P21 defect contributing to oncogenesis [ ADR Type 2 ] | Hypothalamic digoxin mediated model for oncogenesis
|
| Oncogenesis | P21 protein (P78460) | Digoxin induced alteration in intracellular calcium/magnesium ratios and low ubiquinone levels can lead to a mitochondrial dysfunction resulting in increased free radical generation and reduced scavenging & caspase-3 activation producing a P21 defect contributing to oncogenesis. [ ADR Type 2 ] | Hypothalamic digoxin mediated model for oncogenesis
|