|
Nitrated proteins | Activity | Hepatic indication (observed or expected) | References |
|
Carbamoyl phosphate synthase-1 (CPS-1) | Decrease | Hyperammonemia, hepatic encephalopathy | [33] |
Glutamine synthetase (GS) | Decrease | Hyperammonemia, hepatic encephalopathy related to sepsis | [34] |
3-Ketoacyl-CoA thiolase (Thiolase) | Decrease | Decreased β-oxidation of fatty acids with increased hepatic steatosis | [35] |
Aldehyde dehydrogenase 2 (ALDH2) | Decrease | Accumulation of acetaldehyde and lipid peroxides with increased aldehyde-related liver toxicity | [35] |
Complex I (NADH ubiquinone oxidoreductase) | Decrease | ROS leakage, contributing to decreased energy production and increased apoptosis or necrosis | [36] |
Complex V (ATP synthase) | Decrease | Decreased energy production with increased sensitivity toward necrotic liver injury | [11, 35–38] |
Cytochrome p450 2E1, B6 (CYP2E1, CYP2B6) | Decrease | Drug metabolism: ROS production and ethanol- and drug-induced liver toxicity | [39] |
Cytosolic Cu/Zn-SOD (SOD1) | Decrease | Decreased antioxidant defense with increased drug- or toxin-mediated hepatic damage | [35, 40] |
Mitochondrial Mn-SOD (SOD2) | Decrease | Same as above | [35, 41] |
Glutathione peroxidase (GPX) | Decrease | Same as above | [35] |
Glutathione reductase (GR) | Decrease | Increased oxidative stress with elevated levels of oxidized glutathione | [42, 43] |
AKT, IRβ, IRS-1, IRS-2 | Decrease | Decrease insulin signaling with increased hepatic insulin resistance and fatty liver | [44] |
CD95 | Decrease | Increased hepatic anti-inflammatory defense | [45] |
List of nitrated mitochondrial and cytosolic proteins | Not confirmed* | Not confirmed but likely contributing to mitochondrial dysfunction, ER stress, and liver damage | [35] |
List of nitrated mitochondrial proteins | Not confirmed | Not confirmed but likely contributing to mitochondrial dysfunction and liver damage | [46] |
List of nitrated proteins in different compartments | Not confirmed | Not confirmed but likely contributing to mitochondrial dysfunction, ER stress, and liver damage | [47] |
Glutathione-S-transferase (GST) | Increase | Increased hepatic antioxidant defense | [41] |
Heat shock protein 90 (Hsp90)** | Increase | Conversion to a toxic protein, contributing to increased liver toxicity | [48] |
Protein phosphatase type 2A (PP2A)** | Increase | Increased microvascular endothelial permeability | [49] |
|