Pub. Date : 2016 Mar
PMID : 26721299
6 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Low Dose Acetaminophen Induces Reversible Mitochondrial Dysfunction Associated with Transient c-Jun N-Terminal Kinase Activation in Mouse Liver. | Acetaminophen | mitogen-activated protein kinase 8 | Mus musculus |
| 2 | Acetaminophen (APAP) overdose causes hepatotoxicity involving mitochondrial dysfunction and c-jun N-terminal kinase (JNK) activation. | Acetaminophen | mitogen-activated protein kinase 8 | Mus musculus |
| 3 | Acetaminophen (APAP) overdose causes hepatotoxicity involving mitochondrial dysfunction and c-jun N-terminal kinase (JNK) activation. | Acetaminophen | mitogen-activated protein kinase 8 | Mus musculus |
| 4 | Acetaminophen (APAP) overdose causes hepatotoxicity involving mitochondrial dysfunction and c-jun N-terminal kinase (JNK) activation. | Acetaminophen | mitogen-activated protein kinase 8 | Mus musculus |
| 5 | Acetaminophen (APAP) overdose causes hepatotoxicity involving mitochondrial dysfunction and c-jun N-terminal kinase (JNK) activation. | Acetaminophen | mitogen-activated protein kinase 8 | Mus musculus |
| 6 | In conclusion, low dose APAP produces reversible MPT-dependent mitochondrial dysfunction and steatosis in hepatocytes without causing ALT release or necrosis, whereas high dose leads to irreversible mitochondrial dysfunction and cell death associated with sustained JNK activation. | Acetaminophen | mitogen-activated protein kinase 8 | Mus musculus |