Table 8.
Mechanisms of action of omeprazole implicated in genomic instability, which are associated with cancer risks.
| Dose/concentration | Study | Study model | Mechanism of action | Prevention/risk for genetic material | References |
|---|---|---|---|---|---|
| 100 mg/kg | In vivo | Rats | Hypergastrinemia and pancreatic metaplasia | Genomic instability | [216] |
| 20 mg/kg | Clinical | Case study | Hyperplasia, gastric carcinoma, hypoacidity | Cell proliferation | [211] |
| Not reported | Clinical | Human (n = 230) patients with H. pylori | Metaplasias, gastric atrophy | Gastric cancer | [217] |
| 276 mg/kg | In vivo | Rats | Induction of ROS. 8-0Hd6 | Apoptosis Tumors |
[212, 213] |
| — | Several | Several | Premalignant lesions | Genetic alterations | [214] |
| 30 mg/kg | In vivo | Rats | Inhibition of lysosomal hydrolase activity decreases P21 and mammalian target of rapamycin (mTOR) in the stomach | Changes in apoptosis and cell cycle | [215] |
| — | In silico | Artificial system | Formation of metabolites | Genomic instability | [218] |