One of the atypical antipsychotic drugs is olanzapine (OLZ). Enhancing metabolic and detoxifying activities requires zinc (Zn). Thus, the objective of the current study was to determine if Zn supplementation might effectively reduce hepatic lesions induced by OLZ. The oxidative stress, inflammatory, and fibrotic indicators of the liver tissues were evaluated, and electrophoretic methods were used to analyze the native protein and isoenzyme patterns. Furthermore, the liver tissues were examined histopathologically. The dynamic motion of the extracted hemoglobin was also examined. In addition to the serious damage identified histopathologically, our results show that OLZ treatment altered the liver tissue’s antioxidant and inflammatory indicators. The zinc sulfate (ZnSO 4 ) salt solution, given in a dose-dependent fashion, reduced these changes. Additionally, the ZnSO 4 salt solution enhanced the natural protein, lipid, and calcium moieties of the protein pattern that were electrophoretically detected and changed by OLZ. In terms of the isoenzyme patterns, the ZnSO 4 salt solution reduced the electrophoretic catalase (CAT), peroxidase (POX), and β-esterase (β-EST) isoenzyme patterns that were hampered by OLZ in a dose-dependent manner. Rats treated with OLZ in addition to ZnSO 4 showed an increase in heme-heme interactions, suggesting that zinc therapy stabilized oxyhemoglobin. This promotes a more effective folding process that improves the use of oxygen. A dosage of 100 mg/kg of ZnSO 4 was shown to normalize physiological, histological, and biochemical markers. It also improved interactions between heme molecules.
| Journal | Biological Trace Element Research |
|---|---|
| Publisher | Springer |
| Publication Date | 2025-05-30 |
| Publication Year | 2025 |
| Volume | 204 |
| Issue | 1 |
| Pages | 189-205 |
| Document Type | Journal Article |
| eISSN | 1559-0720 |
| DOI | 10.1007/s12011-025-04673-3 |
| NARA Access Coverage | 1979-01-01~Current |
|---|---|
| Journal Homepage | https://www.springer.com/journal/12011 |
| Publisher Page | Open Publisher Page |