Enter your email address
Submit
Write your message
Volume 20, Issue 3 (July 2026)
IJT 2026, 20(3): 130-138 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Gabari A, Salamat N, Mohammadi A. Can Medical Pharmaceutical Residues Affect Non-target Aquatic Organisms? A Model of Environmental Drug Contamination. IJT 2026; 20 (3) :130-138
URL: http://ijt.arakmu.ac.ir/article-1-1567-en.html
URL: http://ijt.arakmu.ac.ir/article-1-1567-en.html
1- Department of Marine Biology, Faculty of Marine Science and oceanography, Khorramshahr University of Marine Science and Technology, Khorramshahr, Iran.
2- Department of Marine Biology, Faculty of Marine Science and oceanography, Khorramshahr University of Marine Science and Technology, Khorramshahr, Iran. ,salamatnegin@yahoo.com
3- Department of Basic Sciences, Abadan University of Medical Sciences, Abadan, Iran.
2- Department of Marine Biology, Faculty of Marine Science and oceanography, Khorramshahr University of Marine Science and Technology, Khorramshahr, Iran. ,
3- Department of Basic Sciences, Abadan University of Medical Sciences, Abadan, Iran.
Abstract: (519 Views)
Background: The present study was carried out to identify potential effects of dexamethasone (DEX) on antioxidant parameters of Acanthopagrus arabicus, in vitro.
Methods: Cultured hepatocytes from A. arabicus were exposed to 3, 3×10, 3×10², and 3×10³ µg/ml of DEX for 48 h. Then, the toxic effects of DEX on the total antioxidant capacity (TAC), glutathione (GSH) enzyme activity, lipid peroxidation (LPO), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured at 12, 24, and 48 h of the experiment.
Results: The results indicated that the sensitivity of cultivated liver cells to DEX increased in a dose-dependent manner. The levels of TAC and GSH activity increased significantly in cells exposed to 3 and 3×10 µg/ml of DEX after 48 h of the experiment. In contrast, higher concentrations of DEX (3×10² and 3×10³ µg/ml) induced a significant decrease in TAC value and GSH activity in treated hepatocytes throughout the experiment. The LPO, AST, ALT, and ALP activities increased dose- and time-dependently in cultivated hepatocytes exposed to 3×10² and 3×10³ µg/ml and reached their peak following 48 h of exposure.
Conclusion: DEX can suppress the antioxidant defense system, as evidenced by the significant increase in lipid peroxides and decrease in antioxidant factors in the liver.
Methods: Cultured hepatocytes from A. arabicus were exposed to 3, 3×10, 3×10², and 3×10³ µg/ml of DEX for 48 h. Then, the toxic effects of DEX on the total antioxidant capacity (TAC), glutathione (GSH) enzyme activity, lipid peroxidation (LPO), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured at 12, 24, and 48 h of the experiment.
Results: The results indicated that the sensitivity of cultivated liver cells to DEX increased in a dose-dependent manner. The levels of TAC and GSH activity increased significantly in cells exposed to 3 and 3×10 µg/ml of DEX after 48 h of the experiment. In contrast, higher concentrations of DEX (3×10² and 3×10³ µg/ml) induced a significant decrease in TAC value and GSH activity in treated hepatocytes throughout the experiment. The LPO, AST, ALT, and ALP activities increased dose- and time-dependently in cultivated hepatocytes exposed to 3×10² and 3×10³ µg/ml and reached their peak following 48 h of exposure.
Conclusion: DEX can suppress the antioxidant defense system, as evidenced by the significant increase in lipid peroxides and decrease in antioxidant factors in the liver.
Keywords: Acanthopagrus arabicus, Dexamethasone, Glutathione, Liver enzymes, Total antioxidant capacity
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
The Iranian Journal of Toxicology
Arak University of Medical Sciences in collaboration with the Iranian Society of Toxicology
Website: http://ijt.arakmu.ac.ir
Email: tox.journal@gmail.com
