ATP depletion and oxidative damage of hepatic cells following acute exposure to malathion in rat: beneficial role of porphyrin–fullerene nanoparticles carrying magnetic magnesium

The objective of the present study was to investigate the role of nanocarrier of magnetic isotope of 25-Mg2+ (PMC16) in liver toxicity, ATP content and oxidative stress due to malathion (MAL) exposure. PMC16 nanoparticles were administered in different doses (0.05, 0.1 and 0.2 LD50) intravenously (i...

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Veröffentlicht in:Pharmaceutical and biomedical research 2015-06, Vol.1 (2), p.10-19
Hauptverfasser: Bakhtiarian, Azam, Abdollahi, Mohammad, Rezayat, Seyed Mahdi, Mohammadi, Hamid Reza
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Sprache:eng
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Zusammenfassung:The objective of the present study was to investigate the role of nanocarrier of magnetic isotope of 25-Mg2+ (PMC16) in liver toxicity, ATP content and oxidative stress due to malathion (MAL) exposure. PMC16 nanoparticles were administered in different doses (0.05, 0.1 and 0.2 LD50) intravenously (iv) 40 minutes after a single MAL (0.25 LD50= 207 mg/kg) intraperitoneal (ip) injection as a complement to standard therapy of pralidoxime (PAM) and atropine (AT). MgSO4 was used as another supplement for comparison with PMC16. ATP/ADP ratio, antioxidant enzymes including catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and oxidative stress biomarker including lipid peroxidation (LPO) were evaluated in liver tissue cells. Results indicated that after MAL administration, ADP/ATP ratio had a significant increase in liver tissues in comparison with control but this ratio was improved using various doses of PMC16. LPO was significantly decreased at all doses of PMC16 and MgSO4 when compared with MAL-exposed group. SOD and CAT activities significantly were increased in MAL-treated group as compared to saline group. SOD was reduced by all doses of PMC16 and CAT activity was decreased in PMC16-0.1 group. These results lead us to conclude that PMC16 and MgSO4 are so useful for protection against MAL-induced liver toxicity, ATP depletion and oxidative damages.
ISSN:2423-4486
2423-4494
DOI:10.18869/acadpub.pbr.1.2.10