Benefit of nanocarrier of magnetic magnesium in rat malathion-induced toxicity and cardiac failure using non-invasive monitoring of electrocardiogram and blood pressure

被引：35

作者：

Mohammadi, Hamidreza ^{[1
,2
]}

Karimi, Gholamreza ^{[2
]}

Rezayat, Seyed Mahdi ^{[3
,4
,5
]}

Dehpour, Ahmad Reza ^{[3
]}

Shafiee, Hoda ^{[5
]}

Nikfar, Shekoufeh ^{[1
]}

Baeeri, Maryam ^{[1
]}

Sabzevari, Omid ^{[1
]}

Abdollahi, Mohammad ^{[1
,5
]}

机构：

[1] Univ Tehran Med Sci, Fac Pharm, Pharmaceut Sci Res Ctr, Tehran 1417614411, Iran

[2] Mashhad Univ Med Sci, Med Toxicol Res Ctr, Fac Pharm, Mashhad, Iran

[3] Univ Tehran Med Sci, Dept Pharmacol, Sch Med, Tehran 1417614411, Iran

[4] Univ Tehran Med Sci, Fac Adv Sci & Technol Med, Tehran 1417614411, Iran

[5] Islamic Azad Univ, Pharmaceut Sci Branch, Tehran, Iran

来源：

TOXICOLOGY AND INDUSTRIAL HEALTH | 2011年 / 27卷 / 05期

基金：

美国国家科学基金会;

关键词：

Malathion; organophosphate; Mg-25-magnetic isotope; PMC16; nanoparticle; porphyrin-fullerene nanoparticle; oxidative stress; OXIDATIVE STRESS; LIPID-PEROXIDATION; POTENTIAL ROLE; HYPOXIA; SULFATE; CELL; INHIBITION; ENDOTHELIN-1; ACTIVATION; GENERATION;

D O I：

10.1177/0748233710387634

中图分类号：

R1 [预防医学、卫生学];

学科分类号：

100235 [预防医学];

摘要：

Medical management in acute organophosphate (OP) poisoning is not always successful because of tissue hypoxia which results in a reduction of heart contractility and cell damage. This study reports improvement of malathion (MAL)-induced cardiac failure by a nanocarrier of magnetic isotope of Mg (PMC16). A rat model of acute MAL poisoning was set up. PMC16 nanoparticle at doses of 0.05, 0.1, 0.2 LD50 = 896 mg/kg) were administered intravenously (iv) 30 minutes after a single intraperitoneal (ip) injection of MAL (0.25 LD50 207 mg/kg). Atropine (AT; 40 mg/kg, ip) plus pralidoxime (PAM; 40 mg/kg, ip) and magnesium sulfate (MgSO4; 600 mg/kg, iv) were used as standard therapy or controls. Anesthetized animals were monitored for heart rate, electrocardiogram, blood pressure, and blood oxidative stress biomarkers like cellular lipid peroxidation, total thiol molecules, antioxidant power, gamma glutamil transpeptidase, and acetylcholinesterase (AChE) as a marker of OP toxicity. Results indicated that after MAL administration, heart rate and BP decreased and R-R duration increased. PMC16 markedly restored BP at all doses as compared with MgSO4. PMC16 at the dose of 0.05 LD50 significantly increased BP in comparison toAT + PAM. PMC16 restored heart rate at dose of 0.2 LD50 and reduced lipid peroxidation at dose of 0.05 LD50 as compared to MgSO4. PMC16 also improved total antioxidant power at all doses when compared to AT + PAM and reduced GGT activity at dose of 0.2 LD50 but did not affect total thiolmolecules. MgSO4 could improve MAL-induced reduction of total antioxidant power. After 24 h, PMC16 significantly improved MAL-suppressed AChE activity at doses of 0.05 and 0.1 LD50. PMC16 at all doses significantly recovered MAL-induced arrhythmia when compared to standard therapies. It is concluded that PMC16 is able to control OP-induced cardiac failure and toxicity.

引用

页码：417 / 429

页数：13

共 49 条

[1]

Effect of magnesium sulfate on the calcium-stimulated adenosine triphosphatase activity and lipid peroxidation of red blood cell membranes from preeclamptic women [J].