Magnesium-deficiency potentiates free radical production associated with postischemic injury to rat hearts: vitamin E affords protection.

Abstract

Preexisting magnesium deficiency may alter the susceptibility of rat hearts to postischemic oxidative injury (free radicals). This was examined in rats maintained for 3 weeks on a magnesium-deficient (Mg-D) diet with or without concurrent vitamin E treatment (1.2 mg/day, SC). Magnesium-sufficient (Mg-S) rats received the same diet supplemented with 100 mmol Mg/kg feed. Following sacrifice, isolated working hearts were subjected to 30-, 40-, or 60-min global ischemia and 30-min reperfusion. Postischemic production of free radicals was monitored using electron spin resonance (ESR) spectroscopy and spin trapping with alpha-phenyl-N-tert butylnitrone (PBN, 3 mM final); preischemic and postischemic effluent samples were collected and then extracted with toluene. PBN/alkoxyl adduct(s) (PBN/RO.; alpha H = 1.93 G, alpha N = 13.63 G) were the dominant signals detected in untreated Mg-S and Mg-D postischemic hearts, with comparably higher signal intensities observed for the Mg-D group following any ischemic duration. Time courses of postischemic PBN/RO. detection were biphasic for both groups (maxima: 2-4 and 8.5-12.5 min), and linear relationships between the extent of PBN/RO. production and the severity of both mechanical dysfunction and tissue injury were determined. Following each duration of ischemia, Mg-D hearts displayed greater levels of total PBN adduct production (1.7-2.0 times higher) and lower recovery of cardiac function (42-48% less) than Mg-S hearts. Pretreating Mg-D rats with vitamin E prior to imposing 40-min ischemia/reperfusion, led to a 49% reduction in total PBN/RO. production, a 55% lower LDH release and a 2.2-fold improvement in functional recovery, compared to untreated Mg-D hearts. These data suggest that magnesium deficiency predisposes postischemic hearts to enhanced oxidative injury and functional loss, and that antioxidants may offer significant protection against the pro-oxidant influence(s) of magnesium deficiency.

• Authors: J H Kramer, V Misík, W B Weglicki
• Journal: Free radical biology & medicine (Free Radic Biol Med) Vol. 16 Issue 6 Pg. 713-23 (Jun 1994) ISSN: 0891-5849 [Print] United States
• PMID: 8070674 (Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Free Radicals
• Vitamin E
• L-Lactate Dehydrogenase

Topics

• Animals
• Blood Pressure
• Cardiac Output
• Coronary Circulation
• Electron Spin Resonance Spectroscopy
• Free Radicals (metabolism)
• Heart (physiology, physiopathology)
• Heart Rate
• Hemodynamics (drug effects)
• L-Lactate Dehydrogenase (analysis)
• Magnesium Deficiency (complications, physiopathology)
• Male
• Myocardial Ischemia (complications, physiopathology)
• Myocardial Reperfusion
• Myocardium (metabolism)
• Rats
• Rats, Sprague-Dawley
• Time Factors
• Vitamin E (pharmacology)