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Published on: March 7, 2022
Magnesium deficiency augments myocardial response to reactive oxygen species
1Division of Cellular and Molecular Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram 695 011, India.
Abstract:
Magnesium (Mg) deficiency and oxidative stress are independently implicated in the etiopathogenesis of various cardiovascular disorders. This study was undertaken to examine the hypothesis that Mg deficiency augments the myocardial response to oxidative stress. Electrically stimulated rat papillary muscle was used for recording the contractile variation. Biochemical variables of energy metabolism (adenosine triphosphate (ATP) and creatine phosphate) and markers of tissue injury (lactate dehydrogenase (LDH) release and lipidperoxidation), which can affect myocardial contractility, were assayed in Langendorff-perfused rat hearts. Hydrogen peroxide (100 micromol/L) was used as the source of reactive oxygen species. The negative inotropic response to H2O2 was significantly higher in Mg deficiency (0.48 mmol Mg/L) than in Mg sufficiency (1.2 mmol Mg/L). Low Mg levels did not affect ATP levels or tissue lipid peroxidation. However, H2O2 induced a decrease in ATP; enhanced lipid peroxidation and the release of LDH were augmented by Mg deficiency. Increased lipid peroxidation associated with a decrease in available energy might be responsible for the augmentation of the negative inotropic response to H2O2 in Mg deficiency. The observations from this study validate the hypothesis that myocardial response to oxidative stress is augmented by Mg deficiency. This observation has significance in ischemia-reperfusion injury, where Mg deficiency can have an additive effect on the debilitating consequences.
Insights
Magnesium deficiency worsens the heart
Area of Science:
- Cardiovascular Physiology
- Oxidative Stress Research
- Mineral Metabolism
Background:
- Magnesium (Mg) deficiency and oxidative stress are known contributors to cardiovascular diseases.
- The combined impact of these factors on myocardial function requires further investigation.
Purpose of the Study:
- To investigate if magnesium deficiency amplifies the heart's reaction to oxidative stress.
- To understand the underlying biochemical mechanisms of this interaction.
Main Methods:
- Used electrically stimulated rat papillary muscle to measure contractile force.
- Analyzed biochemical markers including adenosine triphosphate (ATP), creatine phosphate, lactate dehydrogenase (LDH), and lipid peroxidation in Langendorff-perfused rat hearts.
- Induced oxidative stress using hydrogen peroxide (H2O2).
Main Results:
- Magnesium deficiency significantly increased the negative inotropic effect of H2O2 on heart muscle.
- While low Mg did not affect baseline ATP or lipid peroxidation, it exacerbated H2O2-induced ATP reduction, enhanced lipid peroxidation, and increased LDH release.
- These effects were more pronounced in magnesium-deficient hearts.
Conclusions:
- Magnesium deficiency augments the myocardial response to oxidative stress, likely due to increased lipid peroxidation and reduced energy availability.
- This finding is significant for understanding ischemia-reperfusion injury, where Mg deficiency may worsen outcomes.
- Highlights the critical role of adequate magnesium levels in cardiovascular protection against oxidative damage.
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