- The heart muscle has a lower antioxidative capacity making it more susceptible to oxidative stress, which is a result of roaming free radicals.
- Severe lack of zinc is also associated with increased oxidative stress.
- New findings show that short-term zinc deficiency decreased the antioxidative capacity of the heart muscle, while simultaneously increasing the expression of stress-associated gene and zinc concentration.
The level of zinc in the body affects the function of heart muscle in addition to essential metabolic functions. Shortage of zinc maybe the prime factor for oxidative stress, which can be determined by examining the heart muscle.
A study by the Technical University of Munich (TUM) shows the relationship between the total amount of zinc in the body and cardiac function.
Oxidative stress is as a result of roaming free radicals that are generated in the cell. They can be intercepted by antioxidants such as vitamin E.
The muscle has higher metabolic activity and the larger tissue mass in the heart leads to a large number of free radicals. Furthermore, the heart muscle also has a lower antioxidative capacity than other tissues, which makes it more susceptible to oxidative stress. And as a result, oxidative stress maybe the predisposing factor for various heart diseases.
The activity of two antioxidants, glutathione and vitamin E (α-Tocopherol), was monitored. Both these help to disable free radicals. Vitamin E helps to maintain the integrity of the cell membrane, which shields the cell contents from the environment.
How Zinc Status Regulates Oxidative Stress
To test how zinc regulates oxidative stress, young piglets were deprived of nutritional zinc to different extents for a few days. This helped to review how the declining amounts of zinc affected heart muscle function.
The findings showed that the along the decline in zinc status, the concentration of glutathione and vitamin E in the heart muscle declined. This shows that even at an early stage of life, the decline in the zinc status, already affects the heart's ability to deal with oxidative stress.
The decline in zinc status along with the cell stress, upregulates the genes responsible for programmed cell death (apoptosis).
"The body was no longer able to compensate for the resulting shortage of zinc, even though our tests only ran for a few days," said lead author Daniel Brugger from the Chair of Animal Nutrition at TUM.
"After the first phase, during which a reduction in tissue zinc concentration was observed, the heart muscle intervened and increased the amount of zinc back to the basal (control) level. However, this increase took place at the expense of the zinc content of other organs -- above all the liver, kidneys, and the pancreas." Brugger added.
Further studies are needed to validate the findings.
The the study is published in the Journal of Nutrition.
- Daniel Brugger et al. Short-Term Subclinical Zinc Deficiency in Weaned Piglets Affects Cardiac Redox Metabolism and Zinc Concentration1,2,3. Journal of Nutrition; (2017) doi: 10.3945/jn.116.240804
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