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Nanowires to combat cell damage and ageing in humans

Researchers from the Indian Institute of Science have found that nanowires made of vanadia can reduce cell damage in the human body. This discovery can help develop drugs that prevent ageing, cardiac disorders, and several neurological problems like Parkinson's and Alzheimer's disease. Vanadium oxide or vanadia is a form of vanadium, an element found close to titanium on the periodic table.

Reactive Oxygen Species (ROS) are produced during the normal cellular metabolism. When the level of ROS is elevated, the normal redox state of cells is disturbed, leading to damage of cellular components, including proteins, lipids, and DNA. Oxidative stress caused by ROS is responsible for various conditions ranging from a simple premature greying of hair to serious diseases like cancer, diabetes, arthritis, ageing and kidney disorders.

“Many of the antioxidant-based drugs used to control ROS, also produce ROS, though at small proportions. So we wanted to concentrate on a mechanism that mimics the natural detoxification pathways," say Profs G. Mugesh and Patrick D'Silva, who led the research team at IISc. In a paper published in Nature Communications, they have shown that vanadia nanowires actually mimic a natural antioxidant enzyme.

ROS are helpful when their concentrations are optimal. They help in numerous biochemical reactions and act as critical secondary messengers in signalling pathways. They are also essential for the normal metabolism of the human body. Hydrogen peroxide (H2O2) is the most abundant ROS produced in the body, and higher concentrations, they accounts for most of cell damage. Though the body has many ways to deal specifically with this, under certain conditions, the natural defence system may need some outside help.

“The human body has numerous mechanisms to scavenge ROS, and specifically hydrogen peroxide. However, when people are suffering from a disease, the production of ROS shoots up, and the natural scavenging mechanisms are not able to cope with. In such cases, we may have to control ROS levels artificially," says Prof Patrick D’Silva.

The IISc team has demonstrated that, when the ROS levels are too much for the natural defence system to handle, vandia nanowires can control ROS accumulation and stop the resulting cell damage. The entry of nanowires inside the cells is crucial because, the nanowires must get inside the cell to start their scavenging jobs. Therefore, the researchers treated human cells from different organs and made sure through elaborate methodology that the nanowires could efficiently enter the cells. This clearly shows that vanadia nanowires possess detoxifying abilities for a variety of cells.

Interestingly, vanadia in bulk and foam form do the exact opposite: they enhance ROS levels; hence the nanosize of vanadia is critical for its function. “It is remarkable that the material that generates ROS in bulk and foam forms, can actually destroy them at nanoscales," says Prof G. Mugesh, elaborating on the significance of the research.

With the initial positive results, the discovery needs further studies before being translated into drugs that can be administered. “We have shown that nanovanadia works at the cellular level. Next we want to focus on administering it in animals, and see how it performs," say Profs Mugesh and Patrick D'Silva.

About the authors:

 

Govindasamy Mugesh is a Professor at the Department of Inorganic and Physical Chemistry, IISc. http://ipc.iisc.ernet.in/~mugesh/

Amit A Vernekar and Prasath U. Paramasivam are at the Department of Inorganic and Physical Chemistry.

Patrick D’Silva is an Associate Professor at the Department of Biochemistry.  http://biochem.iisc.ernet.in/pdsilva.php

Devanjan Sinha and Shubhi Srivastava are at the Department of Biochemistry.

Contact:

 

Prof G. Mugesh: mugesh@ipc.iisc.ernet.in, 080 - 2360 2566

Prof Patrick D'Silva: patrick@biochem.iisc.ernet.in, 080 - 2293 2821

The paper appeared on 21 November in Nature Communications. Link to paper:

http://www.nature.com/ncomms/2014/141121/ncomms6301/full/ncomms6301.html.