Foods containing rich sources of antioxidants, like blueberries and red peppers, have long been hailed as ‘superfoods’ by various health specialists and supermarkets alike, promoting better health along the way.
The premise was simple: these foods helped against the formation free-radicals, or oxidants, which had long been associated with a variety of conditions, ranging from skin ageing to cancer.
To understand what an oxidant is, one has to look at its atomic structure. Every atom is made up of a nucleus, compromising varying numbers of positive protons and neutral neutrons. Surrounding this core is a cloud of negatively charged electrons, which surround the nucleus in pairs. When the number of protons and electrons are equal the atom is stable, and unlikely to react.
However, should the number of electrons diverge from this equilibrium, the atom becomes highly reactive. At this point, it becomes a free radical.
Free radical formation occurs naturally in the body, typically as a byproduct of oxygen metabolism, usually called a reactive oxygen species.
Seeing as they are extremely reactive, when these compounds enter cells, they are capable of altering genetic information as well as changing the chemical structure of proteins, capable of kick-starting the mechanisms responsible for cell removal. As a result, foods rich in antioxidants, which neutralise the free radicals, have been thoroughly promoted to ensure a healthy lifestyle.
New research has been put forward however that may alter our understanding free radicals, and could completely turn our knowledge, with regards to health aspects of oxidants, upside down.
This new research was published in the scientific journal Cell by scientists at McGill University, Canada.
They examined the effects of free radicals in the mitochondria of nematode worm Caenorhabditis elegans, an organelle within cells responsible for providing energy, and a potent source of free radical leakage.
The team observed that exposure to free radicals triggered a biochemical pathway known as apoptosis, which occurs naturally in cells, and is the process by which cells are deleted.
Around fifty to seventy billion cells undergo this procedure, which white blood cells mopping up the remains, keeping the surrounding tissue healthy. The reasons the cell does this are varied and numerous, including the likes of cancer prevention and the elimination of pathogens.
However, what they discovered showed that these free radicals actually stimulate apoptosis in a certain way, via pro-longevity apoptotic signalling, which lead to the reinforcement of protective mechanisms which meant the organisms lived longer, even under demanding conditions, the paper wrote. This pathway differs from the usual one in which apoptosis is the conclusion.
Using the nematode worm species, where the Nobel Prize-winning discovery of apoptosis was first found, the scientists looked to augment the levels of free radical production, noting how increasing this production increased survival of the organism via this alternative pathway.
“People believe that free radicals […] cause ageing” said Siegfried Hekimi, senior author of the research speaking to the McGill news release. However, his theory may need to be updated. “We have turned this theory on its head by proving that free radical production increases during aging because free radicals actually combat […] ageing. In fact, in our model organism we can elevate free radical generation and thus induce a substantially longer life.”
“Showing the actual molecular mechanisms by which free radicals can have a pro-longevity effect provides strong new evidence of their beneficial effects as signalling molecules” added Hekimi, underlining the importance of his team’s findings.
How relevant is this research for pharmaceutical and cosmetic industries in the production of anti-ageing compounds?