**3. Oxidative stress and ageing**

Free radicals are highly considered as reactive atoms or molecules having one or more unpaired electron(s) in their external shell. These radicals are produced by losing or accepting a single electron, therefore acting as oxidants or reductants [20]. The terms reactive oxygen species (ROS) refer to reactive radical and non-radical derivatives of oxygen. They are produced by all aerobic cells in the mitochondria and play an important role in cell immunity, in ageing as well as in age-related diseases [21] and they are also known to cause oxidative damage to cells and molecules. This, in turn, is widely recognized as a determinant of both lifespan and health span.

Ageing, over time, is considered as a progressive loss of tissue and organ function. It is generally regarded as an endogenous, irreversible and deleterious process poorly understood biologically [22]. However, in spite of considerable research efforts, the endogenous causes of ageing remain elusive. More recently, the free radical theory of ageing, later termed as oxidative stress theory of ageing, has been postulated. This theory is based on the structural damage-based hypothesis that age-associated functional losses are the result of the accumulation of oxidative injury to macromolecules such as lipids, DNA, and proteins by ROS [22]. The theory was later refined by Harman himself to emphasise the role of mitochondrial ROS, as the majority of free radical oxygen species (ROS) production originates in the mitochondria of mammalian cells, and was termed as the mitochondrial theory of ageing (**Figure 2**).

**Figure 2.** *Oxidative stress implication in ageing.*

Even though the exact mechanism of oxidative stress-induced ageing has remained unclear, however, scientists are agreed that the increased ROS levels lead to cellular senescence, a physiological mechanism that stops cellular proliferation in response to damages that occur during replication [23].
