## 3 Lipid Peroxidation, Free Radical Generation, and Antioxidant Defense System  
Cells produce ROS and reactive nitrogen species as a result of their physiological metabolism or as signaling molecules capable of regulating substantial homeostatic functions [24]. However, their overproduction could induce a cascade of oxidative imbalances [24]. It seems that there are two faces of ROS, redox signaling and oxidative stressor, contributing to both physiological and pathological conditions [25]. Within the range of low to moderate concentration levels, ROS regulate normal cell function, whilst at their highest concentrations, their biochemical instability damages cell components such as lipids, proteins, and DNA, resulting in oxidative stress [26]. The induction of oxidative stress and the over-generation of ROS may be crucial triggers that affect livestock, making animals susceptible to diseases [26]. Stress arises in animals in response to unavoidable or adverse environmental conditions (physical, chemical, biological, and psychological stressors) as well [27]. Physical stressors include fluctuations in ambient temperature as well as mechanical injuries [27]. Notably, high ambient temperature is one of the pivotal factors affecting the productivity and the health of livestock [27]. Heat stress causes a decrease in the concentration of fat-soluble vitamins and increases the concentration ROS through the signaling of heat shock proteins [28], severely compromising the antioxidant/pro-oxidants balance.  
The initial product of these oxidative imbalances is considered to be the superoxide anion (\(\mathrm{O_{2}}^{\bullet-}\)), a severe reactive radical which is generated either through the mitochondrial respiratory chain or phagocytic nicotinamide adenine dinucleotide phosphate oxidase [29]. However, the organism regulates an efficient network of mechanisms to counteract the detrimental effect of ROS, which includes enzymatic or endogenous and non-enzymatic (exogenous) factors [30]. More specifically, the superoxide anion is neutralized to hydrogen peroxide (\(\mathrm{H_{2}O_{2}}\)) through the activity of superoxide dismutase (SOD) at an extremely efficient rate [31]. The formed hydrogen peroxide could be either further neutralized via the antioxidant enzymes catalase (CAT) and glutathione peroxidase (GSH-Px) or form other ROS [26]. Amongst these ROS, the generation of hydroxyl radicals (\(\mathrm{HO}^{\bullet}\)) which are originated as a consequence of the Fenton reaction (\(\mathrm{H_{2}O_{2}}+\mathrm{Fe^{2+}}\rightarrow\mathrm{Fe^{3+}}+\mathrm{OH^{-}}+ \mathrm{OH}\)) [32], appears to exert a detrimental effect in cellular homeostasis. More specifically, the hydroxyl and perhydroxyl radicals initiate the lipid peroxidation of the polyunsaturated fatty acids generating deleterious aldehydes, namely malondialdehydedehyde (MDA) and 4-hydroxy-2-nonenal [33]. On the other hand, the high accumulation of hydroxyl radicals could also inhibit the activity of CAT and consequently suppress the neutralization of hydrogen peroxide [34]. Conversely, it has been observed that high concentrations of \(\mathrm{H_{2}O_{2}}\) could inhibit GSH-Px activity as well [35]. Interestingly, further to the crucial impair of lipid peroxidation per se, its metabolites, in combination with the formed ROS, are able to oxidate the side chain of amino acids forming proteins carbonyls [36]. Additionally, it has been reported that proteins carbonyls which are formed through the lipid peroxidation's aldehydes (such as MDA) are more frequently observed [37].  
Considering the above, it is plausible to assume that although cells have an efficient and complex mechanism to neutralize the harmful ROS and their by-products, the rapid biotransformation of these molecules could disturb the organism's homeostasis. Thus, it is of high importance to prevent the detrimental consequences of oxidative stress in its initial step exploiting a wide collection of natural antioxidants.