14 may react with other free radicals and inactivate them. Furthermore, they act as metal chelators, mainly Fe and Cu, thus not allowing them to initiate Fenton and Haber–Weiss reactions (Nijveldt et al. 2001). In addition, they inhibit the activity of enzymes related to reactive species production, such as xanthine oxidase, cyclooxygenase, and lipoxygenase (Rice-Evans et al. 1996; Cotelle 2001). There are numerous studies examining the beneficial effects of polyphenolic compounds on health. It has been demonstrated that consumption of polyphenols results in the prevention of cardiovascular diseases (Hertog et al. 1997) and cancer (Cotelle 2001). Hooper et al. (2010) have also denoted that plants which are stressed by environmental conditions can produce bioactive compounds (including polyphenolic com- pounds) which offer beneficial health effects, such as stress resistance, and survival benefits to the animals that consume them. This biological principle referred to as “xenohormesis” is of high importance and explains how the environmentally stressed plant compounds can activate the animal’s cellular stress response, which in turn results in improving animal fitness and longevity. Oxidative stress, dietary oxidative stress, and reductive stress Oxidative agents and antioxidant mechanisms are in a potential balance. The disturbance of the equilibrium between oxidative mechanisms and antioxidants in favor of the former has been referred to as oxidative stress (Sies 1991). Sixteen years after the first definition of oxidative stress, Sies and Jones (2007) redefined it in a more precise way: “an imbalance between oxidants and antioxidants in favor of the oxidants leading to a disruption of redox signaling and control and/or molecular damage.” Following this line of reasoning, oxidative stress is inextricably linked with the disruption of normal signaling pathways, damage of macromolecules, and the disruption of homeostasis. The aforementioned definitions imply that oxidative stress is a result of pathophysiological circumstances or is even a cause of such processes. However, it should be noted that oxygen is not evenly distributed in tissues and cells, and therefore there are sites that are under physiological oxidative stress (Sies and Jones 2007). What is the threshold between pathological and physiological oxidative stress? This is a difficult question to answer. There are many studies in the redox biology field describing experi- ments in which two or more different treatments are compared. A treatment is usually considered to induce oxidative stress when the concentration of the products derived from the oxidation of macromolecules is elevated compared with another treatment or with baseline values. Nevertheless, it is difficult to adopt a threshold value of the A.S. Veskoukis et al. concentrations of such products in order to monitor oxidative stress. The concentration of oxidation products and antioxidant molecules could serve as a useful parameter in this regard, however (Sies and Jones 2007). In 1995, Levander et al. (1995) introduced a new term, the “dietary oxidative stress.” It denotes the disturbance of cell redox status caused exclusively by diet via the excess uptake of oxidative load or the impaired availability of antioxidants. The use of the term “dietary oxidative stress” confirms the excessive role that has been given to nutrition from scientists, but apparently follows the rules of redox biology. Every reference in the condition called oxidative stress is absolutely linked to a balance between the pool of oxidant and antioxidant mechanisms. There are two sides in this balance which have not been equally studied. On one side, oxidative stress occurs when the disturbance of the balance favors the oxidants, and reductive stress is generated after the enhance- ment of the antioxidant pool. A search of the Medline database in May 2011 turned up 84,020 papers using the keyword term “oxidative stress,” but only 69 using the term “reductive stress.” This is proof that the literature has emphasized research on oxidative stress, whereas reductive stress has been rather neglected. However, this huge discrep- ancy does not reflect the high importance of the reducing side of the equation. Albert Wendel was the first to use the term “reductive stress” in 1987 (Wendel 1987). The term has never been precisely defined, but scientists usually refer to it in relation to the oxidative side of the equation. This is probably because oxidative stress has been extensively studied, whereas reductive stress has been mainly theoreti- cally examined. Common sense tells us that reductive stress is related to conditions in which cells or organelles are in a reductive state. This could be an outcome of respiratory inhibition, a situation that results in decreased reactive species generation. Although it has not been thoroughly examined, reductive stress contributes in signal transduction regulation and gene expression (Kehrer 2007). The indices that have mostly been used for the assessment of reductive stress are the amounts of nicotinamide adenine dinucleotide (NAD+), NADH (the reduced form of nicotinamide adenine dinucleotide), nicotinamide adenine dinucleotide phosphate (NADP+), and NADPH (the reduced form of nicotinamide adenine dinucleotide phosphate), as well as the increase in the lactate/pyruvate ratio (Kehrer 2007). Finally, it appears that there is high biological affinity between oxidative stress and reductive stress, and they both play an important role in the redox biology field. The oxidative potential of plant antioxidants The regulation of the cellular redox status is an outcome of several different factors. Thus, the increase in the produc-