FAQ

Oxidative stress is an imbalance between the production of free radicals and the ability of antioxidants to inhibit these toxic compounds before they cause damage to cells. This “stress” may be involved in the appearance of more than 200 pathologies and the aging of our cells.

Many studies agree to recognize the involvement of oxidative stress in damaged cells, whether at the level of DNA, membrane lipids or proteins. For example, during the process of lipid peroxidation which is characterized by three stages: initiation, propagation and termination, there is an overproduction and an accumulation of hydroperoxide within the cell. The hydroperoxide concentration can serve as an indicator of oxidative damage to the cell or biological tissue.

Within the matrices, the antioxidants act as a protective system by fighting against the action of free radicals. There are two main classes of antioxidants: enzymatic and non-enzymatic.

Unfortunately, few means exist to know if one is in a state of oxidative stress or not. In order to have an idea of ​​his state of oxidative stress, it is necessary to go through an evaluation of the antioxidant / oxidant balance, in order to offer an appropriate treatment if possible. However, not all people react in the same way when they are under oxidative stress. Each individual has their own unique antioxidant potential, depending on their genetic characteristics, lifestyle and the environment in which they live. In order to maintain the antioxidant potential at an optimal level, it is important to have good eating habits since this factor has a primordial role in the state of oxidative stress.

Oxidative stress is defined by an imbalance of the antioxidant / oxidant balance in the body.

Currently, several endogenous factors are considered to be responsible in the increase in oxidative stress, such as:

• The dysfunction of the respiratory chain in the mitochondria can be caused by ischemia-reperfusion induced during organ transplantation, surgery, or an obstruction of a blood vessel by a clot.
• The over-activation of leukocytes when a tissue is infected or damaged, leading to the consumption of oxygen which will be transformed into reactive oxygen species (ROS). This phenomenon results in inflammation of the affected area.
• Other factors such as the activation of xanthine oxidase or the oxidation of hemoglobin promoting the overproduction of oxidants.

Exogenous factors can also be responsible for an increase in oxidative stress:

• Physical inactivity
• Natural aging
• Prolonged exposure to sunlight
• Exposure to ionizing radiation
• Contact with CMR products (Carcinogens, Mutagens, Reprotoxic) such as lead, asbestos, certain chemical agents, etc.
• Smoking
• Taking medication, contraceptive pill
• Intensive sport
• Excess alcohol
• Psychological, physical, thermal stress
• Poor diet, etc.

Since oxidative stress is involved in various pathophysiologies, a review is recommended:

• In order to prevent certain pathologies linked to oxidative stress such as cancer, diabetes, heart disease, Alzheimer’s, etc.
• When the body has undergone stressful episodes (surgical operations, radical changes in the environment, etc.).
• In order to monitor oxidative stress during a prescribed treatment, thus allowing appropriate management.
• In case of progressive chronic pathology

Regarding the frequency, in the case of a first abnormal assessment, it is advisable to do a monthly follow-up to check the effectiveness of the treatment. In other cases (absence of pathology), a half-yearly or even annual follow-up assessment is sufficient to diagnose oxidative stress and the treatment.

Since oxidative stress corresponds to an imbalance of the antioxidant / oxidant balance in favor of the latter, it is necessary to rebalance this balance. For this, we can increase the concentration of antioxidants and / or decrease the production of free radicals.

The exogenous intake of antioxidants – whether by the oral, parenteral or cutaneous-mucous membranes – makes it possible to increase the concentration of antioxidant compound. However, in some cases, a simple change in lifestyle can significantly correct the balance of oxidative stress. This obviously involves a healthy and varied diet or even the practice of regular physical activity.

An antioxidant can be defined as a molecule which significantly inhibits or delays the oxidation of a substrate and this, at minimal concentrations [Haliwell et al, 1992]. They protect biological systems against the harmful effects of excessive oxidation processes [Krinsky, 1992] by preventing the formation of reactive oxygen species or neutralizing those already produced. The terms “antioxidants” and “free radical scavengers” are used interchangeably to describe these different protective mechanisms. Their presence in the body is therefore essential to maintain a correct state of health.

We can distinguish two main classes of antioxidants: enzymatic antioxidants as well as intra and extracellular non-enzymatic antioxidants intervening in a very specific order [Buettner., 1993; Haramaki et al, 1998; Bankson et al, 1993].

Enzymatic antioxidants

• Superoxide dismutases (SOD) are metalloproteins possessing enzymatic activity. They have the ability to neutralize the action of superoxide radicals by transforming them into hydrogen peroxide (H2O2), a molecule which will subsequently be transformed into water and oxygen thanks to the action of catalase.
• Catalase (CAT): Enzyme mainly present in red blood cells and peroxisomes. It catalyzes the reactions of disproportionation of oxygen peroxide into water and oxygen, which makes it possible to avoid the Haber-Weiss reaction, that is to say the genesis of extremely reactive hydroxyl radicals [Scholz et al, 1997] .
• Glutathione peroxidase: Enzyme present in extracellular fluids but also in the cytosol and mitochondria of cells, it has the capacity to neutralize hydroperoxides such as oxygen peroxide, lipid peroxides, etc.
• Melatonin: It is a neurohormone with antioxidant properties. It limits oxidative lesions on DNA, lipids, proteins, etc.

Non-enzymatic antioxidants

The enzymatic action of antioxidants is complemented by that of various non-enzymatic antioxidants that scavenge reactive oxygen species. These act as an antioxidant shield and ensure the structural integrity of nucleic acids, proteins and lipids. We can distinguish two groups of non-enzymatic antioxidants: fat-soluble and water-soluble antioxidants.

Fat-soluble antioxidants: They are naturally incorporated into membrane or circulating lipoprotein structures, due to their lipophilicity (Blache et al, 1997)

• Α-Tocopherol (Vitamin E): This vitamin inhibits the spread of lipid peroxidation [Leger, 2000]. This molecule is an excellent scavenger of lipid radicals. Each α-Tocopherol molecule can react with two radicals. After reaction, it is converted into an α-tocopheroxyl radical, a very little reactive molecule, and migrates to the surface of the cell membrane where it is reconverted into α-Tocopherol thanks to ascorbic acid (Vitamin C) [Wefers et al, 1988].
• Carotenoids: These molecules are mainly represented by α-carotene, β-carotene, lycopene, lutein, zeaxanthin, β-cryptoxanthin and canthaxanthin [Krinsky, 1992]. Carotenoids, including vitamin A, are excellent scavengers of radical species thanks to their conjugated double bond system. It seems that β-carotene is particularly reactive since it neutralizes at least two peroxyl radicals [Handelman et al, 1991].
• Bilirubin: It is the end product of heme metabolism. This molecule can effectively inhibit lipid peroxidation thanks to a mechanism similar to α-Tocopherol [Stocker et al, 1987].
• Ubiquinol (Coenzyme Ql0): Carrier of electrons in the respiratory chain of the mitochondria. This coenzyme prevents radical reactions in the mitochondria, therefore the genesis of oxidative compounds, it is an effective fat-soluble antioxidant. In addition to preventing lipid peroxidation, ubiquinol can also regenerate the α-Tocopheroxyl radical to form α-Tocopherol, like vitamin C.