To prevent oxidative or nitrosative stress, attention must be paid to reducing individual risk factors. Behavioral risk factors
- Diet
- Malnutrition and undernutrition – including over- and undernutrition.
- Diet low in micronutrients (few cereal products, less than 5 servings of vegetables and fruits (< 400 g/day; 3 servings of vegetables and 2 servings of fruits), few milk and dairy products, less than one to two fish per week, etc) – see prevention with micronutrients
- Pleasure food consumption
- Tobacco (smoking) – the substances inhaled in a single puff from a cigarette form 1015 free radicals in the lungs – a hundred times more than we ourselves have body cells. Detoxification of tar inhaled at the same time creates an additional 1014 free radicals.
- Physical activity
- Extreme physical work
- Competitive and high-performance sports
- UV rays – for example, sunlight, solarium.
Environmental pollution – intoxications (poisonings)
- Occupational contact with carcinogens
- Liver damage from, for example, hydrogen tetrachloride poisoning, ethanol (ethanol), etc.
What are the protective mechanisms against oxidative or nitrosative stress?
The cells of the body are not defenseless against the attacks of free radicals. So-called antioxidants – see micronutrient therapy (vital substances) for more information – intercept the free radicals and defuse them even before they can damage the cells. Antioxidants are chemical or biological substances that are able to neutralize the potential effect of free radicals. Some antioxidants, e.g. the enzymes superoxide dismutase and catalase, are endogenous, i.e. they are normal components of the body, while others (e.g. vitamins C and E) are exogenous and must be supplied in sufficient quantities every day through the diet. However, a reduced mode of action of such a system is partly responsible for an absolute or relative inefficiency of the antioxidant defense system.
| Etiology | Examples |
| ReducedAO intake | Hypovitaminosis, unbalanced diet |
| ReducedAO absorption | Malabsorption: celiac disease, Crohn’s disease, ulcerative colitis, etc. |
| ReducedAO bioavailability | Impaired uptake and transport carriers due to, e.g., aging or biochemical individuality |
| EnzymaticAO deficit | Genetic and/or iatrogenic factors |
| Abnormally increasedAO uptake | Abnormally increased production of oxidative species (e.g., smoking) |
| Medication/drug abuse | Microsomal overload |
| Diseases | See above under “Disease-related risk factors” |
AO=Antioxidants.
Vitamin B12 works best against nitrosative stress (as antagonist of NO.).
Pro oxidative stress!
- Reactive oxygen species (ROS) led to extended lifespan in studies of various model organisms:
- ROS serve as a signal for endogenous defense mechanisms → results in increased stress resistance and lifespan.
Free Radical Theory of Aging (FRTA) vs Mitohormesis.
- Free Radical Theory of Aging (FRTA)
- Free radicals are the cause of the aging process (Harman, 1956).
- Damage to cells, DNA or lipids causes the complex aging process.
- Hormesis (Greek : “stimulation”, “impetus”).
- Small doses of harmful substances can have a positive effect on the organism (Paracelsus, 1493 – 1541).
Physiological formation (eg, sports) of free radicals in the mitochondria favors health-promoting effects in the organism.
Are antioxidants now superfluous? No. They serve:
- Maintain a balance of prooxidant and antioxidant processes.
- Physiological processes
Micronutrients (vital substances) in the low dose range up to 3 times RDA (Recommended Dietary Allowances) are safe in terms of negative suppression of oxidative stress!(Positive effects of oxidative stress are not suppressed in this dose range).