To certain level the antioxidants protect the system from free radicals. The enzymes level will increase depending on organs of an organism. Liver is primary organ to defense, mitochondria is primary organelle to workout on free radical scavenging to generate water, kidney is essential to remove unnecessary molecules from the system to maintain equilibrium. Brain has more of GSH because it protects neurons/ glial cells/matter from brain etc if not it has to use DNA as nucleophile for protection from electrophile. So considering the system, effect and other related situations one has to think of functioning of organs and organelles. Eg plants release Oxygen and animals release Carbon di oxide. Recently people are commenting that because of over production of carbon from nature and consumption of carbon by plant, there is possibility that plants can also release carbon. So it is up to the work at where you are working and the system one is using. However to a level of insult concentration there definitely exists defense in any organism after that the cell forego defense. If insult is going to bind to an enzyme then there is possibility to lose enzyme activity since it may serve as enzyme inhibitor by binding to its catalytic site.

Inflammation basically involves generation of free radicals. Biological role of these enzymes are to scavenge the free radicals. Free radicals are also produced under physiological conditions and is implicated in several biological functions. However, if the levels of free radicals are higher they need to be scavenged by these enzymes. At times, these enzymes  can be inactivated by free radicals and/or by several other factors such as hormonal imbalance, environmental pollution under chronic conditions. Several factors associated with inflammation are implicated in imbalance in the ROS/Antioxidant system. 

Hello,

In normal organisms, antioxidant enzymes' activities should increase under oxidative stress conditions to protect the organisms against harmful effects. Therefore, if you induce oxidative stress in a healthy subject, you should find increased enzyme activity, at least at early stages. If oxidative condition is very severe or last for a long time, the body will exhausted, so enzyme activity may decrease, although oxidative stress is present, yet. So, you should ensure that the subject was first healthy, then faced oxidative stress. Sometimes, you may find decreased enzyme activity despite the presence of oxidative condition (e.g. increased MDA in the body). In this case, maybe improper enzymatic antioxidant defense caused oxidative stress, not vice versa.

It depends on the state of the cell/ tissue. After a mild increment in reactive oxygen species generation, cells are able to increase the antioxidant response and overcome stress. However, after high oxidative damage, cells are no longer able to protect themselves and even antioxidant enzymes could be degraded

Inflammation and oxidative stress are the bed conditions for cells, physiologically there is less chance of developing inflammation and oxidative stress. But in pathological conditions, during mild inflammatory response the cell defence/immune system activated with Anti-Oxidative property. Roxana Mayra Gorojod is correct, up to certain level competition between cell protection and cell damage occur and finally when the cell machinery (signaling molecules, messengers, factors) impaired and fails to protect against oxidative damage, as a result cell death/burst occur. It is not only the improper functioning of antioxidant enzymes level but also cell machinery tool (signaling molecules, messengers, factors) is responsible for cell damage/death.  

It depends on the inducers and depressor of the antioxidant genes. If the inducers are high the synthesis (Transcription and synthesis) of the antioxidant enzymes level will be elevated. Free radicals can be considered as inducers for that genes

The question is very interesting. To my knowledge, there are two scenarios which can lead to the decreased antioxidant enzyme level at oxidative stress. First one is an obvious "defense exhaust", when the cell cannot produce more protective enzymes under the free radical attack. The other is not so obvious: cyclic oscillations when the defense and attack have equal force. At the first stage of attack, the cell produces many protective enzymes, and one can observe elevated antioxidant enzymes at this stage. After the enzymes scavenge excessive free radicals, the oxidative stress condition will temporary disappear, and the cell will cease the production of defense enzymes. E.g. this is realized through a mechanism of negative feedback in the synthesis of NRF2 antioxidant transcription factor that activates production of protective enzymes: the expression of NRF2 gene is inhibited by its own protein product NRF2. So, at this descending stage of the cycle, the level of antioxidant enzymes will drop even lower than normal baseline, as the system has some inertia. It results in a registration of a decreased level of antioxidant enzymes at this stage. But if the pathological state persists, the free radicals will accumulate and the oxidative stress conditions will appear again - and the cycle repeats.

I hypothesized and analysed this oscillatory character of the antioxidant enzyme-free radical antagonism with co-authors in the artice available here on ResearchGate:  https://www.researchgate.net/publication/272842066_Active_ribosomal_genes_translational_homeostasis_and_oxidative_stress_in_the_pathogenesis_of_schizophrenia_and_autism

Article Active ribosomal genes, translational homeostasis and oxidat...

Dear Doctors

Thank you very much for the clarifications 

Your model dr Lev Porokhovnik  is a very interesting reproduction of the oxidative stress balance. However, i dont know if there is an endpoint to this oscillatory events

Also in cyclic or periodic response. There is intensity. This intensity should correlate maybe to the period of the stress (how long).

It will be really interesting to follow enzyme release under oxidative stress over a long period.

Thank you Dr Roxana for your short and interesting answer. I am wondering if in the case of animal models we can predict the response under stress. And if we got the results how it can be possible to explain both cases. 

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For exemple :

- in the case of increased levels : we are in the protective phase

Treated groups express lower values compared to untreated animals

- in the case of decreased levels : High stress levels

Treated groups express higher values than untreated animals

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The use of markers like MDA in parallel i think is suitable. Since MDA levels only increase with increased stress.

Thank you again for your answers Drs (Thyagaraju K - Sridhar Muthusami - Seyyed Morteza Hoseini- Abdul Hafeez Kandhro - Mahmoud Ahmed Mansour )

this is a very interesting topic. Does anybody know if polyphenols are inducers of oxidative stress enzymes in normal conditions? that is without inducing stress damage?

It depends on the type of stress: acute or long-termed; In both cases there are different physiological mechanisms copping with stress. It also depends on type of tissue; different tissues respond differently concerning antioxidant enzymes.

Sometimes the results depends on the existence of multiple stress sources (different pollutants etc) which interplay with each other modifying the oxidative enzyme's expression.

Please see the attached file as an additional information. 

Article Evaluation of antioxidant deficit and lipid profile in type ...

Most of the times the activity of antioxidant enzymes is reduced in oxidative stress

it is according to the causative agent and other host defense mechanisms.

for example, in case of infections there are WBCs that clear the infection so, you may find antioxidant enzymes still high not consumed while in case of chemical_ inducedoxidative stress the antioxidant enzymes decrease as enzymes here are the main keeper.

also, it depends on the disease state in acute disease enzymes are toward normal while in chronic state enzymes consumed contiuosely

This question is interesting. One of the components (Nrf2)of the signaling pathway (Nrf2/ARE signaling) orchestrating the transcription of in vivo antioxidant genes called (SOD, Catalase, GSH etc), had been noted to increase in protein level at the early stage of any oxidative stress-mediated diseases, meaning, all the transcripts which include catalase will definitely increase at both protein and mRNA levels. This is the stage at which the cells defense system are been activated. At the later stage, Nrf2 transcription factor reduced which infer that the strength of the defense system is not strong enough to combat the situation and the levels of Nrf2 transcripts (including Catalase) reduced as well. So, in order words, the issue could be viewed in two different perspectives (The early stage and the latter stage). I hope this helps you.

Dear @ Ilia's,

Level of antioxidants decrease as the free radicals increased.

To me I think levels of antioxidant enzymes should decrease with increased toxicity and inflammation since the enzymes are being used up while performing their catalytic function. Or does it differ in vivo?