One of the modern techniques of analyzing oxidative stress is to measure redox status of cells. Many times redox status is also referred as redox stress. By nature all molecules tend to be in reduced stress. So more reduced state seems to be often desired by cells. So for a lay man, why should redox stress be expected and analysed in cells?
You bring up a point that is often discussed in the redox world. The key to answering the question is the endpoint of the redox event. For example, if you treat cells with a known harmful drug and the redox status becomes incredibly oxidizing and THEN the cell dies... this would be oxidative or redox STRESS. On the other hand, if you treat a cell with signaling molecule (e.g. TNFalpha, angiotensin, etc) and you see that the redox status has increased oxidatively BUT THE cell does not have any adverse effects, we would call this oxidative or redox SIGNALING.
The problem in the literature is many people are not experts in redox, and as such refer to everything as "stress" when it is clearly not. Another example is ER "stress." While the unfolded protein response is well documented to have adverse effects on cells such as autophagy and apoptosis, not everything that increases chaperones involved in protein folding (e.g. Grp78, BiP, etc) is a stressful event or ER stress for the cell.
So overall, you are very correct in your assumption that cells prefer a more reducing environment during normal homeostasis, and that oxidizing events can be both signaling and stressful in nature. This is why it is absolutely critical that our methods of measuring SPECIFIC ROS and RNS species gets more rigorous, so we can understand if this is a signaling or stressful event more clearly. Additionally, non-experts in the redox field need to be trained on the difference, but this is a difficult feat as you would expect.
Good question...
~Adam
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