Dear sir, kindly send me your email id. i will send you the some of the data which related to measure the OS. Thank you...

I agree with you - much of what is defined as oxidative stress is determined by context. Tissue type, stress conditions and also method of assay,  whether this is by using luminescence probes, or oxidatized products TBARS , carbonylated residues, nitrosylated residues or loss of antioxidant potential GSH/GSSG NADH/NAD etc.  One would not expect oxidative stress necessarily to be manifest in the same way in synovial fluid, as in blood or tissues which are subject to infarction e.g.  heart or kidney or brain.  

Additional  complexities arise  the degree to which the tissue or cells are capable of accumulating ascorbate and or iron e.g. macrophages versus rbc's. and the degree to which ROS products from mitochondria can affect apoptosis.  

In my personal experience availability of labile iron mobilized from intracellular sources and redox cycling due to ascorbate in combination with trace metal ions are very important contributors to oxidative stress which will be very much context dependent.  

Hi Dov,

We have measured serum TBARS and TAS (commercial kit) and urinary isoprostanes (GC/MS) in a cohort of 40 individuals before and after overfeeding. Happy to send the data. Hope you're well!

Dear Dorit

Glad to hear from you. I hope you are well and pleased to see that you are  doing well. We miss you and will be glad to meet you sooner than later. We are in a reltively good shape, still active and productive. I am looking forward to analysing your data (to be accepted by mail?). Happy Passover

Dov

Dear Thanga

Thanks for your prompt reply. I look forward to your results and hope that the analysis of all the results will yield understanding of the secrets of OS.

My e-mail address is [email protected]

Yours

Dov

Dear Richard

Thank you for adding more arguments regarding the complexities  associated with quantitation of the term oxidative stress (OS).

Both  "the degree to which the tissue or cells are capable of accumulating ascorbate and/ or iron and the degree to which ROS products from mitochondria can affect apoptosis" are of course very important and I think that they make a major composition to the OS, as assayed by different biomarkers. The only approach I can think about that  can be taken on the road to understanding of the meaning of differences between the results of different assays is  to study the correlations between such results.

 Do you determine OS by two or more assays? If you do, we'll apprichiate a copy of the results for us to atudy the correlations .

Thank you  Dov

Yes I have comparisons on chemiluminescence assays with lucigenin and L-012 which show differences in response to the same redox effects of ascorbate and iron on ferritin ROS production of hydroxyl superoxide and ascorbyl radicals. I can send you the figures which are about to be submitted to a journal -by email can you send your email address to mine

Thank you very much. My email addews is [email protected]

Do you trust both with respect to the redox effect? 

Looking forward to your mail

"Trust" is a rather loaded word  when it comes to luminescence... there are significant differences in the responses of these reporters which suggests they are reporting different type of ROS.  I think It is best to keep an open mind  and not be over persuaded by overly prescriptive authoritarians.