SODs are specific for superoxide.

We have published 23 years ago a paper :(http://www.ncbi.nlm.nih.gov/pubmed/1937144)

which showed tha SOD can penetrate into endothelial cells. I think that SOD is  the only specific scavenger of superoxide radical.

Yes, I will say SOD or PEG-SOD. Other antioxidants may be more nonspecific. However, H2O2 can form after SOD treatment and in some report H2O2 can enhance superoxide formation so it may not be the perfect one.

After going through your problem, I was wondering if we approach in a different way like we use CPTIO, which is rather specific as NO scavenger and acetaminophen which is peroxynitrite scavenger, may we be in a better position to avoid the non specificity of super-oxide inhibitor? Since it is well known that in a system where both NO and Super-oxide prevail they usually form peroxynitrite, so if we use acetaminophen we are supposed to get total inhibition whereas with CPTIO we will inhibit only NO, therefore theoretically we may the contribution of Super-oxide by subtraction. This proposal may be tried to see whether it works to answer your research question.

D.S.PUSHPARANI

In normal physiology, there is a dynamic equilibrium between reactive oxygen species (ROS) activity and antioxidant defence capacity. Once that equilibrium shifts in favour of ROS, either by a reduction in antioxidant defences or an increase in ROS production or activity, it results in oxidative stress leading to potential damage. Lipid peroxidize, Superoxide dismutase (SOD), Catalase, total Thiol group and reduced Glutathione can be used for assessment. The tissue concentrations of antioxidants or free radical scavengers may be either in the form of enzymes (eg. Superoxide dismutase (SOD), Catalase and Glutathione peroxide) or as low molecular weight free radical scavengers (eg. vitamin E, total thiol, Glutathione etc). When there is an excess of free radicals from exogenous or endogenous sources, the available tissue antioxidant system may become overwhelmed leading to oxidative damage to tissues. Works done on the status of antioxidants, proved that GSH is a scavenger of hydroxyl radicals and singlet oxygen. It functions as a substrate for the hydrogen peroxide removing enzyme, Glutathione peroxidase (GPx). This might be due to more flux of hydrogen peroxide and hydroxyl radicals. Exposure of tissues to a large flux of hydrogen peroxide and hydroxyl radicals might result in an imbalance of GSH and oxidized Glutathione (GSSG) ratio.

We have used PEG-SOD, a cell permeable analogue to dismutate superoxide, but, you have to take in account the kinetics of the enzymes, doses and toxicity. Other compound you can use is TIRON. It is very effective and specific for superoxide.

Free Radic Biol Med. 2014 Jun;71:146-56. doi: 10.1016/j.freeradbiomed.2014.03.011. Epub 2014 Mar 15.

Acute hypoxia produces a superoxide burst in cells.

Supplementary material.

Hey Kazushi,

Tiron (1,2-dihydroxybenzene-3,5-disulfonate) is a vitamin E analog, cell-permeable

and acts as a global superoxide scavenger as an alternative for TEMPOL.

If you like you can have a look at our recent review:

"Functions of ROS in macrophages and antimicrobial immunity".

In this review, we give an introduction to ROS and their sources in macrophages, summarize the versatile roles of ROS in direct and indirect antimicrobial immune defense and provide an overview of commonly used ROS probes, ROS source inhibitors and ROS scavengers (also the difference between ROS scavengers and antioxidants, which are not synonymous, is explained).

Functions of ROS in Macrophages and Antimicrobial Immunity

February 2021, Antioxidants 10(2):313

DOI: https://doi.org/10.3390/antiox10020313

All the best and stay healthy,

Marc