When an organism is exposed to a type of stress, and this stress originates ROS, after a certain amount a significant difference between the control and the exposed organisms can be found. But did anyone get better results for LPO within organisms exposed to this type of stress and the control who were not exposed? Does anyone has any explanation for this results? Can it be a problem resulting from the use of the TBAR method?
Dear collegue, yours and our results are similar! At first, about TBARS method: what samples and method of "reactive substances" extraction did you use?
At second, is possible explanation - stress adaptation/disadaptation? Look: Dasgupta A., Malhorta D., Levy H., Marcadis D., Blackwell W., Johnston D (1997). Decreased Total Antioxidant Capacity but normal lipid hydroperoxide concentrations in sera of critically ill patients. Life Sciences, 60(4-5), 335-340
Dear Natalia Koretskaia, thank you for the answer, I'm using the TBARS protocol from Bird and Draper (1984) and Ohkawa et al. (1979), and I'm sampling terrestrial isopods. I was wondering if it was not an artifict due to antioxidants who mask the presence of peroxidized lipids and I will take a look to the paper.
Oh, how intresting yours researching objects! Whether correctly did I understand that TBARS were absent in control and stress groups? Our samples demonstrated artifict overestimated results and butanol extractions for lipids (protocol Mihara M., Uchiyama M. et al, Biochem.,Med, С 1980, С v.23, С р.302.) helped.
Dear Natalia and Alaaeldin, I had TBARS in both the control and treatment, but with the increase of the dose in treatments instead of higher TBARS rates, I was getting exactly the oposite but with a clear pattern of decrease. After reading several studies I think that non enzimatic antioxidants (since the enzimatic ones were measured and are not the responsibles for that TABRS decrease) may be the reason for these results
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