sod activity should go up if superoxide is being produced more...that is rational...moreover you should look in to the activities of different kinds of SODs that exist....some research also suggests that more superoxide inactivates SODs via free radical damage...but the data that you are getting is fine

The result you are getting is very valuable and interesting, looking to determine at the expense of which SOD isoform is increased the total activity. This work could guide you.

Mol Microbiol. 2001 Jun;40(5):1175-86.

Accumulation of manganese in Neisseria gonorrhoeae correlates with resistance to oxidative killing by superoxide anion and is independent of superoxide dismutase activity.

Tseng HJ1, Srikhanta Y, McEwan AG, Jennings MP.

Author information

Abstract

As a facultative aerobe with a high iron requirement and a highly active aerobic respiratory chain, Neisseria gonorrhoeae requires defence systems to respond to toxic oxygen species such as superoxide. It has been shown that supplementation of media with 100 microM Mn(II) considerably enhanced the resistance of this bacterium to oxidative killing by superoxide. This protection was not associated with the superoxide dismutase enzymes of N. gonorrhoeae. In contrast to previous studies, which suggested that some strains of N. gonorrhoeae might not contain a superoxide dismutase, we identified a sodB gene by genome analysis and confirmed its presence in all strains examined by Southern blotting, but found no evidence for sodA or sodC. A sodB mutant showed very similar susceptibility to superoxide killing to that of wild-type cells, indicating that the Fe-dependent SOD B did not have a major role in resistance to oxidative killing under the conditions tested. The absence of a sodA gene indicated that the Mn-dependent protection against oxidative killing was independent of Mn-dependent SOD A. As a sodB mutant also showed Mn-dependent resistance to oxidative killing, then it is concluded that this resistance is independent of superoxide dismutase enzymes. Resistance to oxidative killing was correlated with accumulation of Mn(II) by the bacterium. We hypothesize that this bacterium uses Mn(II) as a chemical quenching agent in a similar way to the already established process in Lactobacillus plantarum. A search for putative Mn(II) uptake systems identified an ABC cassette-type system (MntABC) with a periplasmic-binding protein (MntC). An mntC mutant was shown to have lowered accumulation of Mn(II) and was also highly susceptible to oxidative killing, even in the presence of added Mn(II). Taken together, these data show that N. gonorrhoeae possesses a Mn(II) uptake system that is critical for resistance to oxidative stress.

PMID:

11401721

[PubMed - indexed for MEDLINE]

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Dear collegue,

it is well known that superoxide has a half-life time of about 2 µs. That means that even without any enzyme to dismutate superoxide it would be metabolized very quickly (and should not accumulate).

There are some considerations from my side:

- Is the method to determine superoxide exclusively sensitive to superoxide or perhaps also to hydrogen peroxide (which could accumulate due to the elevated SOD activity); did You conduct simple control experiments with H2O2? 

- Is MitoSOX loading and behavior in mitochondria of protozoa the same as in mitochondria of "higher animals"  (where it was validated)?

- How is the state of defense in Your parasites? All cells try to balance the "redox state" by different means. What is changed in the manipulated animals?

- If You manipulate the lipid metabolism there should be a difference in reactions like lipid peroxidation; You should consider this, too.

- ROS metabolism in mitochondria (as well as in other compartments) could be strongly dependent on the calcium concentration in the same compartment. Did You compare these to control ones?

Perhaps the comments can help You.