*3.5. Mitochondrial Enzymes Linked to Oxidative Metabolism*

Several mitochondrial enzymes linked to oxidative metabolism were assayed with the purpose of searching for possible modifications in energy metabolism and in reactions leading to the production of NADPH for feeding the glutathione cycle with reducing equivalents. To the latter category belong L-glutamate dehydrogenase (which also operates with NADP+) and the NADP+-dependent isocitrate dehydrogenase. The activity of the first one was not modified by arthritis or by the subsequent MeJA treatment (not shown). The NADP+-dependent isocitrate dehydrogenase, however, was diminished in arthritic rats by 23%, as shown in Figure 5a. The MeJA treatment increased this enzyme in both healthy and arthritic rats. In the latter, this effect led to a complete prevention of the diminution caused by arthritis.

**Figure 5.** Effects of MeJA treatment on selected mitochondrial enzyme activities. (**a**) Succinate dehydrogenase; (**b**) isocitrate dehydrogenase; (**c**) L-malate dehydrogenase; (**d**) NADH dehydrogenase. Abbreviations: C, controls; C300, controls treated with 300 mg/kg MeJA; A, arthritic rats; A75, A150 and A300, arthritic rats treated with 75, 150 and 300 mg/kg MeJA, respectively; AIBU, arthritic rats treated with 30 mg/kg ibuprofen. Data are the means ± standard errors of the mean of five animals for each experimental condition. Statistical analysis: ANOVA one-way with Newman–Keuls post-hoc testing. \* *p* < 0.05, different from the controls (C); # *p* < 0.05, different from non-treated arthritic rats (A).

The other enzymatic activities linked to oxidative metabolism that were measured were ATPase, α-ketoglutarate dehydrogenase, L-malate dehydrogenase, succinate dehydrogenase and NADHdehydrogenase. No modifications by arthritis or MeJA treatment were found for the first two. The other three, however, suffered modifications. Succinate dehydrogenase was increased by a factor of 1.8 in arthritic rats; almost the same increment was caused by the MeJA treatment of healthy rats. The latter effect was apparently maintained in arthritic rats in which the already higher activity was further increased by the MeJA treatment. For the 300 mg/kg dose this led to an increase of 2.76-fold when compared to the healthy controls. The activities of the other two enzymes were diminished by arthritis. The L-malate dehydrogenase activity was diminished by 30%. Although the MeJA treatment of healthy rats produced an increase in the L-malate dehydrogenase activity, this effect was not prominent enough in arthritic rats so as to conduct to a significant recovery. The diminution of NADH dehydrogenase caused by arthritis amounted to 31%. The treatment of healthy rats with 300 mg/kg MeJA did not produce modifications. However, the same treatment of arthritic rats almost completely prevented the diminution of the NADH-dehydrogenase activity.
