Inhibition of endogenous thioredoxin in the heart increases oxidative stress and cardiac hypertrophy
J. Clin. Invest. Mitsutaka Yamamoto, et al. 112:1395 doi:10.1172/JCI17700 [Go to this article.]

Figure 2
(a) Heart homogenates were prepared from Tg-DN-Trx1 mice and NTg littermates. Tissue levels of MDA alone and MDA plus 4-HAE, markers of lipid peroxidation, were found to be increased in Tg-DN-Trx1 mice. (b) LV myocardial sections were subjected to immunostaining with 8-OHdG, a marker of oxidative DNA damage, which was increased in Tg-DN-Trx1 mice. The result is representative of three experiments. (c) Heart homogenates were prepared from Tg-DN-Trx1 mice and NTg littermates. Immunoblot analyses of MnSOD, CuZnSOD, and catalase are shown. Note that neither the level of MnSOD nor the level of catalase differed between Tg-DN-Trx1 and NTg mice, while that of CuZnSOD was higher (about 2.5-fold) in Tg-DN-Trx1 mice. n = 3. (d) Tissue levels of GSSG and GSH were determined using fresh samples.