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Perceptions of hostile criticism (PHC) from close others are associated with poor individual functioning and low relationship satisfaction, whereas perceptions of constructive criticism (PCC) are associated with better relationship satisfaction. There is little empirical knowledge, however, regarding individual factors that contribute to such perceptions. The present study examined associations of overall emotion regulation difficulties, as well as the specific use of expressive suppression and cognitive reappraisal, with PHC and PCC. Both partners of 63 community couples completed global self-report measures. Sixty-one couples also completed similar measures immediately following each of three discussions during a laboratory session. Multilevel modeling analyses of global data indicated that individuals' reports of PHC were higher when they used more suppression and when both they and their partners reported greater difficulty in emotion regulation. Results with discussion-specific data were similar: Participants reported higher PHC in discussions when both they and their partners reported using more suppression or when they had more difficulties in emotion regulation during the discussions. Individuals reported higher levels of PCC when their partners reported using less suppression, both globally and in discussions. Finally, participants also reported higher levels of PCC in discussions when they reported using more reappraisal.

Mitoquinone (MitoQ) is a synthetically modified, redox-active ubiquinone compound that accumulates predominantly in mitochondria. We found that MitoQ is 30-fold more cytotoxic to breast cancer cells than to healthy mammary cells. MitoQ treatment led to irreversible inhibition of clonogenic growth of breast cancer cells through a combination of autophagy and apoptotic cell death mechanisms. Relatively limited cytotoxicity was seen with the parent ubiquinone coenzyme Q(10.) Inhibition of cancer cell growth by MitoQ was associated with G(1)/S cell cycle arrest and phosphorylation of the checkpoint kinases Chk1 and Chk2. The possible role of oxidative stress in MitoQ activity was investigated by measuring the products of hydroethidine oxidation. Increases in ethidium and dihydroethidium levels, markers of one-electron oxidation of hydroethidine, were observed at cytotoxic concentrations of MitoQ. Keap1, an oxidative stress sensor protein that regulates the antioxidant transcription factor Nrf2, underwent oxidation, degradation, and dissociation from Nrf2 in MitoQ-treated cells. Nrf2 protein levels, nuclear localization, and transcriptional activity also increased following MitoQ treatment. Knockdown of Nrf2 caused a 2-fold increase in autophagy and an increase in G(1) cell cycle arrest in response to MitoQ but had no apparent effect on apoptosis. The Nrf2-regulated enzyme NQO1 is partly responsible for controlling the level of autophagy. Keap1 and Nrf2 act as redox sensors for oxidative perturbations that lead to autophagy. MitoQ and similar compounds should be further evaluated for novel anticancer activity.