Why Victimized Employees Become Less Engaged at Work: An Integrated Model for Testing the Mediating Role of Sleep Quality.

Recent studies have shown that workplace victimization is negatively related to work engagement. The explanations for the underlying mechanisms, however, are still in a nascent stage. Drawing on the limited resource theory of self-regulation and research on workplace aggression and sleep, we develop and test an integrated model, which explains that victimized employees may have impaired sleep quality and thus have less energy and be less likely to be engaged in their work. The results of logistic regression and structural equation modeling analyses of large-scale survey data collected from 90,272 employees across the years 2010, 2011, 2014, and 2017, indicate that workplace victimization is negatively related to sleep quality and subsequent workplace engagement, even controlling for alternative explanations-job insecurity and basic psychological needs for competence, autonomy, and relatedness. Our findings advance our knowledge on the detrimental consequences of workplace victimization and suggest that, while unmet basic psychological needs matter, impaired sleep quality is one reason why victimized employees find it difficult to engage at work.

Inhibitory effects of tetrahydropapaverine on serotonin biosynthesis in murine mastocytoma P815 cells.

The inhibitory effects of tetrahydropapaverine on serotonin biosynthesis in serotonin-producing murine mastocytoma P815 cells were investigated. Tetrahydropapaverine at concentration ranges of 5-20 microM decreased serotonin content in a concentration-dependent manner in P815 cells and showed 42.1% inhibition of serotonin content at 5.0 microM at 24 hr. The value of 50% inhibitory concentration, IC50, of tetrahydropapaverine was 6.2 microM. Under these conditions, tryptophan hydroxylase (EC 1.14.16.4, TPH) was inhibited for 24-36 hr after treatment with tetrahydropapaverine in P815 cells (49.1% inhibition at 7.5 microM). However, aromatic L-amino acid decarboxylase activity was not affected by tetrahydropapaverine. In addition, tetrahydropapaverine inhibited the activity of TPH, prepared from the P815 cells (P815-TPH), with the IC50 value of 5.7 microM. Tetrahydropapaverine un-competitively inhibited P815-TPH with the substrate L-tryptophan, and non-competitively with the cofactor DL-6-methyl-5,6,7,8-tetrahydropteridin. The Ki value of tetrahydropapaverine with L-tryptophan was 10.1 microM. These data indicate that tetrahydropapaverine leads to a decrease in serotonin content by the inhibition of TPH activity in P815 cells.

Reduction of serotonin content by tetrahydropapaveroline in murine mastocytoma P815 cells.

The inhibitory effects of tetrahydropapaveroline on serotonin biosynthesis in serotonin-producing murine mastocytoma P815 cells were investigated. Tetrahydropapaveroline decreased serotonin content in a concentration-dependent manner in P815 cells and showed 44.9% reduction of serotonin content at a concentration of 5.0 microM for 24 h. The value of 50% inhibitory concentration, IC(50), of tetrahydropapaveroline was 7.5 microM. Under these conditions, tryptophan hydroxylase (EC 1.14.16.4, TPH) was inhibited for 24-36 h after treatment with tetrahydropapaveroline in P815 cells (46.6% inhibition at 7.5 microM). In addition, tetrahydropapaveroline inhibited the activity of TPH, prepared from the P815 cells (P815-TPH), with the IC(50) value of 8.4 microM. Inhibition of P815-TPH by tetrahydropapaveroline was found to be non-competitive both with the substrate L-tryptophan and with the cofactor DL-6-methyl-5,6,7,8-tetrahydropterine. The K(i) value of tetrahydropapaveroline with L-tryptophan was 9.29 microM. These data indicate that tetrahydropapaveroline leads to a decrease in serotonin content by inhibiting TPH activity in P815 cells.