Cytogenetic Activity of Diazepam in Normal Human Lymphocyte Cultures

Akritopoulou, Kiriaki; Iakovidou‐Kritsi, Zafiroula; Mioglou-Kalouptsi, E.; Ekonomopoulou, Maria T.; Mourelatos, D.

doi:10.1089/gtmb.2008.0116

Cited by 16 publications

(7 citation statements)

References 20 publications

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“…In this case, all the parameters did not differ from those in the control animals. These results are consistent with the data on the effects of diazepam on proliferation of lymphocytes in vitro [7]. Since chronic administration of diazepam has a pronounced anxiolytic effect [3] and inhibits the effects of CSDS on parameters of cellular immunity [6], we can conclude that expressed anxiety developing under these conditions is the pathogenic factor forming immunodefi cient state with changes in subpopulation composition of lymphocytes and cell cycle disturbances in immunocompetent organs.…”

Section: Parametersupporting

confidence: 91%

Cell Cycle Arrest in the Thymus and Spleen in Male Mice under Conditions of Chronic Social Defeat Stress: Effects of Diazepam

et al. 2011

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The effects of chronic social defeat stress on the percentage of cells in different phases of the cell cycle and in apoptosis in the thymus and spleen of male mice were studied by the method of flow cytofluorometry. In stressed males, thymus weight decreased, the percent of proliferating thymocytes was significantly lower, and the percentage of G0-G1 cells was higher than in intact males. Stress substantially reduced the percentage of splenocytes in the G0-G1 phase and apoptotic cells, but the percentage of S and G2-M cells and proliferation index significantly increased. Chronic administration of anxiolytic diazepam prevented the majority of the changes in the percentage of cells in different phases of the cell cycle, but apoptosis in the thymus increased under these conditions. Possible association between cell cycle disorders, impairment of cell immunity, and chronic anxiety developing under conditions of long-term social defeat stress is considered.

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Section: Parametersupporting

confidence: 91%

Cell Cycle Arrest in the Thymus and Spleen in Male Mice under Conditions of Chronic Social Defeat Stress: Effects of Diazepam

et al. 2011

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“…Furthermore, micromolar diazepam concentration decreased the intensity of 5CMF-DA fl uorescence, thus indicating that diazepam induced a decrease in cellular content of glutathione. The diazepam-induced rat thymocytes apoptosis associated with the collapse of MTP has been confi rmed earlier (24), as well as the genotoxic effects of diazepam in human lymphocytes (1). On the other hand, there is increasing evidence suggesting that the toxicity of diazepam is mediated by oxidative stress.…”

Section: Discussionmentioning

confidence: 80%

Protective role of vitamin C in diazepam-induced apoptosis in rat thymocytes

Pavlović¹,

Pavlović²,

Kamenov³

et al. 2012

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Diazepam, a peripheral-type benzodiazepine receptor ligand, is widely used as a therapeutic agent. On the other hand, peripheral-type benzodiazepines have been shown to induce apoptosis in different immune cell types. In this study, we examined the possible protective role of vitamin C in diazepam-induced apoptosis and evaluated the cellular content of glutathione during this process. Rat thymocytes were incubated for 24 hours with diazepam and increasing concentrations of vitamin C or with diazepam alone. The exposure to diazepam resulted in an increase in apoptotic cell death and decrease in glutathione content in rat thymocytes. Vitamin C was effective in ameliorating the effect of diazepam in rat thymocytes by decreasing the proportion of apoptotic cells and increasing the cellular content of glutathione. These results suggest that vitamin C reduced the diazepam-induced apoptosis in rat thymocytes by restoring the cellular content of glutathione, which may be useful in preventing the diazepam-induced immunosupression (Tab. 1, Fig. 1

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“…SCEs have been frequently used as a highly sensitive indicator of DNA damage and/or of subsequent DNA repair mechanisms' effectiveness. Recognition and signaling of DNA damage are a prerequisite for the induction of subsequent cellular responses such as increased repair, cell cycle arrest and apoptosis (Akritopoulou et al, ). The high SCE values after OLZ treatment could be either due to a large number of DNA damages, which couldn't be repaired before the cells reach S phase, or/and due to the inability of the repair mechanisms to restore the damages, while these lesions seem not to affect the cell cycle.…”

Section: Discussionmentioning

confidence: 98%