Akacid Medical Formulation Induces Apoptosis in Myeloid and Lymphatic Leukemic Cell Lines In Vitro and In Vivo

Neuwirt, Hannes; Wabnig, Elisabeth; Feistritzer, Clemens; Eder, Iris E.; Salvador, Christina; Puhr, Martin; Čulig, Zoran; Massoner, Petra; Tiefenthaler, Martin; Steurer, Michael; Konwalinka, Guenther

doi:10.1371/journal.pone.0117806

Cited by 2 publications

(2 citation statements)

References 43 publications

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“…38 In another study, they also reported that AMF has antiproliferative effects on cell lines derived from human leukemia and lymphoma and demonstrated that AMF induced caspase 8, −9 and −3/−7 and caused apoptosis both intrinsically and extrinsically. 39 These findings were found to be compatible with the results we obtained in this study. Mafra et al evaluated the cytotoxic effects of CHG and PHMB; although both solutions were found to have toxic effects on HUVEC and HCEC, similar to our results, the cytotoxic effects of PHMB occur through apoptosis, while CHG increases necrosis.…”

Section: Discussionsupporting

confidence: 92%

Comparison of cytotoxic, apoptotic and oxidative properties of Akacid plus and chlorhexidine in corneal epithelial cell culture

Kucukoduk,

Durmus Bilgiseven,

Aksoy

et al. 2023

European Journal of Ophthalmology

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Purpose This study aims to compare the cytotoxic, apoptotic, and oxidative effects of a new cationic disinfectant, Akacid Plus, with chlorhexidine, on the human corneal epithelial cell line. Methods Time-dependent cytotoxicity studies were performed with the Alamar Blue method. Apoptotic activity was investigated by flow cytometric methods. Reactive oxygen species levels were measured with the ROS cellular test kit. BAX, BCL2 and caspase 3, 9, 12 mRNA expressions were evaluated by PCR, as well as BAX and BCL2 protein expressions by Western-Blot. Results At the fifth minute of the treatment, the viability was 68.15% with Akacid Plus and 43.95% with chlorhexidine. At the 15th minute, no significant difference was observed with both solutions. In the apoptotic evaluation, Akacid Plus significantly increased the early and late apoptotic activity in the cell line ( p < 0.0001), while a significant increase was observed in late apoptosis and necrosis levels with chlorhexidine ( p < 0.001). Chlorhexidine also induced gene expression of BAX, BCL2, caspase 3, 9 and BAX proteins ( p < 0.05), while reducing protein expression of BCL2 ( p < 0.001). Akacid Plus induced the gene expressions of BCL2, CASP3 and caspase 9, reduced gene expressions of BAX and caspase 12 and protein expression of BCL2 ( p < 0.05). No significant difference was observed in the ROS level with both solutions ( p > 0.05). Conclusion Due to the widespread use of cationic polymers in ophthalmology, this new molecule with high antimicrobial activity and relatively low cytotoxicity may be of interest for clinical use. Further investigations are necessary to fully understand the ophthalmologic potential of this solution.

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Section: Discussionsupporting

confidence: 92%

Comparison of cytotoxic, apoptotic and oxidative properties of Akacid plus and chlorhexidine in corneal epithelial cell culture

Kucukoduk,

Durmus Bilgiseven,

Aksoy

et al. 2023

European Journal of Ophthalmology

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“…This was compared to the counts of the total population, including G1‐/S‐/G2‐phase cells. For assessment of annexin V and PI, we used the Annexin V‐FITC Apoptosis Detection Kit (Enzo Lifescience Inc., Lausen, Austria) according to the manufacturer´s protocol as previously described .…”

Section: Methodsmentioning

confidence: 99%

Calcineurin inhibitor‐induced complement system activation via ERK1/2 signalling is inhibited by SOCS‐3 in human renal tubule cells

et al. 2017

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One factor that significantly contributes to renal allograft loss is chronic calcineurin inhibitor (CNI) nephrotoxicity (CIN). Among other factors, the complement (C-) system has been proposed to be involved CIN development. Hence, we investigated the impact of CNIs on intracellular signalling and the effects on the C-system in human renal tubule cells. In a qPCR array, CNI treatment upregulated C-factors and downregulated SOCS-3 and the complement inhibitors CD46 and CD55. Additionally, ERK1/-2 was required for these regulations. Following knock-down and overexpression of SOCS-3, we found that SOCS-3 inhibits ERK1/-2 signalling. Finally, we assessed terminal complement complex formation, cell viability and apoptosis. Terminal complement complex formation was induced by CNIs. Cell viability was significantly decreased, whereas apoptosis was increased. Both effects were reversed under complement component-depleted conditions. In vivo, increased ERK1/-2 phosphorylation and SOCS-3 downregulation were observed at the time of transplantation in renal allograft patients who developed a progressive decline of renal function in the follow-up compared to stable patients. The progressive cohort also had lower total C3 levels, suggesting higher complement activity at baseline. In conclusion, our data suggest that SOCS-3 inhibits CNI-induced ERK1/-2 signalling, thereby blunting the negative control of C-system activation.

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Akacid Medical Formulation Induces Apoptosis in Myeloid and Lymphatic Leukemic Cell Lines In Vitro and In Vivo

Cited by 2 publications

References 43 publications

Comparison of cytotoxic, apoptotic and oxidative properties of Akacid plus and chlorhexidine in corneal epithelial cell culture

Comparison of cytotoxic, apoptotic and oxidative properties of Akacid plus and chlorhexidine in corneal epithelial cell culture

Calcineurin inhibitor‐induced complement system activation via ERK1/2 signalling is inhibited by SOCS‐3 in human renal tubule cells

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