Di-ethanolamine Causes the Mortality of Bone Marrow Mesenchymal Stem Cell Due to Metabolic Imbalance and Oxidative Stress

Abstract

Background: Cell toxicity due to diethanolamine (DEA) is well known but no data are available regarding its mechanism. The present study investigated the cell viability and proliferation ability of rat bone marrow mesenchymal stem cells (BMSCs) treated with DEA. Methods: At 3rd passages, BMSCs were treated for 12, 24, and 48 hours with 0.025 to 16 mM of bis(2- ethylhexyl) phthalate. The cell viability was estimated using the trypan blue and MTT, then 1, 4, and 16 mM, and 48 hours were selected as well. Next, other parameters were determined, including proliferation ability, cell morphology, sodium and potassium levels, as well as the concentration of calcium, total protein, and the activity of metabolic enzymes (i.e., alanine transaminase [ALT], aspartate transaminase [AST], and lactate dehydrogenase [LDH]). Finally, malondialdehyde (MDA), total antioxidant capacity (TAC), and the activity of antioxidant enzymes such as superoxide dismutase and catalase were measured based on the aim of the study. Results: Based on the results, the viability reduced significantly from 0.6 mM at 12 hours and 0.2 for 24 and 48 hours (P<0.05). In addition, the proliferation ability showed a significant reduction (P<0.05) while the activity of LDH, ALT, and AST increased significantly (P<0.05). The level of electrolytes at 1 mM treatment demonstrated no change (P>0.05) whereas 4 mM concentration caused a decline in the calcium level while increased the sodium significantly (P<0.05). The results further revealed that the level of MDA increased although the activity of antioxidant enzymes and TAC represented a significant reduction (P<0.05). No change was detected in the morphology of nuclei while cytoplasm shrinkage and roundness were observable. Conclusion: In general, the findings of this study showed that DEA reduced the viability and proliferation of BMSCs via metabolic change, electrolyte imbalance, and the induction of oxidative stress.