Di-ethanolamine Might Cause Bone-related Complications Due to the Reduction of Osteogenic Differentiation and Induction of Oxidative Stress

Document Type : Research Article

Authors

Department of Biology, Faculty of Sciences, Arak University, Arak, Iran

Abstract

Di-ethanolamine (DEA) is a well-known environmental pollutant used in manufacturing soap, detergent, body lotion, and other sanitary products. DEA has been reported to cause cytotoxicity in different tissue and cell, but no study was found to explain the toxic effect of DEA on rat bone marrow mesenchymal stem cells (BMSCs) differentiation. Thus in the present study, the differentiation property of BMSCs treated with DEA was investigated. BMSCs after 3rd passage were cultured in osteogenic media in presence of 1 and 4 mM of DEA for 21 days. Then, the viability, based on 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide or MTT) and morphology of nuclei and cytoplasm (using fluorescent dye), as well as osteoblasts mineralization property (based on quantitative alizarin red and calcium concentration), were studied. Also, sodium and potassium level, the activity of alanine transaminase, aspartate transaminase, alkaline phosphatase, and lactate dehydrogenase (LDH) were determined. The level of total-antioxidant capacity (TAC), malondialdehyde (MDA), and the activity of antioxidant enzymes (superoxide dismutase and catalase) also were estimated. The DEA treated cells showed nuclear enlargement and cytoplasm shrinkage as well as an increase in potassium level. Also based on LDH activity elevation, we observed a cellular anaerobic metabolism. Also, a significant increase in MDA was shown, while TAC and antioxidant enzyme activity was reduced.  Finally, a significant decreased in cell viability and differentiation ability of BMSCs was observed. Since BMSCs are the cellular backup to generate osteoblasts, therefore its intoxication with DEA might cause bone complications, thus we recommend, prevention of DEA utilization in health-related products.

Keywords

References

Abnosi MH, Babolghani ZA. 2020. The inhibitory role of Di-2-ethylhexyl phthalate on osteogenic differentiation of mesenchymal stem cells via down-regulation of RUNX2 and membrane function impairment. Int J Med Toxicol Forensic Med 10(2): 26673.
Abnosi MH, Masoomi S. 2020. p-Nonylphenol impairment of osteogenic differentiation of mesenchymal stem cells was found to be due to oxidative stress and down-regulation of RUNX2 and BMP. Endocr Metab Immune 20: 1-11.
Abnosi MH, Masoomi S. 2019. Para-nonylphenol toxicity induces oxidative stress and arrests the cell cycle in mesenchymal stem cells of bone marrow. Iran J Toxicol 13: 1-8.
Bailey J. 2007. DEA in consumer products is safe. FASEB J 21: 296-297.
Blair HC, Robinson LJ, Huang CL, Sun L, Friedman PA, Schlesinger PH, Zaidi M. 2011. Calcium and bone disease. Biofactors 37: 159-167.
Clausen MV, Hilbers F, Poulsen H. 2017. The structure and function of the Na,K-ATPase isoforms in health and disease. Front.Physiol 8: 371.
Nelson DL, Cox MM. 2008. Glycolysis, gluconeogenesis, and the pentose phosphate pathway. Lehninger principles of biochemistry 4th Ed. New York: chapter 14. Pp 521-59.
De Ritis F, Coltorti M, Giusti G. 1972. Serum transaminase activities in liver disease. Lancet 1: 685-687.
Ewing RD, Clegg JS. 1969.  Lactate dehydrogenase activity and anaerobic metabolism during embryonic development in Artemia salina. Comp Biochem Physiol 31: 297-307.
Frauenkron M, Melder JP, Ruider G,  Rossbacher R,  Höke H.  2012. Ethanolamines and propanolamines. Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim. DOI: 10.1002/14356007.a10_001.
Gardiner J, Overall R, Marc J. 2013. The nervous system cytoskeleton under oxidative stress. Diseases 1: 36-50.
Ighodaro OM, Akinloye OA. 2018. First line defense antioxidants-superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX): their fundamental role in the entire antioxidant defence grid. Alexandria Med J 54: 287-293.
Jevtić P, Edens LJ, Vuković LD, Levy DL. 2014. Sizing and shaping the nucleus: mechanisms and significance. Curr Opin Cell Biol 28: 16-27.
Kraeling ME, Yourick JJ, Bronaugh RL. 2004. In vitro human skin penetration of diethanolamine. Food Chem Toxicol 42: 1553-1561.
Libralato G, Volpi Ghirardini A, Avezzù F. 2010. Seawater ecotoxicity of monoethanolamine, diethanolamine and triethanolamine. J Hazard Mater 176: 535-539.
Long EG, Buluk M, Gallagher MB, Schneider JM, Brown Justin L, 2019. Human mesenchymal stem cell morphology, migration, and differentiation on micro and nano-textured titanium. Bioact Mater 4: 249-255.
Lowry OH, Rosebrough NJ, Farr AL, Randall RJ, 1951. Protein measurement with the folin phenol reagent. J Biol Chem 193: 265-275.
Mathews JM, Garner CE, Black SL, Mathews HB. 1997. Diethanolamine absorption, metabolis, and disposition in rat and mouse following oral, intravenous and dermal administration. Xenobiotica 27: 733-746.
Mathews JM, Garner CE, Mathews HB. 1995.  Metabolism, bioaccumulation, and incorporation of diethanolamine into phspholipids. Chem Res Toxicol. 8: 625-633.
Melnick RL, Mahler J, Bucher JR, Thompson M, Hejtmancik M, Ryan MJ, Mezza LE. 1994a. Toxicity of diethanolamine. 1. Drinking water and topical application exposure in F344 rats. J Appl Toxicol 14: 1-9.
Melnick RL, Mahler J, Bucher JR, Hejtmancik M, Singer A, Persing RL. 1994b. Toxicity of diethanolamine. 2. Drinking water and topical application exposures in B6C3F1 mice. J Appl Toxicol‎ 14: 11-19.
Melnick R. 1992. NTP technical report on the toxicity studies of Diethanolamine (CAS No. 111-42-2) administered topically and in drinking water to F344/N Rats and B6C3F1 Mice. Toxic Report Series 20:1-10.
Niculescu MD, Renan W, Zhong G, Kerry AC, Steven HZ. 2007. Diethanolamine alters proliferation and choline metabolism in mouse neural precursor cells. Toxicol Sci 96: 321-326.
Oliyai M, Abnosi MH, Momeni HR. 2017. Myo-inositol at high concentration reduced viability and proliferation of rat bone marrow mesenchymal stem cells via electrolyte imbalance and elevation of aerobic metabolism. J Genet Resour 3: 18-25
Panchal S, Prajapati H, Verma RJ. 2014. Diethanolamine cytotoxicity on red blood corpuscles. Int Res J Biological Sci 3: 67-69.
Panchal S, Verma RJ. 2016. Effect of diethanolamine on testicular steroidogenesis and its amelioration by curcumin. Asian Pascific J Reprod 5: 128-131.
Shum LC, White NS, Mills BN, de Mesy Bentley KL, Eliseev RA. 2016. Energy metabolism in mesenchymal stem cells during osteogenic differentiation. Stem Cells Dev 25: 114-122.
Vrtačnik P, Zupan J, Mlakar V, Kranjc T, Marc J, Kern B, Ostanek B. 2018. Epigenetic enzymes influenced by oxidative stress and hypoxia mimetic in osteoblasts are differentially expressed in patients with osteoporosis and osteoarthritis. Sci Rep 8:1-2.
Yoon KB, Park KR, Kim SY, Han SY. 2016. Induction of nuclear enlargement and senescence by sirtuin inhibitors in glioblastoma cells. Immune Netw 16: 183-188.
Yordy JR, Alexander M. 1981. Formation of N-nitrosediethanolamine from diethanolamine in lake water and sewage. J Environl Qual 10: 266-270.
Zheng CX, Sui BD, Qiu XY, Hu CH, Jin Y. 2020. Mitochondrial regulation of stem cells in bone homeostasis. Trends Mol Med 1: 89-104.
Journal of Genetic Resources
Volume 6, Issue 2
September 2020
Pages 185-194

Files

Share

How to cite

Statistics