Ülkan KILIÇ, Mehmet OZANSOY, Ertuğrul KILIÇ, Muzaffer Beyza OZANSOY, Mehmet Özgen ALTINTAŞ, Necmeddin GÜNAY

Two boron-containing compounds affect the cellular viability of SH-SY5Y cells in an in vitro amyloid-beta toxicity model

Boron is a naturally occurring trace element found in organic and inorganic complexes. Boron-containing compounds are required for living organisms for diverse metabolic functions, including nitrogen fixation in microorganisms, cell wall stability in plants, and bone and carbohydrate metabolism in animals. The number of studies about the effect of boron in biological model systems is very limited; so far, there has been no study on the correlation between boron and amyloid-beta toxicity. Here, we investigated the possible effects of 2 boron-containing compounds-sodium borate decahydrate and boric acid-against amyloid-beta toxicity. In our in vitro amyloid-beta toxicity model, we showed that these 2 compounds increase the survival of the SH-SY5Y cells. Furthermore, boron in these 2 forms increases the expression of Sirt1, which has protective functions against cellular stress. The compounds also change the expressions of GSK-3 alpha/beta; by doing so, boron may contribute to the stimulation of intracellular prosurvival pathways. This is the first experimental study indicating the prosurvival effect of boron in an amyloid-beta toxicity model.

PDF

___

Aysan E, Sahin F, Telci D, Yalvac ME, Emre SH et al. (2011). Body weight reducing effect of oral boric acid intake. International Journal of Medical Sciences 8 (8): 653-658. doi: 10.7150/ ijms.8.653
Bennett DA, Schneider JA, Wilson RS, Bienias JL, Arnold SE (2004). Neurofibrillary tangles mediate the association of amyloid load with clinical Alzheimer disease and level of cognitive function. Archives of Neurology 61 (3): 378-384. doi: 10.1001/ archneur.61.3.378
Blennow K, De Leon MJ, Zetterberg H (2006). Alzheimer’s disease. Lancet 368 (9533): 387-403. doi: 10.1016/S0140- 6736(06)69113-7
Deitrich RA (1967). Diphosphopyridine nucleotide-linked aldehyde dehydrogenase: 3. Sulfhydryl characteristics of the enzyme. Archives of Biochemistry and Biophysics 119 (1): 253-263. doi: 10.1016/0003-9861(67)90452-3
Gizem D, Leonard G (2010). Aging and disease: connections to sirtuins. Aging Cell 9 (2): 285-290. doi: 10.1111/j.1474- 9726.2010.00548.x
Götz J, Lim YA, Ke YD, Eckert A, Ittner LM (2010). Dissecting toxicity of tau and beta-amyloid. Neurodegenerative Disease 7 (1-3): 10-12. doi: 10.1159/000283475
Howe PD (1998). A review of boron effects in the environment. Biological Trace Element Research 66 (1-3): 153-166. doi: 10.1007/BF02783135
Hunt CD (2012). Dietary boron: progress in establishing essential roles in human physiology. Journal of Trace Elements in Medicine and Biology 26 (2-3): 157-160. doi: 10.1016/j. jtemb.2012.03.014
Hunt CD, Halas ES, Eberhardt, MJ (1988). Long-term effects of lactational zinc deficiency on bone mineral composition in rats fed a commercially modified Luecke diet. Biological Trace Element Research 16 (2): 97-113. doi: 10.1007/BF02797095
Elibol B (2019). Both activation and inhibition of SIRT1 may act via exosomal GSK3α/β in the in vitro amyloid-beta toxicity model. Advances in Clinical Toxicology 4 (175): 1-8. doi: 10.23880/ act-16000175
Khan SS, Bloom GS (2016). Tau: the center of a signaling nexus in Alzheimer’s disease. Frontiers in Neuroscience 10 (31): 1-5. doi: 10.3389/fnins.2016.00031
Kim D, Nguyen MD, Dobbin MM, Fischer A, Sananbenesi F et al. (2007). SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer’s disease and amyotrophic lateral sclerosis. The EMBO Journal 26 (13): 3169-3179. doi: 10.1038/ sj.emboj.7601758
Larson B (2016). BioTek instruments, technical resources application notes: analysis of the effect of aggregated β-amyloid on cellular signaling pathways critical for memory in Alzheimer’s disease. Available online at https://www.biotek.com/resources/ application-notes/analysis-of-the-effect-of-aggregatedamyloid-on-cellular-signaling-pathways-critical-for-memoryin-alzheimers-disease/
Michan S, Sinclair D (2007). Sirtuins in mammals: insights into their biological function. The Biochemical Journal 404 (1): 1-13. doi: 10.1042/BJ20070140
Nielsen FH (1997). Boron in human and animal nutrition. Plant and Soil 193 (1-2): 199-208. doi: 10.1023/A:1004276311956
Penland JG (1998). The importance of boron nutrition for brain and psychological function. Biological Trace Element Research 66 (1-3): 299-317. doi: 10.1007/BF02783144
Rahman S, Islam R (2011). Mammalian Sirt1: insights on its biological functions. Cell Communication and Signaling 9 (11): 1-8. doi: 10.1186/1478-811X-9-11
Sadigh-Eteghad S, Sabermarouf B, Majdi A, Talebi M, Farhoudi M et al. (2015). Amyloid-beta: a crucial factor in Alzheimer’s disease. Medical Principles and Practice 24 (1): 1-10. doi: 10.1159/000369101
Selkoe DJ, Hardy J (2016). The amyloid hypothesis of Alzheimer’s disease at 25 years. EMBO Molecular Medicine 8 (6): 595-608. doi: 10.15252/emmm.201606210
Shankar GM, Li S, Mehta TH, Garcia-Munoz A, Shepardson NE et al. (2008). Amyloid-beta protein dimers isolated directly from Alzheimer’s brains impair synaptic plasticity and memory. Nature Medicine 14 (8): 837-842. doi: 10.1038/nm1782
Strittmatter P (1964). Reversible direct hydrogen transfer from reduced pyridine nucleotides to cytochrome b5 reductase. Journal of Biological Chemistry 239 (9): 3043-3050.
Sutherland B, Strong P, King JC (1998). Determining human dietary requirements for boron. Biological Trace Element Research 66 (1-3): 193-204. doi: 10.1007/BF02783138
World Health Organization, International Atomic Energy Agency & Food and Agriculture Organization of the United Nations (1996). Trace elements in human nutrition and health. Geneva, Switzerland: World Health Organization.