BIOLOGICAL ROLE OF COPPER IN PATHOGENESIS OF AUTISM IN CHILDREN: A LITERATURE REVIEW


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Abstract

The article summarizes the evidence on the biological role of copper and the role of copper metabolism disorders in neurodegenerative processes and pathogenesis of autism. The neuromodulating effects of copper ions and their role for cognitive functions are described. The results of original studies on copper metabolism in children with autistic disorders (AD) arepresented. Our review suggests that the current evidence is contradictory. While several publications indicate an increased level of copper in blood, hair, teeth, nails of AD patients, other studies do not report any difference in the concentration of copper between AD and healthy children. It isassumed that the dysregulation of copper metabolism in children with AD is associated with dysfunction of transport proteins. Data on copper involvement in the processes of management of free radical in children with AD arediscussed. Monitoring of metal-ligand homeostasis in children with AD iswarranted as well as the development of effective methods of correction of copper metabolism disorders.

About the authors

O. V. Kostina

Privolzhsky Research Medical University

Email: olkosta@rambler.ru
кандидат биологических наук, старший научный сотрудник группы биохимии отдела лабораторных исследований Научно-исследовательского института профилактической медицины Университетской клиники

M. V. Presnyakova

Privolzhsky Research Medical University

Zh. V. Albitskaya

Privolzhsky Research Medical University

References

  1. Давыдова Н. О., Нотова С. В., Кван О. В. Влияние элементного статуса организма на когнитивные функции // Микроэлементы в медицине. 2014. № 15 (3). С. 3-9
  2. Новиков В. С., Шустов Е. Б. Роль минеральных веществ микроэлементов в сохранении здоровья человека // Вестник образования и развития науки Российской академии естественных наук. 2017. № 3. С. 5-16
  3. Парахонский А. П. Роль меди в организме и значение ее дисбаланса // Естественно-гуманитарные исследования. 2015. Т. 10, № 4. С. 72-83
  4. Ребров В. Г., Громова О. А. Витамины, макро- и микроэлементы. М.: ГЭОТАР-Медиа, 2008. 960 c
  5. Сидоров А. В. Активные формы кислорода и регуляция нейронных функций // Новости медико-биологических наук. 2011. Т. 4, № 4. С. 224-231
  6. Роль ионов цинка и меди в механизмах патогенеза болезней Альцгеймера и Паркинсона / Е.В. Стельмашук [и др.] // Биохимия. 2014. T. 79, вып. 5. C. 501-508
  7. A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States / R. Dufault [et al.]. Clin. Epigenetics. 2012, 4 (1), p. 6.
  8. Ackerman C. M., Chang C. J. Copper signaling in the brain and beyond. J Biol Chem. 2018, 30 (13), pp. 4628-4635.
  9. Assessment of gender and age effects on serum and hair trace element levels in children with autism spectrum disorder.A.V. Skalny [et al.]. Metab. Brain Dis. 2017, 32 (5), pp. 1675-1684.
  10. Baecker T. Loss of COMMD1 and copper overload disrupt zinc homeostasis and influence an autism-associated pathway at glutamatergic synapses. Biometals. 2014, 27 (4), pp. 715-730.
  11. Blood lipid peroxidation, antioxidant enzyme activities and hemorheological changes in autistic children. A. Laszlo [et al.]. Ideggyogy Sz. 2013, 66 (1-2), pp. 23-28.
  12. Capturing a reactive state of amyloid aggregates: Nmr-based characterization of copper-bound Alzheimer disease amyloid в-fibrils in a redox cycle. S. Parthasarathy [et al.]. J. Biol. Chem. 2014, 289 (14), pp. 9998-10010.
  13. Ceruloplasmin, superoxide dismutase and copper in autistic patients. G. Tуrsdуttir [et al.]. Basic Clin. Pharmacol. Toxicol. 2005, 96 (2), pp. 146-148.
  14. Copper is required for oncogenic BRAF signalling and tumorigenеsis. D. C. Brady [et al.]. Nature. 2014, 509, pp. 492-496.
  15. Csiszar K. Lysyl oxidases: a novel multifunctional amine oxidase family. Prog. Nucleic Acid Res. Mol. Biol. 2001,70 (1), pp. 1-32.
  16. Dietary copper and human health: Current evidence and unresolved issues. M. Bost_[ et al.]. Journal of Trace Elements in Medicine and Biology. 2016, 35, pp. 107-115.
  17. Dietary Zinc Supplementation Prevents Autism Related Behaviors and Striatal Synaptic Dysfunction in Shank3 Exon 13-16 Mutant Mice. C. Fourie [et al.]. Front Cell Neurosci. 2018, 12, p. 374
  18. Dodani S. C. Copper is an endogenous modulator of neural circuit spontaneous activity. Proc Natl Acad Sci USA. 2014, 18 (1 11-46), pp. 16280-16285
  19. Dynamical features in fetal and postnatal zinc-copper metabolic cycles predict the emergence of autism spectrum disorder. P. Curtin [et al.]. Sci. Adv. 2018, 4 (5), pp. 1-8.
  20. Evaluation of oxidative stress in autism: defective antioxidant enzymes and increased lipid peroxidation. N. A. Meguid [et al.]. Biol. Trace Elem. Res. 2011, 143 (1), pp. 58-65.
  21. Evaluation of whole blood zinc and copper levels in children with autism spectrum disorder. E. C. Crrciun [et al.]. Metab. Brain Dis. 2016, 3 (4), pp. 887-890.
  22. Exploiting innate immune cell activation of a copper-dependent antimicrobial agent during infection. R. A. Festa [et al.]. Chem. Biol. 2014, 21, pp. 977-987.
  23. Gaetke L. M., Chow-Johnson H. S., Chow C. R. Cooper: toxicological relevance and mechanisms. Arch Toxicol. 2014, 88 (1 1), pp. 1929-1938.
  24. Hagmeyer S., Mangus K., Boeckers T. M., Grabrucker А. М. Effects of Trace Metal Profiles Characteristic for Autism on Synapses in Cultured Neurons. Neural Plasticity. 2015, Article ID 985083, 16 pages. Available at: https://doi. org/10.1 155/2015/985083 (accessed: 23.04.2019).
  25. Hollis F., Kanellopoulos A. K, Bagni C. Mitochondrial dysfunction in Autism Spectrum Disorder: clinical features and perspectives. Curr. Opin. Neurobiol. 2017, 45, pp. 178-187.
  26. Is cognitive function linked to serum free copper levels? A cohort study in a normal population. C. Salustri [et al.]. Clin. Neurophysiol. 2010, 121 (4), pp. 502-507.
  27. Johannesson T., Kristinsson J., Sn®dal J. Neurodegenerative diseases, antioxidative enzymes and copper. A review of experimental research. Laeknabladid. 2003, 9 (9), pp. 659-671.
  28. Kim B. E., Nevitt T., Thiele D. J. Mechanisms for copper acquisition, distribution and regulation. Nat. Chem. Biol. 2008, 4, pp. 176-185.
  29. Levels of metals in the blood and specific porphyrins in the urine in children with autism spectrum disorders. M. Macedoni-Lukљiи [et al.]. Biol. Trace Elem. Res. 2015, 163 (1-2), pp. 2-10.
  30. Nishito Y., Kambe T. Absorption mechanisms of iron, copper and zinc: an overview. J Nutr Sci Vitaminol (Tokyo). 2018, 64 (1), pp. 1-7.
  31. Nutritional and metabolic status of children with autism vs. neurotypical children, and the association with autism severity. J. B. Adams [et al.]. Nutr. Metab. (Lond). 2011, 8 (1), p. 34.
  32. Optic neuropathy, myelopathy, anemia, and neutropenia caused by acquired copper deficiency after gastric bypass surgery. S. S. Yarandi [et al.]. J Clin Gastroenterol. 2014, 8 (10), pp. 862-865.
  33. Oxidative stress in autism: increased lipid peroxidation and reduced serum levels of ceruloplasmin and transferrin--the antioxidant proteins. A. Chauhan [et al.]. Life Sci. 2004, 75 (21), pp. 2539-2549.
  34. Pal A. Copper toxicity induced hepatocerebral and neurodegenerative diseases: An urgent need for prognostic biomarkers. NeuroToxicology. 2014, 40, pp. 97-101.
  35. Plasma antioxidant capacity is reduced in Asperger syndrome. M. Parellada [et al.]. J. Psychiatr. Res. 2012, 46 (3), pp. 394-401
  36. Plasma concentrations of the trace elements copper, zinc and selenium in Brazilian children with autism spectrum disorder. P. F. Saldanha Tschinkel [et al.]. Biomed. Pharmacother. 2018, 106, pp. 605-609.
  37. Predictive value of selected biomarkers related to metabolism and oxidative stress in children with autism spectrum disorder. A. El-Ansary [et al.]. Metab. Brain Dis. 2017, 32 (4), pp. 1209-1221.
  38. Reduced endogenous urinary total antioxidant power and its relation of plasma antioxidant activity of superoxide dismutase in individuals with autism spectrum disorder. K. Yui [et al.]. Int. J. Dev. Neurosci. 2017, 60, pp. 70-77.
  39. Role of the P-Type ATPases, ATP7A and ATP7B in brain copper homeostasis. J. Telianidis [et al.]. Front Aging Neurosci. 2013, 5, p. 44.
  40. Russo A. F. Anti-metallothionein IgG and levels of metallothionein in autistic families. Swiss Med Wkly. 2008, 138 (5-6), pp. 70-77.
  41. Russo A. J., de Vito R. Analysis of Copper and Zinc Plasma Concentration and the Efficacy of Zinc Therapy in Individuals with Asperger’s Syndrome, Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS) and Autism. Biomark Insights. 2011, 6, pp. 127-133.
  42. Scheiber I. F., Dringen R. Astrocyte functions in the copper homeostasis of the brain. Neurochemistry International. 2013, 62 (5), pp. 556-565.
  43. Serum copper and zinc levels in individuals with autism spectrum disorders. S. O. Li [et al.]. Neuroreport. 2014, 25 (15), pp. 1216-1220.
  44. Squitt R. M., Siotto M., Polimanti R. Low-copper diet as a preventive strategy for Alzheimer’s disease. Neurobiology of Aging. 2014, 35 (2), pp. 40-50.
  45. Status of essential elements in autism spectrum disorder: systematic review and meta-analysis. A. Saghazadeh [et al.]. Rev. Neurosci. 2017, 28 (7), pp. 783-809.
  46. Study of some biomarkers in hair of children with autism. E. Elsheshtawy [et al. Middle East Current Psychiatry. 2011, 18 (1), pp. 6-10.
  47. The link between intraneuronal N-truncated amyloid-P peptide and oxidatively modified lipids in idiopathic autism and dup(15q11.2-q13)/autism. J. Frackowiak J. [et al.]. Acta Neuropathol. Commun. 2013, 1, pp. 1-15.
  48. Vasak M., Meloni G. Mammalian Metallothionein-3: New Functional and Structural Insights. International journal of molecular sciences. 2017, 18 (6), p. 1117.
  49. Yamada Y., Prosser R. A. Copper chelation and exogenous copper affect circadian clock phase resetting in the suprachiasmatic nucleus in vitro. Neuroscence. 2014, 256, pp. 252-261.
  50. Yasuda H., Tsutsui T. Assessment of infantile mineral imbalances in autism spectrum disorders (ASDs). Int. J. Environ. Res. Public Health. 2013, 10 (11), pp. 6027-6043.

Copyright (c) 2020 Kostina O.V., Presnyakova M.V., Albitskaya Z.V.

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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
 


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