PL EN


Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Czasopismo

2019 | 78 | 3 |

Tytuł artykułu

Acrylamide-induced adverse cerebellar changes in rats: possible oligodendrogenic effect of omega 3 and green tea

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Background: Humans are widely exposed to acrylamide (ACR) and its neurotoxicity is a significant public health issue attracting wide attention. The aim of the study was to investigate ACR-induced adverse cerebellar changes in rats and study the possible oligodendrogenic effect of omega 3 and green tea. Materials and methods: Twenty-four adult albino rats weighing 150–200 g were randomly divided into four equal groups (6 rats each): control group (Group I), the rats that received ACR 45 mg/kg/day (Group II), the rats that received ACR concomitant with omega 3 at a dosage of 200 mg/kg/day (Group III), the rats that received ACR concomitant with green tea dissolved in drinking water at a dosage of 5 g/L (Group IV). The rats were euthanized after 8 weeks of the experiment. Malondialdehyde (MDA) and glutathione (GSH) were measured in cerebellar homogenates. Sections of 5 µm thickness from specimens from the cerebellum were stained with haematoxylin and eosin, silver stain and immunohistochemical stains: platelet-derived growth factor alpha (PDGFα; for oligodendrocytes), glial fibrillary acidic protein (GFAP; for astrocytes) and BCL2 (antiapoptotic). Results: Omega 3 and green tea had improved MDA and GSH as compared to the ACR group. Histologically, the ACR group showed variable degrees of cellular degeneration. Omega 3 had induced oligodendrogenesis in Group III. The optical density of silver stain was significantly (p < 0.05) increased in Groups III and IV as compared to the ACR group. Area per cent of positive PDGFα was significantly increased in the ACR + omega 3 group as compared to the ACR group. Area per cent of positive GFAP was significantly decreased in Groups III and IV as compared to the ACR group. Area per cent of positive BCL2 was significantly increased in the omega 3-trated group as compared to the ACR group. Conclusions: Concomitant administration of omega 3 or green tea with ACR might mitigate the adverse cerebellar changes caused by ACR thanks to an oligodendrogenic effect of omega 3. (Folia Morphol 2019; 78, 3: 564–574)

Słowa kluczowe

Wydawca

-

Czasopismo

Rocznik

Tom

78

Numer

3

Opis fizyczny

p.564–574,fig.,ref.

Twórcy

autor
  • Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Cairo, Egypt
  • Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Cairo, Egypt

Bibliografia

  • 1. Allam A, El-Ghareeb AA, Abdul-Hamid M, et al. Prenatal and perinatal acrylamide disrupts the development of cerebellum in rat: Biochemical and morphological studies. Toxicol Ind Health. 2011; 27(4): 291–306, doi: 10.1177/0748233710386412, indexed in Pubmed: 21310778.
  • 2. Bancroft JD, Layton C. Connective and other mesenchymal tissues with their stains. In: Suvarna SK, Bancroft, JD, Editors. Bancroft’s Theory and Practice of Histological Techniques, Eighth Edition, Elsevier Limited. 2019: 53–175.
  • 3. Begum G, Yan HQ, Li L, et al. Docosahexaenoic acid reduces ER stress and abnormal protein accumulation and improves neuronal function following traumatic brain injury. J Neurosci. 2014; 34(10): 3743–3755, doi: 10.1523/JNEUROSCI.2872-13.2014, indexed in Pubmed: 24599472.
  • 4. Brahmbhatt V, Oliveira M, Briand M, et al. Protective effects of dietary EPA and DHA on ischemia-reperfusion-induced intestinal stress. J Nutr Biochem. 2013; 24(1): 104–111, doi: 10.1016/j.jnutbio.2012.02.014, indexed in Pubmed: 22819560.
  • 5. Buja LM, Krueger GRF. Nervous System. In:, Krueger GRF editors. 2nd edition. Netter’s Illustrated Human Pathology, Saunders, an imprint of Elsevier Inc, Philadelphia, 2014: 441–513.
  • 6. Carere A. Genotoxicity and carcinogenicity of acrylamide: a critical review. Ann Ist Super Sanita. 2006; 42(2): 144–155, indexed in Pubmed: 17033134.
  • 7. Catalá A. The ability of melatonin to counteract lipid peroxidation in biological membranes. Curr Mol Med. 2007; 7(7): 638–649, indexed in Pubmed: 18045142.
  • 8. Crossman AR, Neary D. Cells of the nervous system. In:, editors. Neuroanatomy: An Illustrated Colour Text, 5th edition, Churchil Livingstone an imprint of Elsevier Limited. 2015: 32–35.
  • 9. Dominiczak MH. Lipoprotein Metabolism and Atherogenesis. In: Baynes JW, Hab M, editors. Medical Biochemistry, 5th edition, Elsevier, Saunders. 2019: 489–506.
  • 10. Erasmus MA, Lawlis P, Duncan IJH, et al. Using time to insensibility and estimated time of death to evaluate a nonpenetrating captive bolt, cervical dislocation, and blunt trauma for on-farm killing of turkeys. Poult Sci. 2010; 89(7): 1345–1354, doi: 10.3382/ps.2009-00445, indexed in Pubmed: 20548061.
  • 11. Esmaeelpanah E, Rahmatkhah A, Poormahmood N, et al. Protective Effect of Green Tea Aqueous Extract on Acrylamide Induced Neurotoxicity. Jundishapur J Nat Pharm Prod. 2015; 10(2), doi: 10.17795/jjnpp-18406.
  • 12. Esmaeelpanah E, Razavi BM, Vahdati Hasani F, et al. Evaluation of epigallocatechin gallate and epicatechin gallate effects on acrylamide-induced neurotoxicity in rats and cytotoxicity in PC 12 cells. Drug Chem Toxicol. 2018; 41(4): 441–448, doi: 10.1080/01480545.2017.1381108, indexed in Pubmed: 29072525.
  • 13. Felten D, O’Banion M, Maida M. Neurons and their properties. 3rd edition. Netter’s Atlas of Neuroscience. 2016: 1–42, doi: 10.1016/b978-0-323-26511-9.00001-1.
  • 14. Gartner LP. Nervous tissue In: Textbook of Histology, 4th edition, Elsevier, Philadelphia. 2017: 211–249.
  • 15. Ghorbel I, Amara IB, Ktari N, et al. Aluminium and Acrylamide Disrupt Cerebellum Redox States, Cholinergic Function and Membrane-Bound ATPase in Adult Rats and Their Offspring. Biol Trace Elem Res. 2016; 174(2): 335–346, doi: 10.1007/s12011-016-0716-1, indexed in Pubmed: 27116954.
  • 16. Harvey LD, Yin Y, Attarwala IY, et al. Administration of DHA Reduces Endoplasmic Reticulum Stress-Associated Inflammation and Alters Microglial or Macrophage Activation in Traumatic Brain Injury. ASN Neuro. 2015; 7(6), doi: 10.1177/1759091415618969, indexed in Pubmed: 26685193.
  • 17. Hasadsri L, Wang BH, Lee JV, et al. Omega-3 fatty acids as a putative treatment for traumatic brain injury. J Neurotrauma. 2013; 30(11): 897–906, doi: 10.1089/neu.2012.2672, indexed in Pubmed: 23363551.
  • 18. Hasebe M, Matsumoto I, Imagawa T, et al. Effects of an anti-thyroid drug, methimazole, administration to rat dams on the cerebellar cortex development in their pups. Int J Dev Neurosci. 2008; 26(5): 409–414, doi: 10.1016/j.ijdevneu.2008.03.007, indexed in Pubmed: 18456449.
  • 19. He Y, Tan D, Mi Y, et al. Effect of epigallocatechin-3-gallate on acrylamide-induced oxidative stress and apoptosis in PC12 cells. Hum Exp Toxicol. 2017; 36(10): 1087–1099, doi: 10.1177/0960327116681648, indexed in Pubmed: 27920337.
  • 20. Hering H, Lin CC, Sheng M. Lipid Rafts in the Maintenance of Synapses, Dendritic Spines, and Surface AMPA Receptor Stability. J Neurosci. 2003; 23(8): 3262–3271, doi: 10.1523/jneurosci.23-08-03262.2003.
  • 21. Lu H, Yuan G, Yin Z, et al. Effects of subchronic exposure to lead acetate and cadmium chloride on rat’s bone: Ca and Pi contents, bone density, and histopathological evaluation. Int J Clin Exp Pathol. 2014; 7(2): 640–647, indexed in Pubmed: 24551284.
  • 22. Hügel HM. Brain food for alzheimer-free ageing: focus on herbal medicines. Adv Exp Med Biol. 2015; 863: 95–116, doi: 10.1007/978-3-319-18365-7_5, indexed in Pubmed: 26092628.
  • 23. Khalaf AA, Moselhy WA, Abdel-Hamed MI. The protective effect of green tea extract on lead induced oxidative and DNA damage on rat brain. Neurotoxicology. 2012; 33(3): 280–289, doi: 10.1016/j.neuro.2012.02.003, indexed in Pubmed: 22342836.
  • 24. Khorramirouz R, Go JL, Noble C, et al. A novel surgical technique for a rat subcutaneous implantation of a tissue engineered scaffold. Acta Histochem. 2018; 120(3): 282–291, doi: 10.1016/j.acthis.2018.02.010, indexed in Pubmed: 29519681.
  • 25. LoPachin RM. The changing view of acrylamide neurotoxicity. Neurotoxicology. 2004; 25(4): 617–630, doi: 10.1016/j.neuro.2004.01.004, indexed in Pubmed: 15183015.
  • 26. LoPachin RM, Barber DS, He D, et al. Acrylamide inhibits dopamine uptake in rat striatal synaptic vesicles. Toxicol Sci. 2006; 89(1): 224–234, doi: 10.1093/toxsci/kfj005, indexed in Pubmed: 16207938.
  • 27. Meisenberg G, Simmons W. The metabolism of membrane lipids. Principles of Medical Biochemistry. 4 th edition. Elsevier, Philadelphia. 2012: 412–423, doi: 10.1016/b978-0-323-07155-0.00024-1.
  • 28. Mescher AL. Nerve Tissue & The Nervous System. In: Junqueira’s Basic Histology Text and Atlas, Thirteen’s edition, McGraw-Hill Education, USA. 2013: 170.
  • 29. Ovalle WK, Nahirney PC. Nervous Tissue. In: Netter’s Essential Histology, 2nd Edition, Elsevier, Philadelphia. 2013: 101–130.
  • 30. Pu H, Jiang X, Wei Z, et al. Repetitive and Prolonged Omega-3 Fatty Acid Treatment After Traumatic Brain Injury Enhances Long-Term Tissue Restoration and Cognitive Recovery. Cell Transplant. 2017; 26(4): 555–569, doi: 10.3727/096368916X693842, indexed in Pubmed: 27938482.
  • 31. Rajeh NA, Al-Dhaheri NM. Antioxidant effect of vitamin E and 5-aminosalicylic acid on acrylamide induced kidney injury in rats. Saudi Med J. 2017; 38(2): 132–137, doi: 10.15537/smj.2017.2.16049, indexed in Pubmed: 28133684.
  • 32. Rang HP, Ritter JM, Flower RJ, et al. Rang & Dale’s Pharmacology, 8th edition, Elsevier, Churchil Livingstone, 23; Atherosclerosis and lipoprotein metabolism. 2016: 285–292.
  • 33. Ren H, Yang Z, Luo C, et al. Enriched endogenous omega-3 fatty acids in mice ameliorate parenchymal cell death after traumatic brain injury. Mol Neurobiol. 2017; 54(5): 3317–3326, doi: 10.1007/s12035-016-9931-1, indexed in Pubmed: 27167127.
  • 34. Ross MH, Pawlina W. Histology: a text and atlas — with correlated cell and molecular biology. 7th edition, chapter 12. Wolters Kluwer Health, Philadelphia 2016: 378.
  • 35. Sanderson S, Wild G, Cull AM, et al. Immunohistochemical and immunofluorescent techniques. In: Suvarna SK, Layton C, Bancroft, JD, Editors. Bancroft’s Theory and Practice of Histological Techniques, Eighth Edition, Elsevier Limited. 2019: 337–394.
  • 36. Sarubbo F, Moranta D, Pani G. Dietary polyphenols and neurogenesis: Molecular interactions and implication for brain ageing and cognition. Neurosci Biobehav Rev. 2018; 90: 456–470, doi: 10.1016/j.neubiorev.2018.05.011, indexed in Pubmed: 29753753.
  • 37. Shi J, Ma Y, Zheng M, et al. Effect of sub-acute exposure to acrylamide on GABAergic neurons and astrocytes in weaning rat cerebellum. Toxicol Ind Health. 2012; 28(1): 10–20, doi: 10.1177/0748233711401264, indexed in Pubmed: 21444355.
  • 38. Shim JiS, Kim DH, Bae JH, et al. Effects of omega-3 fatty acids on erectile dysfunction in a rat model of atherosclerosis-induced chronic pelvic ischemia. J Korean Med Sci. 2016; 31(4): 585–589, doi: 10.3346/jkms.2016.31.4.585, indexed in Pubmed: 27051243.
  • 39. Subramony SH, Xia G. Disorders of the cerebellum, including the degenerative ataxias. Neurology in Clinical Practice. 2012: 1802–1823, doi: 10.1016/b978-1-4377-0434-1.00097-9.
  • 40. Tanaka H, Katoh A, Oguro K, et al. Disturbance of hippocampal long-term potentiation after transient ischemia in GFAP deficient mice. J Neurosci Res. 2002; 67(1): 11–20, doi: 10.1002/jnr.10004, indexed in Pubmed: 11754076.
  • 41. Yousef MI, El-Demerdash FM. Acrylamide-induced oxidative stress and biochemical perturbations in rats. Toxicology. 2006; 219(1-3): 133–141, doi: 10.1016/j.tox.2005.11.008, indexed in Pubmed: 16343728.
  • 42. Yousef MI. Aluminium-induced changes in hemato-biochemical parameters, lipid peroxidation and enzyme activities of male rabbits: protective role of ascorbic acid. Toxicology. 2004; 199(1): 47–57, doi: 10.1016/j.tox.2004.02.014, indexed in Pubmed: 15125998.

Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

bwmeta1.element.agro-92d14bf0-0e75-4010-98f3-dfb669f23e24
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.