Journals / Dokuz Eylül Üniversitesi Tıp Fakültesi Dergisi / 2002 / Cilt: 16 - Sayı: 3

Cell death due to methamphetamine in primary oligodendrocyte culture

Primer oligodendrosit kültüründe metamfetamine bağlı hücre ölümü

Pages
141–147
DOI
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusions: These results suggest that neurotoxic effects that are observed in chronic mediamphetamine users may be partly due to the toxic effect of methamphetamine on oligodendrocyte.

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: The neurotoxic effect of methamphetamine which is a psyhcostimulant drug has been established by in vitro and in vivo studies.
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Key Findings & Data:For this purpose cultures have been exposed to the various concentrations of methamphetamine (10-1000 $\mu$M with various incubation time (24-96 hours).
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Conclusion & Impact:Conclusions: These results suggest that neurotoxic effects that are observed in chronic mediamphetamine users may be partly due to the toxic effect of methamphetamine on oligodendrocyte.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Apoptoz · Hayvanlar · yenidoğan

Abstract

Objective: The neurotoxic effect of methamphetamine which is a psyhcostimulant drug has been established by in vitro and in vivo studies. In this study, the cytotoxic effect of mediamphetamine on oligodendrocytes has been investigated. Material and Method: The cytotoxic effect of metamphetamine was determined by lactate dehydrogenase (LDH) test in neonatal Wistar rat oligodendrocyte cultures. The apoptosis inducing effect of methamphetamine was evaluated by apostain immunfluorescence staining method. For this purpose cultures have been exposed to the various concentrations of methamphetamine (10-1000 $\mu$M with various incubation time (24-96 hours). Results LDH measures show that mediamphetamine leads dose and time-dependent oligodendrocyte death. Apostain method points that methamphetamine results in apoptotic oligodendrocyte death especially at low (10 $\mu$M and high (1000 $\mu$M doses. Conclusions: These results suggest that neurotoxic effects that are observed in chronic mediamphetamine users may be partly due to the toxic effect of methamphetamine on oligodendrocyte.

Özet

Amaç: Psikostimülan bir ilaç olan metamfetaminin nörotoksik etkisi in vitro ve in vivo çalışmalarla kanıtlanmıştır. Bu çalışmada ise metamfetaminin yenidoğan Wistar sıçan oligodendrosit kültürlerinde sitotoksik etkisi araştırıldı. Gereç ve Yöntem: Metamfetaminin sitotoksik etkisi laktat dehidrogenaz (LDH) testiyle, apoptoz indükleyici etkisi ise apostain immünfloresan boyama yöntemiyle araştırıldı. Bu amaçla kültürler değişen konsantrasyonlarda (10-1000 $\mu$M arası) ve değişik enkübasyon sürelerinde (24-96 saat arası) metamfetamiııe maruz bırakıldı. Bulgular: LDH ölçümleri metamfetaminin doza ve zamana bağımlı olarak oligodendrosit ölümüne yol açtığını göstermektedir. Apostain yöntemi ise metamfetaminin düşük (10 $\mu$M) ve yüksek (1000 $\mu$M) dozlarda daha belirgin apoptoza neden olduğunu işaret etmektedir. Sonuç: Bu sonuçlar kronik metamfetamin kullanıcılarında gözlenen nörotoksik etkilerin kısmen bu maddenin oligodendrositler üzerine toksik etkisine de bağlı olabileceğini düşündürmektedir.

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Cite This Article

GENÇ, K. K., GENÇ, Ş., SÖNMEZ, Ü., YILMAZ, O., SÖNMEZ, A., TUĞYAN, K., ERGÜR, B., BULDAN, Z. (2002). Cell death due to methamphetamine in primary oligodendrocyte culture. Dokuz Eylül Üniversitesi Tıp Fakültesi Dergisi, Cilt: 16 - Sayı: 3, 141–147. https://ajindex.com/articles/213397

References (14)

  1. Davidson. C, Gow AJ, Lee TH, et al. Methamp- hetamine neurotoxicity: necrotic and apoptotic mechanisms and relevance to human abuse and treatment. Brain Res Brain Res Rev 2001;36:l-22
  2. Zimmerman EF. Substance abuse in pregnancy: teratogenesis. Pediatr Ann 1991;20:541-544
  3. Yamamoto Y, Yamamoto K, Abiru H, et al. Effects of methamphetamine on rat embryos cultured in vitro. BiolNeonate 1995;68:33-38
  4. Clio DH, Lyu HM, Lee HB, et al. Behavioral teratoge- nicity of memamphetamine. J Toxicol Sci 1991;16:37-49
  5. Choi HJ, Yoo TM, Chung SY, et al. Methamphe- tamine-induced apoptosis in a CNS-derived catec- holammergic cell Hue. Mol Cells 2002;13:221-227
  6. Cadet JL, Ordonez SV, Ordonez JV. Metliamphe¬ tamine induces apoptosis in immortalized neural cells: protection by the proto-oncogene, bcl-2. Synapse 1997;25:176-184
  7. Deng X, Wang Y, Chou J, et al. Methamphetamine causes widespread apoptosis in the mouse brain: evidence from using an improved TUNEL iiistochemical method. Brain Res Mol Brain Res 2001;93:64-69
  8. Deng X, Cai NS, McCoy MT, et al. Methamphetamine induces apoptosis in an immortalized rat striatal cell line by activating the mitochondrial cell death pathway. Neuropharmacology 2002;42:837-845. 9. 'Ernst T, Chang L, Leonido-Yee M, et al. Evidence for lung-term neurotoxicity associated with methamphe¬ tamine abuse: A 1H MRS study. Neurology 2000;54:1344-1349
  9. De Velüs J, Espinosa de los Monteros A. Oligodend- rocytes. In "Practical Cell Culture Techniques" A. A. Boulton, G. B. Baker, W. Walz (eds.), p. 323-353, Humana Press, Totowa, New Jersey, 1992
  10. Ying HS, Gottron FJ, Choi DW. Assessment of cell viability in primary neuronal cultures. Current Protocols in Neuroscience 2000;7.18.1-7.18.17. 12. irankfurt OS. Detection of apoptosis in leukemic and breast cancer cells with monoclonal antibody to single-stranded DNA. Anticancer Res 1994;14:1861-1869
  11. Benn T, Halfpenny C, Scolding N. Glial cells as targets for cvtotoxic immune mediators. Glia 2001;36:200-211
  12. Casaccia-Bonnefil P. Cell death in the oligodendrocyte lineage: a molecular perspective of life/death decisions in development and disease. Glia 2000;29:l24-135
  13. Charriaut-Marlangue C, Ben-Ari J. A cautionary note on the use of the TUNEL stain to determine apoptosis. Neuroreport 1995;7:61-64
  14. Stadclmann C, Brack W, Bancher C, et al. Alzheimer disease: DNA fragmentation ndicates increased neuronal vulnerability, but not apoptosis. J Neuropathol Exp Neurol 1998;57