Dergiler / Nöropsikiyatri Arşivi / 2020 / Cilt: 57 - Sayı: 4

High KEAP1, NRF2 and Low HO-1 Serum Levels in Children with Autism

Otizmli Çocuklarda Yüksek KEAP1, NRF2 ve Düşük HO-1 Serum Düzeyleri

Sayfa
274–279
DOI
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Conclusion: This study suggests that oxidative stress is higher in children with ASD and that HO-1 levels are insufficient to achieve oxidative balance.

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Amaç & Hipotez:Introduction: The purpose of our study was to investigate heme oxygenase-1 (HO-1), nuclear factor erythroid-2-related factor 2 (NRF2), and kelch-like ECH-associated protein 1 (KEAP1) levels in children with autism spectrum disorder (ASD) and to reveal their association with the severity of autism.
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Temel Bulgular & Veri:Methods: This study measured serum HO-1, KEAP1, and NRF2 levels in 43 patients with ASD (aged 3–12 years) and in 41 age– and gendermatched healthy controls.
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Sonuç & Katkı:Conclusion: This study suggests that oxidative stress is higher in children with ASD and that HO-1 levels are insufficient to achieve oxidative balance.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Alan Parametreleri

Özet

Introduction: The purpose of our study was to investigate heme oxygenase-1 (HO-1), nuclear factor erythroid-2-related factor 2 (NRF2), and kelch-like ECH-associated protein 1 (KEAP1) levels in children with autism spectrum disorder (ASD) and to reveal their association with the severity of autism. Methods: This study measured serum HO-1, KEAP1, and NRF2 levels in 43 patients with ASD (aged 3–12 years) and in 41 age– and gendermatched healthy controls. ASD severity was rated using the Childhood Autism Rating Scale (CARS). HO-1, KEAP1, and NRF2 levels were determined in the biochemistry laboratory using the ELISA technique. Results: HO-1 levels were significantly lower in patients aged 3–12 years compared to controls aged 3–12, while KEAP1 and NRF2 levels were significantly higher (p=0.020, p 0.05). Conclusion: This study suggests that oxidative stress is higher in children with ASD and that HO-1 levels are insufficient to achieve oxidative balance.

Abstract

Amaç: Çalışmamızın amacı otizm spektrum bozukluğu (OSB) tanılı çocuklarda heme oksijenaz-1 (HO-1), nükleer faktör eritroid-2 ile ilişkili faktör 2 (NRF2) ve kelch benzeri ECH ile ilişkili protein 1 (KEAP1) düzeylerini araştırmak otizmin ciddiyeti ile ilişkilerini ortaya koymaktır. Yöntem: Bu çalışmada, OSB tanılı 43 hasta (yaş 3-12 yaş) ve yaş, cinsiyet uyumlu 41 sağlıklı kontrolde serum HO-1, KEAP1 ve NRF2 düzeyleri ölçülmüştür. OSB şiddeti, çocukluk otizm değerlendirme ölçeği (ÇODÖ) kullanılarak derecelendirildi. ELISA tekniği kullanılarak biyokimya laboratuarında HO-1, KEAP1 ve NRF2 seviyeleri belirlendi. Bulgular: 3-12 yaş arası hastalarda HO-1 düzeyleri 3-12 yaş arası kontrollere göre anlamlı derecede düşükken, KEAP1 ve NRF2 düzeyleri anlamlı olarak yüksek bulundu (sırasıyla p = 0.020, p 0.05). Sonuç: Bu çalışma, OSB’li çocuklarda oksidatif stresin daha yüksek olduğunu ve HO-1 seviyelerinin oksidatif dengeyi sağlamak için yetersiz olduğunu göstermektedir.

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Bu Makaleye Atıf Yap

AYAYDIN, H., AKALTUN, İ., KOYUNCU, İ., ÇELİK, H., KİRMİT, A., TAKATAK, H. (2020). High KEAP1, NRF2 and Low HO-1 Serum Levels in Children with Autism. Nöropsikiyatri Arşivi, Cilt: 57 - Sayı: 4, 274–279. https://ajindex.com/articles/292043

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Kaynakça (3)

  1. American Psychiatric Association (APA). Diagnostic and statistical manual of mental disorders (DSM-5®): American Psychiatric Pub; 2013
  2. Grice DE, Buxbaum JD. The genetics of autism spectrum disorders. Neuromolecular Med 2006;8:451–460. [Crossref] 3. Rutter M. Genetic Influences and Autism. In: Volkmar FR, Paul R, Klin A, Cohen D, editors. Handbook of autism and pervasive developmental disorders: Diagnosis, development, neurobiology, and behavior (3rd ed.). Hoboken, NJ, USA: John Wiley & Sons; 2005. p.425–453. [Crossref] 4. Rossignol DA, Frye RE. A review of research trends in physiological abnormalities in autism spectrum disorders: immune dysregulation, inflammation, oxidative stress, mitochondrial dysfunction and environmental toxicant exposures. Mol Psychiatry 2012;17:389–401. [Crossref] 5. Gutteridge JM, Halliwell B. Antioxidant Protection and Ixygen Radical Signaling. In: Colton CA, Gilbert DL, editors. Reactive oxygen species in biological systems. Boston, MA. Springer; 2002. p.189–218
  3. Tonnies E, Trushina E. Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease. J Alzheimers Dis 2017;57:1105–1121. [Crossref] 7. Ng F, Berk M, Dean O, Bush AI. Oxidative stress in psychiatric disorders: evidence base and therapeutic implications. Int J Neuropsychopharmacol 2008;11:851–876. [Crossref] 8. Camkurt MA, Findikli E, Izci F, Kurutas EB, Tuman TC. Evaluation of malondialdehyde, superoxide dismutase and catalase activity and their diagnostic value in drug naive, first episode, non-smoker major depression patients and healthy controls. Psychiatry Res 2016;238:81–85. [Crossref] 9. Oztop D, Altun H, Baskol G, Ozsoy S. Oxidative stress in children with attention deficit hyperactivity disorder. Clin Biochem 2012;45:745–748. [Crossref] 10. Smaga I, Niedzielska E, Gawlik M, Moniczewski A, Krzek J, Przegalinski E, Pera J, Filip M. Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 2. Depression, anxiety, schizophrenia and autism. Pharmacol Rep 2015;67:569–580. [Crossref] 11. James SJ, Cutler P, Melnyk S, Jernigan S, Janak L, Gaylor DW, Neubrander JA. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. Am J Clin Nutr 2004;80:1611– 1617. [Crossref] 12. Han Y, Xi QQ, Dai W, Yang SH, Gao L, Su YY, Zhang X. Abnormal transsulfuration metabolism and reduced antioxidant capacity in Chinese children with autism spectrum disorders. Int J Dev Neurosc