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Examining the link between dose-dependent dietary iron intake and Alzheimer's disease through oxidative stress in the rat cortex.
J Trace Elem Med Biol 2019; 56:198-206JT

Abstract

BACKGROUND

Neurodegenerative diseases such as Alzheimer's and Parkinson's disease are characterized by the progressive deterioration of the structure and function of the nervous system. A number of environmental risk factors including potentially toxic elements such as iron, lead to negative effects on many metabolic reactions as well as neuroprotection. The aim of this study is to reveal whether long-term iron overload is one of the underlying factors in the pathogenesis of Alzheimer's disease (AD).

METHODS

15 young-adult male rats were randomly divided into 5 groups treated with iron through drinking water for 4 months. Following feeding, the iron content, reduced glutathione (GSH), and hydrogen peroxide (H2O2) levels of cortex tissues were measured. Specific enzyme activities were determined spectrophotometrically. mRNA expression profiles were measured using real-time PCR (qPCR).

RESULTS

Iron levels were elevated in case of non-toxic (0.87 and 3 μg/mL) iron administration. However, no changes were observed in toxic (30 and 300 μg/mL) iron administration. GSH and H2O2 levels altered with long-term iron overload. Glutathione peroxidase (GPx) enzyme activities significantly increased in all groups, while glutathione S-transferase (GST) activity increased only in case of 0.87 and 30 μg/mL iron administration. Expression levels of neuroprotective and AD-related genes were altered by 3 μg/mL iron overload in a dose-dependent manner. The expression and activity of acetylcholinesterase (AChE) were elevated at 3 μg/mL iron concentration.

CONCLUSION

The findings of the present study allow us to conclude that long-term dietary iron intake, especially at a dose of 3 μg/mL demonstrates negative effects on the rat cortex by provoking antioxidant metabolism and AD pathology in a dose-dependently.

Authors+Show Affiliations

Science Faculty, Department of Molecular Biology and Genetics, Atatürk University, Erzurum, Turkey. Electronic address: hamid.ceylan@atauni.edu.tr.Science Faculty, Department of Molecular Biology and Genetics, Atatürk University, Erzurum, Turkey.Science Faculty, Department of Molecular Biology and Genetics, Atatürk University, Erzurum, Turkey; Vocational School, Department of Medical Services and Techniques, Muş Alparslan University, Mus, Turkey.Science Faculty, Department of Molecular Biology and Genetics, Atatürk University, Erzurum, Turkey.Science Faculty, Department of Molecular Biology and Genetics, Atatürk University, Erzurum, Turkey.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31525623

Citation

Ceylan, Hamid, et al. "Examining the Link Between Dose-dependent Dietary Iron Intake and Alzheimer's Disease Through Oxidative Stress in the Rat Cortex." Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS), vol. 56, 2019, pp. 198-206.
Ceylan H, Budak H, Kocpinar EF, et al. Examining the link between dose-dependent dietary iron intake and Alzheimer's disease through oxidative stress in the rat cortex. J Trace Elem Med Biol. 2019;56:198-206.
Ceylan, H., Budak, H., Kocpinar, E. F., Baltaci, N. G., & Erdogan, O. (2019). Examining the link between dose-dependent dietary iron intake and Alzheimer's disease through oxidative stress in the rat cortex. Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS), 56, pp. 198-206. doi:10.1016/j.jtemb.2019.09.002.
Ceylan H, et al. Examining the Link Between Dose-dependent Dietary Iron Intake and Alzheimer's Disease Through Oxidative Stress in the Rat Cortex. J Trace Elem Med Biol. 2019;56:198-206. PubMed PMID: 31525623.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Examining the link between dose-dependent dietary iron intake and Alzheimer's disease through oxidative stress in the rat cortex. AU - Ceylan,Hamid, AU - Budak,Harun, AU - Kocpinar,Enver Fehim, AU - Baltaci,Nurdan Gonul, AU - Erdogan,Orhan, Y1 - 2019/09/09/ PY - 2019/06/13/received PY - 2019/08/01/revised PY - 2019/09/08/accepted PY - 2019/9/17/pubmed PY - 2019/9/17/medline PY - 2019/9/17/entrez KW - Alzheimer's disease KW - Neurotoxicity KW - Oxidative stress KW - Rat cortex KW - Toxic element SP - 198 EP - 206 JF - Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) JO - J Trace Elem Med Biol VL - 56 N2 - BACKGROUND: Neurodegenerative diseases such as Alzheimer's and Parkinson's disease are characterized by the progressive deterioration of the structure and function of the nervous system. A number of environmental risk factors including potentially toxic elements such as iron, lead to negative effects on many metabolic reactions as well as neuroprotection. The aim of this study is to reveal whether long-term iron overload is one of the underlying factors in the pathogenesis of Alzheimer's disease (AD). METHODS: 15 young-adult male rats were randomly divided into 5 groups treated with iron through drinking water for 4 months. Following feeding, the iron content, reduced glutathione (GSH), and hydrogen peroxide (H2O2) levels of cortex tissues were measured. Specific enzyme activities were determined spectrophotometrically. mRNA expression profiles were measured using real-time PCR (qPCR). RESULTS: Iron levels were elevated in case of non-toxic (0.87 and 3 μg/mL) iron administration. However, no changes were observed in toxic (30 and 300 μg/mL) iron administration. GSH and H2O2 levels altered with long-term iron overload. Glutathione peroxidase (GPx) enzyme activities significantly increased in all groups, while glutathione S-transferase (GST) activity increased only in case of 0.87 and 30 μg/mL iron administration. Expression levels of neuroprotective and AD-related genes were altered by 3 μg/mL iron overload in a dose-dependent manner. The expression and activity of acetylcholinesterase (AChE) were elevated at 3 μg/mL iron concentration. CONCLUSION: The findings of the present study allow us to conclude that long-term dietary iron intake, especially at a dose of 3 μg/mL demonstrates negative effects on the rat cortex by provoking antioxidant metabolism and AD pathology in a dose-dependently. SN - 1878-3252 UR - https://www.unboundmedicine.com/medline/citation/31525623/Examining_the_link_between_dose-dependent_dietary_iron_intake_and_Alzheimer's_disease_through_oxidative_stress_in_the_rat_cortex L2 - https://linkinghub.elsevier.com/retrieve/pii/S0946-672X(19)30384-0 DB - PRIME DP - Unbound Medicine ER -