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Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism.
Life Sci. 2008 Jul 18; 83(3-4):96-102.LS

Abstract

Oxidative stress is one of the hypothesized pathogenic mechanisms for neurodegenerative diseases, including Alzheimer's disease (AD); numerous studies suggest that Abeta is toxic to neurons by free radical mediated mechanism. A constant feature in AD brain is selective neuronal loss, accompanied by dysfunction of several neurotransmitter systems, such as cholinergic, serotoninergic and noradrenergic systems. In the present study, we studied the neuroprotective role of melatonin against amyloid protofibrils and the toxicity of protofibrils on serotoninergic and noradrenergic systems. Mice were divided into four groups (n=8 each), control, Scrambles Abeta(35-25) treated, Abeta(25-35) injected, and melatonin treated. A single dose of Abeta(25-35) (25 microg) was administered to mice via intraperitoneal injection. Melatonin (50 mg/kg body weight) was administered intraperitoneally for 3 days to the Abeta(25-35) injected mice. Control mice received only physiological saline and Scrambles receives Abeta(35-25) single intraperitoneal injection of 25 microg of Abeta(35-25). Our study showed that melatonin significantly reduces reactive oxygen species (ROS) production in the astrocytes, lymphocytes and hepatocytes of Abeta injected mice by increasing the levels of scavenging enzymes, SOD, catalase and GSH when compared to the untreated group. Immunohistochemistry study reveals that melatonin prevents the activation of GFAP in neocortex and transcription factor NF-kappaB in liver and neocortex of Abeta injected mice. It also prevents the elevation of dopamine depletion and its degradation products. Thus, while melatonin may be a potential therapeutic agent in the prevention of oxidative stress associated with Abeta and AD, it can also prevent dopamine turnover induced by Abeta.

Authors+Show Affiliations

Bio-Organic and Neurochemistry Laboratory, Central Leather Research Institute, Chennai, India.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18590917

Citation

Gunasingh, Masilamoni J., et al. "Melatonin Prevents Amyloid Protofibrillar Induced Oxidative Imbalance and Biogenic Amine Catabolism." Life Sciences, vol. 83, no. 3-4, 2008, pp. 96-102.
Gunasingh MJ, Philip JE, Ashok BS, et al. Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism. Life Sci. 2008;83(3-4):96-102.
Gunasingh, M. J., Philip, J. E., Ashok, B. S., Kirubagaran, R., Jebaraj, W. C., Davis, G. D., Vignesh, S., Dhandayuthapani, S., & Jayakumar, R. (2008). Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism. Life Sciences, 83(3-4), 96-102. https://doi.org/10.1016/j.lfs.2008.05.011
Gunasingh MJ, et al. Melatonin Prevents Amyloid Protofibrillar Induced Oxidative Imbalance and Biogenic Amine Catabolism. Life Sci. 2008 Jul 18;83(3-4):96-102. PubMed PMID: 18590917.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism. AU - Gunasingh,Masilamoni J, AU - Philip,Jesudason E, AU - Ashok,Ben S, AU - Kirubagaran,R, AU - Jebaraj,W Charles E, AU - Davis,G Dicky John, AU - Vignesh,S, AU - Dhandayuthapani,S, AU - Jayakumar,R, Y1 - 2008/05/27/ PY - 2008/01/15/received PY - 2008/04/14/revised PY - 2008/05/09/accepted PY - 2008/7/2/pubmed PY - 2008/9/24/medline PY - 2008/7/2/entrez SP - 96 EP - 102 JF - Life sciences JO - Life Sci VL - 83 IS - 3-4 N2 - Oxidative stress is one of the hypothesized pathogenic mechanisms for neurodegenerative diseases, including Alzheimer's disease (AD); numerous studies suggest that Abeta is toxic to neurons by free radical mediated mechanism. A constant feature in AD brain is selective neuronal loss, accompanied by dysfunction of several neurotransmitter systems, such as cholinergic, serotoninergic and noradrenergic systems. In the present study, we studied the neuroprotective role of melatonin against amyloid protofibrils and the toxicity of protofibrils on serotoninergic and noradrenergic systems. Mice were divided into four groups (n=8 each), control, Scrambles Abeta(35-25) treated, Abeta(25-35) injected, and melatonin treated. A single dose of Abeta(25-35) (25 microg) was administered to mice via intraperitoneal injection. Melatonin (50 mg/kg body weight) was administered intraperitoneally for 3 days to the Abeta(25-35) injected mice. Control mice received only physiological saline and Scrambles receives Abeta(35-25) single intraperitoneal injection of 25 microg of Abeta(35-25). Our study showed that melatonin significantly reduces reactive oxygen species (ROS) production in the astrocytes, lymphocytes and hepatocytes of Abeta injected mice by increasing the levels of scavenging enzymes, SOD, catalase and GSH when compared to the untreated group. Immunohistochemistry study reveals that melatonin prevents the activation of GFAP in neocortex and transcription factor NF-kappaB in liver and neocortex of Abeta injected mice. It also prevents the elevation of dopamine depletion and its degradation products. Thus, while melatonin may be a potential therapeutic agent in the prevention of oxidative stress associated with Abeta and AD, it can also prevent dopamine turnover induced by Abeta. SN - 0024-3205 UR - https://www.unboundmedicine.com/medline/citation/18590917/Melatonin_prevents_amyloid_protofibrillar_induced_oxidative_imbalance_and_biogenic_amine_catabolism_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(08)00215-4 DB - PRIME DP - Unbound Medicine ER -