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mTOR Modulates Methamphetamine-Induced Toxicity through Cell Clearing Systems
المؤلفون المشاركون
Biagioni, Francesca
Fornai, Francesco
Lenzi, Paola
Lazzeri, Gloria
Busceti, Carla L.
Fulceri, Federica
Scavuzzo, Maria C.
Ippolito, Chiara
Salvetti, Alessandra
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-22، 22ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-10-29
دولة النشر
مصر
عدد الصفحات
22
التخصصات الرئيسية
الملخص EN
Methamphetamine (METH) is abused worldwide, and it represents a threat for public health.
METH exposure induces a variety of detrimental effects.
In fact, METH produces a number of oxidative species, which lead to lipid peroxidation, protein misfolding, and nuclear damage.
Cell clearing pathways such as ubiquitin-proteasome (UP) and autophagy (ATG) are involved in METH-induced oxidative damage.
Although these pathways were traditionally considered to operate as separate metabolic systems, recent studies demonstrate their interconnection at the functional and biochemical level.
Very recently, the convergence between UP and ATG was evidenced within a single organelle named autophagoproteasome (APP), which is suppressed by mTOR activation.
In the present research study, the occurrence of APP during METH toxicity was analyzed.
In fact, coimmunoprecipitation indicates a binding between LC3 and P20S particles, which also recruit p62 and alpha-synuclein.
The amount of METH-induced toxicity correlates with APP levels.
Specific markers for ATG and UP, such as LC3 and P20S in the cytosol, and within METH-induced vacuoles, were measured at different doses and time intervals following METH administration either alone or combined with mTOR modulators.
Western blotting, coimmunoprecipitation, light microscopy, confocal microscopy, plain transmission electron microscopy, and immunogold staining were used to document the effects of mTOR modulation on METH toxicity and the merging of UP with ATG markers within APPs.
METH-induced cell death is prevented by mTOR inhibition, while it is worsened by mTOR activation, which correlates with the amount of autophagoproteasomes.
The present data, which apply to METH toxicity, are also relevant to provide a novel insight into cell clearing pathways to counteract several kinds of oxidative damage.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Lazzeri, Gloria& Biagioni, Francesca& Fulceri, Federica& Busceti, Carla L.& Scavuzzo, Maria C.& Ippolito, Chiara…[et al.]. 2018. mTOR Modulates Methamphetamine-Induced Toxicity through Cell Clearing Systems. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-22.
https://search.emarefa.net/detail/BIM-1211751
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Lazzeri, Gloria…[et al.]. mTOR Modulates Methamphetamine-Induced Toxicity through Cell Clearing Systems. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-22.
https://search.emarefa.net/detail/BIM-1211751
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Lazzeri, Gloria& Biagioni, Francesca& Fulceri, Federica& Busceti, Carla L.& Scavuzzo, Maria C.& Ippolito, Chiara…[et al.]. mTOR Modulates Methamphetamine-Induced Toxicity through Cell Clearing Systems. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-22.
https://search.emarefa.net/detail/BIM-1211751
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1211751
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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