scholarly journals Molecular crowding effects on the biochemical properties of amyloid β–heme, Aβ–Cu and Aβ–heme–Cu complexes

2020 ◽  
Vol 11 (28) ◽  
pp. 7479-7486 ◽  
Author(s):  
Meng Li ◽  
Zhenqi Liu ◽  
Jinsong Ren ◽  
Xiaogang Qu
Keyword(s):  
Oxidative Damage ◽  
Amyloid Β ◽  
Biochemical Properties ◽  
Molecular Crowding ◽  
Crowding Effects ◽  
Cu Complexes

Our findings highlight the significance of hydration contributions to the interactions of Aβ–heme and Aβ–Cu as well as their peroxidase activities. Aβ40–Cu but not Aβ40–heme may play more important roles in the oxidative damage in the etiology of AD.

scholarly journals The Amyloid β Protein Induces Oxidative Damage of Mitochondrial DNA

1997 ◽  
Vol 56 (12) ◽  
pp. 1356-1362 ◽  
Author(s):  
PETER BOZNER ◽  
VALENTINA GRISHKO ◽  
SUSAN P. LEDOUX ◽  
GLENN L. WILSON ◽  
Y-C CHYAN ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Oxidative Damage ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Β Protein

Two dimensional crowding effects on protein folding at interfaces observed by chiral vibrational sum frequency generation spectroscopy

2018 ◽  
Vol 20 (35) ◽  
pp. 22421-22426 ◽  
Author(s):  
Wei Liu ◽  
Li Fu ◽  
Zhuguang Wang ◽  
Zahra Sohrabpour ◽  
Xiaobai Li ◽  
...  
Keyword(s):  
Protein Folding ◽  
Sum Frequency Generation ◽  
Molecular Crowding ◽  
Two Dimensional ◽  
Sum Frequency ◽  
Crowding Effects ◽  
Sum Frequency Generation Spectroscopy ◽  
Frequency Generation

Vibrational sum frequency generation studies demonstrate the effects of two-dimensional molecular crowding on protein folding at interfaces.

scholarly journals 57 Carnosine prevents oxidative damage in myoblast cells derived from porcine skeletal muscle

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 59-59
Author(s):  
Marie-France Palin ◽  
Jérôme Lapointe ◽  
Claude Gariépy ◽  
Danièle Beaudry ◽  
Claudia Kalbe
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Metal Ion ◽  
Antioxidant Activities ◽  
Radical Scavenging ◽  
Biochemical Properties ◽  
Antioxidant Enzyme Activities ◽  
Antioxidant Genes ◽  
Mitochondrial Functions ◽  
Myoblast Cells

Abstract Carnosine (β-alanyl-L-histidine) is a molecule naturally and exclusively present in muscle food with the highest concentrations found in skeletal muscles and brain of the animal. Among its numerous biochemical properties, carnosine has antioxidant activity which include metal ion chelation and free radical scavenging. We have recently reported that high muscle carnosine content in pig is associated with better meat quality. Moreover, supplementing pigs with β-alanine reduced oxidative damage to Longissimus muscle (LM) lipids and proteins. Among previously reported antioxidant activities, carnosine was found to limit the production of reactive oxygen species (ROS) and increase antioxidant enzyme activities. However, these studies were mainly conducted in rodents and cell lines and mechanisms in play remain to be characterized. To determine the effect of carnosine in preventing oxidative damage and characterize the mechanisms in play, we have undertaken experiments using the progeny (myoblasts) of satellite cells isolated from the LM of newborn piglets. Cells were treated with carnosine (0, 10, 25 and 50 mM) for 48 h and were then either collected immediately or treated with H2O2 (0.3 mM, 1 h) to induce an oxidative stress. Our results showed that carnosine prevents oxidative stress through the reduction of total intracellular ROS and by modulating the antioxidant system in myoblasts.Carnosine increased the mRNA abundance of NEF2L2, a transcription factor activated by oxidative stress, and several of its downstream regulated antioxidant genes. Western blot analyses further suggest that the protective effect of carnosine on H2O2-induced oxidative stress is mediated through the p38 MAPK intracellular pathway. Finally, the addition of carnosine to H2O2-treated myoblasts increased the basal cellular oxygen consumption rate (OCR), the ATP-linked OCR and proton leaks, thus suggesting an effect of carnosine on mitochondrial functions. Taken together, these findings demonstrate the important role of carnosine in preventing oxidative damage in porcine muscle cells.

scholarly journals Ginsenoside Re Inhibits ROS/ASK-1 Dependent Mitochondrial Apoptosis Pathway and Activation of Nrf2-Antioxidant Response in Beta-Amyloid-Challenged SH-SY5Y Cells

Molecules ◽  
2019 ◽  
Vol 24 (15) ◽  
pp. 2687 ◽  
Author(s):  
Meichen Liu ◽  
Xueyuan Bai ◽  
Shiting Yu ◽  
Wenxue Zhao ◽  
Juhui Qiao ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Related Factor ◽  
Ros Scavenging ◽  
Cytochrome C Release ◽  
Apoptotic Pathway ◽  
Ginsenoside Re ◽  
Apoptosis Pathway

Accumulation of amyloid-β (Aβ), which results in the formation of senile plaques that cause oxidative damage and neuronal cell death, has been accepted as the major pathological mechanism of Alzheimer’s disease (AD). Hence, inhibition of Aβ-induced oxidative damage and neuronal cell apoptosis represents the effective strategies in combating AD. Ginsenoside Re (Re) has pharmacological effects against Aβ-induced neurotoxicity. However, its molecular mechanism remains elusive. The present study evaluated the effect of Re against Aβ-induced cytotoxicity and apoptosis in SH-SY5Y cells, and investigated the underlying mechanism. We demonstrate that Re inhibits the Aβ-triggered mitochondrial apoptotic pathway, as indicated by maintenance of mitochondrial functional, elevated Bcl-2/Bax ratio, reduced cytochrome c release, and inactivation of caspase-3/9. Re attenuated Aβ-evoked reactive oxygen species (ROS) production, apoptosis signal-regulating kinase 1 (ASK1) phosphorylation, and JNK activation. ROS-scavenging abrogated the ability of Re to alter ASK-1 activation. Simultaneously, inhibition of JNK abolished Re-induced Bax downregulation in Aβ-challenged SH-SY5Y cells. In addition, Re enhanced activation of the nuclear factor-E2-related factor 2 (Nrf2) in Aβ-induced SH-SY5Y cells. Knockdown of Nrf2 by small interfering RNA targeting Nrf2 abolished the protective effect of Re. Our findings indicate that Re could be a potential therapeutic approach for the treatment of AD.

scholarly journals The Effects of Molecular Crowding on the Structure and Stability of G-Quadruplexes with an Abasic Site

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Takeshi Fujimoto ◽  
Shu-ichi Nakano ◽  
Daisuke Miyoshi ◽  
Naoki Sugimoto
Keyword(s):  
Site Effects ◽  
Enthalpy Change ◽  
Molecular Crowding ◽  
Abasic Site ◽  
Structure And Stability ◽  
Quadruplex Structure ◽  
Abasic Sites ◽  
Crowding Effects ◽  
G Quadruplex ◽  
Quadruplex Formation

Both cellular environmental factors and chemical modifications critically affect the properties of nucleic acids. However, the structure and stability of DNA containing abasic sites under cell-mimicking molecular crowding conditions remain unclear. Here, we investigated the molecular crowding effects on the structure and stability of the G-quadruplexes including a single abasic site. Structural analysis by circular dichroism showed that molecular crowding by PEG200 did not affect the topology of the G-quadruplex structure with or without an abasic site. Thermodynamic analysis further demonstrated that the degree of stabilization of the G-quadruplex by molecular crowding decreased with substitution of an abasic site for a single guanine. Notably, we found that the molecular crowding effects on the enthalpy change for G-quadruplex formation had a linear relationship with the abasic site effects depending on its position. These results are useful for predicting the structure and stability of G-quadruplexes with abasic sites in the cell-mimicking conditions.

Metal-Catalyzed Oxidative Damage and Oligomerization of the Amyloid-β Peptide of Alzheimer′s Disease

ChemInform ◽  
2004 ◽  
Vol 35 (33) ◽  
Author(s):  
Feda E. A. Ali ◽  
Kevin J. Barnham ◽  
Colin J. Barrow ◽  
Frances Separovic
Keyword(s):  
Oxidative Damage ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Metal Catalyzed

scholarly journals Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1353
Author(s):  
Francesca Romana Buccellato ◽  
Marianna D’Anca ◽  
Chiara Fenoglio ◽  
Elio Scarpini ◽  
Daniela Galimberti
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oxidative Damage ◽  
Molecular Mechanisms ◽  
Biomarker Discovery ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Antioxidant Defenses ◽  
Ageing Population

Alzheimer’s disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population. The lack of effective treatments for overt AD urges the discovery of biomarkers for early diagnosis, i.e., in subjects with mild cognitive impairment (MCI) or prodromal AD. The brain is exposed to oxidative stress as levels of reactive oxygen species (ROS) are increased, whereas cellular antioxidant defenses are decreased. Increased ROS levels can damage cellular structures or molecules, leading to protein, lipid, DNA, or RNA oxidation. Oxidative damage is involved in the molecular mechanisms which link the accumulation of amyloid-β and neurofibrillary tangles, containing hyperphosphorylated tau, to microglia response. In this scenario, microglia are thought to play a crucial role not only in the early events of AD pathogenesis but also in the progression of the disease. This review will focus on oxidative damage products as possible peripheral biomarkers in AD and in the preclinical phases of the disease. Particular attention will be paid to biological fluids such as blood, CSF, urine, and saliva, and potential future use of molecules contained in such body fluids for early differential diagnosis and monitoring the disease course. We will also review the role of oxidative damage and microglia in the pathogenesis of AD and, more broadly, in neurodegeneration.

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