Effects of cholesterol oxides on cell death induction and calcium increase in human neuronal cells (SK-N-BE) and evaluation of the protective effects of docosahexaenoic acid (DHA; C22:6 n-3)

Zarrouk, Amira; Nury, Thomas; Samadi, Mohammad; O’Callaghan, Yvonne C.; Hammami, Mohamed; O’Brien, Nora M.; Lizard, Gérard; Mackrill, John J.

doi:10.1016/j.steroids.2015.01.018

Cited by 36 publications

(34 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We attempted to bring additional information on the impact of 7b-OHC on mitochondria with regards on mitochondrial structure, function and metabolism affected in neurodegenerative diseases. In agreement with previous studies [25,80,81], we demonstrated that 7b-OHC induces alterations in mitochondrial function: it inhibits the succinate dehydrogenase activity, decreases DWm and enhances the mitochondrial production of O 2 À . These events were associated with an increased mitochondrial mass which could be a consequence of the loss of DWm.…”

Section: Discussionsupporting

confidence: 93%

Biotin attenuation of oxidative stress, mitochondrial dysfunction, lipid metabolism alteration and 7β-hydroxycholesterol-induced cell death in 158N murine oligodendrocytes

Sghaier

Zarrouk

Nury

et al. 2019

Free Radical Research

Self Cite

View full text Add to dashboard Cite

Lizard (2019) Biotin attenuation of oxidative stress, mitochondrial dysfunction, lipid metabolism alteration and 7β-hydroxycholesterol-induced cell death in 158N murine oligodendrocytes, Free Radical Research, 53:5, 535-561, ABSTRACT Mitochondrial dysfunction and oxidative stress are involved in neurodegenerative diseases associated with an enhancement of lipid peroxidation products such as 7b-hydroxycholesterol (7b-OHC). It is, therefore, important to study the ability of 7b-OHC to trigger mitochondrial defects, oxidative stress, metabolic dysfunctions and cell death, which are hallmarks of neurodegeneration, and to identify cytoprotective molecules. The effects of biotin were evaluated on 158N murine oligodendrocytes, which are myelin synthesizing cells, exposed to 7b-OHC (50 mM) with or without biotin (10 and 100 nM) or a-tocopherol (positive control of cytoprotection). The effects of biotin on 7b-OHC activities were determined using different criteria: cell adhesion; plasma membrane integrity; redox status. The impact on mitochondria was characterized by the measurement of transmembrane mitochondrial potential (DWm), reactive oxygen species (ROS) overproduction, mitochondrial mass, quantification of cardiolipins and organic acids. Sterols and fatty acids were also quantified. Cell death (apoptosis, autophagy) was characterized by the enumeration of apoptotic cells, caspase-3 activation, identification of autophagic vesicles, and activation of LC3-I into LC3-II. Biotin attenuates 7b-OHC-induced cytotoxicity: loss of cell adhesion was reduced; antioxidant activities were normalized. ROS overproduction, protein and lipid oxidation products were decreased. Biotin partially restores mitochondrial functions: attenuation of the loss of DWm; reduced levels of mitochondrial O 2 À overproduction; normalization of cardiolipins and organic acid levels. Biotin also normalizes cholesterol and fatty acid synthesis, and prevents apoptosis and autophagy (oxiapoptophagy). Our data support that biotin, which prevents oligodendrocytes damages, could be useful in the treatment of neurodegeneration and demyelination. ARTICLE HISTORY

show abstract

Section: Discussionsupporting

confidence: 93%

Biotin attenuation of oxidative stress, mitochondrial dysfunction, lipid metabolism alteration and 7β-hydroxycholesterol-induced cell death in 158N murine oligodendrocytes

Sghaier

Zarrouk

Nury

et al. 2019

Free Radical Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…In line with these results, is the ability of n-3 PUFAs to decrease superoxide anion production in mouse aorta [38] and human fibroblasts [39]. In addition, DHA has been reported to decrease oxidative stress in vascular [40], nervous [41] and immune [42] systems. All these data demonstrate the antioxidant properties of DHA in situations where oxidative stress is increased.…”

Section: Discussionmentioning

confidence: 71%

Docosahexaenoic Acid Supplemented Diet Influences the Orchidectomy-Induced Vascular Dysfunction in Rat Mesenteric Arteries

et al. 2017

View full text Add to dashboard Cite

Over the past few decades, the cardiovascular benefits of a high dietary intake of long-chain polyunsaturated fatty acids (PUFAs), like docosahexaenoic acid (DHA), have been extensively studied. However, many of the molecular mechanisms and effects exerted by PUFAs have yet to be well explained. The lack of sex hormones alters vascular tone, and we have described that a DHA-supplemented diet to orchidectomized rats improve vascular function of the aorta. Based on these data and since the mesenteric artery importantly controls the systemic vascular resistance, the objective of this study was to analyze the effect of a DHA-supplemented diet on the mesenteric vascular function from orchidectomized rats. For this purpose mesenteric artery segments obtained from control, orchidectomized or orchidectomized plus DHA-supplemented diet were utilized to analyze: (1) the release of prostanoids, (2) formation of NO and ROS, (3) the vasodilator response to acetylcholine (ACh), as well as the involvement of prostanoids and NO in this response, and (4) the vasoconstrictor response to electrical field stimulation (EFS), analyzing also the effect of exogenous noradrenaline (NA), and the NO donor, sodium nitroprusside (SNP). The results demonstrate beneficial effects of DHA on the vascular function in orchidectomized rats, which include a decrease in the prostanoids release and superoxide formation that were previously augmented by orchidectomy. Additionally, there was an increase in endothelial NO formation and the response to ACh, in which NO involvement and the participation of vasodilator prostanoids were increased. DHA also reversed the decrease in EFS-induced response caused by orchidectomy. All of these findings suggest beneficial effects of DHA on vascular function by reversing the neurogenic response and the endothelial dysfunction caused by orchidectomy.

show abstract

“…12, 13 Meanwhile, lipotoxicity may also occur in the CNS, as has been observed in several neurodegenerative diseases. 14, 15 However, there is still not enough evidence to confirm the toxic damage caused by lipids to the CNS and their participation in metabolic complications associated with insulin resistance and type 2 diabetes. Thus, here we will review new evidence, suggesting the role of inflammation in the central nervous system during lipid accumulation on insulin sensitivity leading to metabolic failure.…”

Section: Lipotoxicity Is a Pathogenic Mechanism In Key Organs For Metmentioning

confidence: 99%

Microglia activation due to obesity programs metabolic failure leading to type two diabetes

et al. 2017

View full text Add to dashboard Cite

Obesity is an energy metabolism disorder that increases susceptibility to the development of metabolic diseases. Recently, it has been described that obese subjects have a phenotype of chronic inflammation in organs that are metabolically relevant for glucose homeostasis and energy. Altered expression of immune system molecules such as interleukins IL-1, IL-6, IL-18, tumor necrosis factor alpha (TNF-α), serum amyloid A (SAA), and plasminogen activator inhibitor-1 (PAI-1), among others, has been associated with the development of chronic inflammation in obesity. Chronic inflammation modulates the development of metabolic-related comorbidities like metabolic syndrome (insulin resistance, glucose tolerance, hypertension and hyperlipidemia). Recent evidence suggests that microglia activation in the central nervous system (CNS) is a priority in the deregulation of energy homeostasis and promotes increased glucose levels. This review will cover the most significant advances that explore the molecular signals during microglia activation and inflammatory stage in the brain in the context of obesity, and its influence on the development of metabolic syndrome and type two diabetes.

show abstract

Effects of cholesterol oxides on cell death induction and calcium increase in human neuronal cells (SK-N-BE) and evaluation of the protective effects of docosahexaenoic acid (DHA; C22:6 n-3)

Cited by 36 publications

References 64 publications

Biotin attenuation of oxidative stress, mitochondrial dysfunction, lipid metabolism alteration and 7β-hydroxycholesterol-induced cell death in 158N murine oligodendrocytes

Biotin attenuation of oxidative stress, mitochondrial dysfunction, lipid metabolism alteration and 7β-hydroxycholesterol-induced cell death in 158N murine oligodendrocytes

Docosahexaenoic Acid Supplemented Diet Influences the Orchidectomy-Induced Vascular Dysfunction in Rat Mesenteric Arteries

Microglia activation due to obesity programs metabolic failure leading to type two diabetes

Contact Info

Product

Resources

About