Peroxisomal metabolism and oxidative stress

Nordgren, Marcus; Fransen, Marc

doi:10.1016/j.biochi.2013.07.026

Cited by 155 publications

(123 citation statements)

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“…Their dysfunctions can lead to serious consequences. For instance, mitochondrial alterations can go as far as to activate apoptosis [48], peroxisomal dysfunction affect the mitochondria, subsequently leading to oxidative stress and cell death [49,50], alterations of the lysosome may have consequences on the induction of autophagy and apoptosis [51], endoplasmic reticulum damages can lead to reticulum stress which can trigger different forms of cell death in extreme cases [52], and Golgi apparatus dysfunctions can disturb post-translational modifications and vesicular transport [53]. The incidence of the cytotoxicity of nanoparticles is often addressed in generalized terms such as induction of cell death, oxidative stress stimulation, inflammation activation and genotoxicity.…”

Section: Influence Of Nanoparticles On the Biogenesis And Activity Ofmentioning

confidence: 99%

Toxicological Risk Assessment of Emerging Nanomaterials: Cytotoxicity, Cellular Uptake, Effects on Biogenesis and Cell Organelle Activity, Acute Toxicity and Biodistribution of Oxide Nanoparticles

Maurizi¹,

Papa²,

Boudon³

et al. 2018

Unraveling the Safety Profile of Nanoscale Particles and Materials - From Biomedical to Environmental Applications

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The lack of toxicological data on nanomaterials makes it difficult to assess the risk related to their exposure, and as a result further investigation is required. This chapter presents the synthesis of controlled oxide nanoparticles followed by the evaluation of their safety profile or toxicity (iron, titanium and zinc oxides). The controlled surface chemistry, dispersion in several media, morphology and surface charge of these nanoparticles are presented (transmission electron microscopy, dynamic light scattering, zeta potential, X-ray photoelectron spectroscopy). Classical cytotoxic and cellular uptake studies on different cancer cell lines from liver, prostate, heart, brain and spinal cord are discussed. The incidence of nanoparticles on biogenesis and activity of cell organelles is also highlighted, as well as their biodistribution in animal models. The acute toxicity on zebrafish embryo model is also presented. Finally, the stress is put on the influence and the necessity of controlling the protein corona, a layer of plasma proteins physically adsorbed at the surface of such nanoparticles as a result of their presence in the bloodstream (or relevant biological fluids).

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Section: Influence Of Nanoparticles On the Biogenesis And Activity Ofmentioning

confidence: 99%

Toxicological Risk Assessment of Emerging Nanomaterials: Cytotoxicity, Cellular Uptake, Effects on Biogenesis and Cell Organelle Activity, Acute Toxicity and Biodistribution of Oxide Nanoparticles

Maurizi¹,

Papa²,

Boudon³

et al. 2018

Unraveling the Safety Profile of Nanoscale Particles and Materials - From Biomedical to Environmental Applications

View full text Add to dashboard Cite

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“…It is also known that many if not all of the abiotic stresses, including temperature, hypoxia, osmotic and pH stress, increase the production of reactive oxygen and nitrogen species (ROS and RNS), in part causing damage to macromolecular cellular structures (Halliwell and Gutteridge, 2007). The cellular sources of ROS during stressful and nonstressful conditions depend on the tissue, but generally involve the mitochondria, endoplasmic reticulum (ER) and peroxisome (Csala et al, 2010;Mailloux et al, 2013;Murphy, 2009;Nordgren and Fransen, 2014).…”

Section: Introductionmentioning

confidence: 99%

Proteomic responses to environmentally induced oxidative stress

Tomanek

2015

Journal of Experimental Biology

137

132

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Environmental (acute and chronic temperature, osmotic, hypoxic and pH) stress challenges the cellular redox balance and can lead to the increased production of reactive oxygen species (ROS). This review provides an overview of the reactions producing and scavenging ROS in the mitochondria, endoplasmic reticulum (ER) and peroxisome. It then compares these reactions with the findings of a number of studies investigating the proteomic responses of marine organisms to environmentally induced oxidative stress. These responses indicate that the thioredoxin-peroxiredoxin system is possibly more frequently recruited to scavenge H 2 O 2 than the glutathione system. Isoforms of superoxide dismutase (SOD) are not ubiquitously induced in parallel, suggesting that SOD scavenging activity is sometimes sufficient. The glutathione system plays an important role in some organisms and probably also contributes to protecting protein thiols during environmental stress. Synthesis pathways of cysteine and selenocysteine, building blocks for glutathione and glutathione peroxidase, also play an important role in scavenging ROS during stress. The increased abundance of glutaredoxin and DyP-type peroxidase suggests a need for regulating the deglutathionylation of proteins and scavenging of peroxynitrite. Reducing equivalents for these scavenging reactions are generated by proteins of the pentose phosphate pathway and by NADP-dependent isocitrate dehydrogenase. Furthermore, proteins representing reactions of the tricarboxylic acid cycle and the electron transport system generating NADH and ROS, including those of complex I, II and III, are frequently reduced in abundance with stress. Protein maturation in the ER likely represents another source of ROS during environmental stress, as indicated by simultaneous changes in ER chaperones and antioxidant proteins. Although there are still too few proteomic analyses of non-model organisms exposed to environmental stress for a general pattern to emerge, hyposaline and low pH stress show different responses from temperature and hypoxic stress. Furthermore, comparisons of closely related congeners differing in stress tolerance start to provide insights into biochemical processes contributing to adaptive differences, but more of these comparisons are needed to draw general conclusions. To fully take advantage of a systems approach, studies with longer time courses, including several tissues and more species comparisons are needed.

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“…Furthermore, the evidence suggests that peroxisomal dysfunction is associated not only with rare peroxisomal disorders, but also with more common age-related diseases including neurodegenerative disorders such as Alzheimer s disease 16 , as well as metabolic diseases related to oxidative stress and chronic inflammation 17,18 . Thus, elevated plasma-saturated VLCFAs seem to be an indication of peroxisomal dysfunction as well as a symptom of age-related diseases 19,20 .…”

Section: Introductionmentioning

confidence: 99%