Reactive Oxygen Species and Male Fertility: The Physiological Role

2017 ◽  
pp. 445-454
Keyword(s):  
Reactive Oxygen Species ◽  
Male Fertility ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Interaction of Oxidative Stress and Misfolded Proteins in the Mechanism of Neurodegeneration

Life ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 101 ◽  
Author(s):  
Andrey Y. Abramov ◽  
Elena V. Potapova ◽  
Viktor V. Dremin ◽  
Andrey V. Dunaev
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Neurodegenerative Disorders ◽  
Structural Changes ◽  
Wide Spectrum ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Misfolded Proteins ◽  
Oxygen Species

Aggregation of the misfolded proteins β-amyloid, tau, huntingtin, and α-synuclein is one of the most important steps in the pathology underlying a wide spectrum of neurodegenerative disorders, including the two most common ones—Alzheimer’s and Parkinson’s disease. Activity and toxicity of these proteins depends on the stage and form of aggregates. Excessive production of free radicals, including reactive oxygen species which lead to oxidative stress, is proven to be involved in the mechanism of pathology in most of neurodegenerative disorders. Both reactive oxygen species and misfolded proteins play a physiological role in the brain, and only deregulation in redox state and aggregation of the proteins leads to pathology. Here, we review the role of misfolded proteins in the activation of ROS production from various sources in neurons and glia. We discuss if free radicals can influence structural changes of the key toxic intermediates and describe the putative mechanisms by which oxidative stress and oligomers may cause neuronal death.

scholarly journals Reactive Oxygen Species Regulate Activity-Dependent Neuronal Structural Plasticity in Drosophila

2016 ◽  
Author(s):  
Matthew C. W. Oswald ◽  
Paul S. Brooks ◽  
Maarten F. Zwart ◽  
Amrita Mukherjee ◽  
Ryan J. H. West ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Structural Changes ◽  
Second Messengers ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Structural Plasticity ◽  
Activity Level ◽  
Oxygen Species ◽  
Network Output ◽  
Activity Dependent

AbstractNeurons are inherently plastic, adjusting their structure, connectivity and excitability in response to changes in activity. How neurons sense changes in their activity level and then transduce these to structural changes remains to be fully elucidated. Working with the Drosophila larval locomotor network, we show that neurons use reactive oxygen species (ROS), metabolic byproducts, to monitor their activity. ROS signals are both necessary and sufficient for activity-dependent structural adjustments of both pre- and postsynaptic terminals and for network output, as measured by larval crawling behavior. We find the highly conserved Parkinson’s disease-linked protein DJ-1ß acts as a redox sensor in neurons where it regulates pre- and postsynaptic structural plasticity, in part via modulation of the PTEN-PI3Kinase pathway. Neuronal ROS thus play an important physiological role as second messengers required for neuronal and network tuning, whose dysregulation in the ageing brain and under neurodegenerative conditions may contribute to synaptic dysfunction.

scholarly journals Reactive Oxygen Species and Male Fertility

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 287 ◽  
Author(s):  
Cristian O’Flaherty
Keyword(s):  
Reactive Oxygen Species ◽  
Male Fertility ◽  
Reactive Oxygen ◽  
Oxygen Species

Human infertility affects ~15% of couples worldwide, and it is now recognized that in half of these cases, the causes of infertility can be traced to men [...]

Functions and effects of reactive oxygen species in male fertility

2020 ◽  
Vol 220 ◽  
pp. 106456
Author(s):  
Zamira Gibb ◽  
Róisín Ann Griffin ◽  
Robert John Aitken ◽  
Geoffry Nunzio De Iuliis
Keyword(s):  
Reactive Oxygen Species ◽  
Male Fertility ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Reactive oxygen species induce chondrocyte hypertrophy in endochondral ossification

2007 ◽  
Vol 204 (7) ◽  
pp. 1613-1623 ◽  
Author(s):  
Kozo Morita ◽  
Takeshi Miyamoto ◽  
Nobuyuki Fujita ◽  
Yoshiaki Kubota ◽  
Keisuke Ito ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endochondral Ossification ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Hypertrophic Chondrocytes ◽  
Cellular Damage ◽  
Oxygen Species ◽  
Chondrocyte Hypertrophy ◽  
Inhibition Of Proliferation

Chondrocyte hypertrophy during endochondral ossification is a well-controlled process in which proliferating chondrocytes stop proliferating and differentiate into hypertrophic chondrocytes, which then undergo apoptosis. Chondrocyte hypertrophy induces angiogenesis and mineralization. This step is crucial for the longitudinal growth and development of long bones, but what triggers the process is unknown. Reactive oxygen species (ROS) have been implicated in cellular damage; however, the physiological role of ROS in chondrogenesis is not well characterized. We demonstrate that increasing ROS levels induce chondrocyte hypertrophy. Elevated ROS levels are detected in hypertrophic chondrocytes. In vivo and in vitro treatment with N-acetyl cysteine, which enhances endogenous antioxidant levels and protects cells from oxidative stress, inhibits chondrocyte hypertrophy. In ataxia telangiectasia mutated (Atm)–deficient (Atm−/−) mice, ROS levels were elevated in chondrocytes of growth plates, accompanied by a proliferation defect and stimulation of chondrocyte hypertrophy. Decreased proliferation and excessive hypertrophy in Atm−/− mice were also rescued by antioxidant treatment. These findings indicate that ROS levels regulate inhibition of proliferation and modulate initiation of the hypertrophic changes in chondrocytes.

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