scholarly journals The effect of intrinsic physiological traits on diapause survival and their underlying mechanisms in an annual bee species Bombus impatiens

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Erin Treanore ◽  
Etya Amsalem
Keyword(s):  
Oxidative Stress ◽  
Life Stage ◽  
Mass Gain ◽  
Nutrient Acquisition ◽  
Bombus Impatiens ◽  
Factors Affecting ◽  
Age Related ◽  
The Face ◽  
Underlying Mechanisms ◽  
Age Range

Abstract In the face of insect declines, identifying phases of the life cycle when insects are particularly vulnerable to mortality is critical to conservation efforts. For numerous annual insect groups, diapause is both a key adaptation that allows survival of inhospitable conditions and a physiologically demanding life stage that can result in high rates of mortality. As bees continue to garner attention as a group experiencing high rates of decline, improving our understanding of how annual bees prepare for diapause and identifying factors that reduce survival is imperative. Here, we studied factors affecting diapause survival length and their underlying mechanisms using an economically and ecologically important annual bee species, Bombus impatiens. We examined how age and mass upon diapause onset correlate with diapause survival length, and the mechanistic role of nutrient acquisition and oxidative stress post pupal eclosion in mediating these effects. Our findings show that both age and mass were strong predictors of diapause survival length. Heavier queens or queens in the age range of ~6–17 days survived longer in diapause. Mass gain was attributed to increases in lipid, protein and glycerol amounts following pupal eclosion, and the ability to deal with oxidative stress was significantly compromised in older pre-diapause queens. Our results demonstrate that age-related shifts in bee physiology and timing of nutrient acquisition may both be critical factors driving diapause survival.

scholarly journals Epigallocatechin gallate prevents senescence by alleviating oxidative stress and inflammation in WI-38 human embryonic fibroblasts

RSC Advances ◽  
2019 ◽  
Vol 9 (46) ◽  
pp. 26787-26798 ◽  
Author(s):  
Qiao Zhang ◽  
Yuqing Wu ◽  
Yue Guan ◽  
Fan Ling ◽  
Ying Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aging Process ◽  
Epigallocatechin Gallate ◽  
Embryonic Fibroblasts ◽  
Age Related ◽  
Underlying Mechanisms ◽  
Human Embryonic Fibroblasts

Increased levels of oxidative stress and inflammation are the underlying mechanisms behind the aging process and age-related diseases.

scholarly journals Carotenoids: How Effective Are They to Prevent Age-Related Diseases?

Molecules ◽  
2019 ◽  
Vol 24 (9) ◽  
pp. 1801 ◽  
Author(s):  
Bee Ling Tan ◽  
Mohd Esa Norhaizan
Keyword(s):  
Oxidative Stress ◽  
Healthy Aging ◽  
The Elderly ◽  
Antioxidant Systems ◽  
Potential Intervention ◽  
Healthy Longevity ◽  
Age Related ◽  
Underlying Mechanisms ◽  
Endogenous Antioxidant

Despite an increase in life expectancy that indicates positive human development, a new challenge is arising. Aging is positively associated with biological and cognitive degeneration, for instance cognitive decline, psychological impairment, and physical frailty. The elderly population is prone to oxidative stress due to the inefficiency of their endogenous antioxidant systems. As many studies showed an inverse relationship between carotenoids and age-related diseases (ARD) by reducing oxidative stress through interrupting the propagation of free radicals, carotenoid has been foreseen as a potential intervention for age-associated pathologies. Therefore, the role of carotenoids that counteract oxidative stress and promote healthy aging is worthy of further discussion. In this review, we discussed the underlying mechanisms of carotenoids involved in the prevention of ARD. Collectively, understanding the role of carotenoids in ARD would provide insights into a potential intervention that may affect the aging process, and subsequently promote healthy longevity.

Calorie Restriction and Aging

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. SCI-2-SCI-2
Author(s):  
Rafael de Cabo
Keyword(s):  
Oxidative Stress ◽  
Life Span ◽  
Calorie Restriction ◽  
Stress Proteins ◽  
Conflicts Of Interest ◽  
Caloric Intake ◽  
Tissue Growth ◽  
Age Related ◽  
Underlying Mechanisms ◽  
And Oxidative Stress

Abstract Abstract SCI-2 A prominent manifestation of aging is a reduced ability to respond to environmental stressors, including heat and oxidative stress. Reduced stress tolerance and decreased ability to maintain homeostasis are at least partially responsible for the increased morbidity and mortality that occurs with advancing age. The age-related attenuation of stress pathways and increased expression of stress-response genes with aging are examples of the growing body of evidence linking reduced stress responsiveness to aging. In 1935, McCay and colleagues first reported that reducing the caloric intake of rodents could significantly lengthen their mean and maximal life span, slowing down basic aging processes. The effect of calorie restriction (CR) on delaying aging has been replicated in many animal species including nonhuman primates, although in these, potential life span alterations cannot be ascertained for several more years due to their longevity CR causes a reduction in body weight, tissue growth, blood glucose, insulin levels and body temperature. In addition, CR prevents the age-related decline in tolerance to different stressors such as oxidative and heat, and the age-related reduction in expression of protective heat shock and oxidative stress proteins. While CR is the only intervention that has consistently been shown to increase maximum life span and prevent or delay the onset of age-associated pathophysiological changes in laboratory rodents, the underlying mechanisms remain elusive. Using calorie restriction (CR) as their benchmark research tool, gerontologists are making progress in identifying dietary and pharmacologic interventions that may be applicable to retarding aging processes in humans. Disclosures: No relevant conflicts of interest to declare.

scholarly journals MEF2D haploinsufficiency downregulates the NRF2 pathway and renders photoreceptors susceptible to light-induced oxidative stress

2017 ◽  
Vol 114 (20) ◽  
pp. E4048-E4056 ◽  
Author(s):  
Saumya Nagar ◽  
Sarah M. Noveral ◽  
Dorit Trudler ◽  
Kevin M. Lopez ◽  
Scott R. McKercher ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Age Related Macular Degeneration ◽  
Mouse Retina ◽  
Nrf2 Pathway ◽  
Multifactorial Diseases ◽  
Downstream Target ◽  
Age Related ◽  
The Face ◽  
Genetic And Environmental Factors

Gaining mechanistic insight into interaction between causative factors of complex multifactorial diseases involving photoreceptor damage might aid in devising effective therapies. Oxidative stress is one of the potential unifying mechanisms for interplay between genetic and environmental factors that contribute to photoreceptor pathology. Interestingly, the transcription factor myocyte enhancer factor 2d (MEF2D) is known to be important in photoreceptor survival, as knockout of this transcription factor results in loss of photoreceptors in mice. Here, using a mild light-induced retinal degeneration model, we show that the diminished MEF2D transcriptional activity in Mef2d+/− retina is further reduced under photostimulation-induced oxidative stress. Reactive oxygen species cause an aberrant redox modification on MEF2D, consequently inhibiting transcription of its downstream target, nuclear factor (erythroid-derived 2)-like 2 (NRF2). NRF2 is a master regulator of phase II antiinflammatory and antioxidant gene expression. In the Mef2d heterozygous mouse retina, NRF2 is not up-regulated to a normal degree in the face of light-induced oxidative stress, contributing to accelerated photoreceptor cell death. Furthermore, to combat this injury, we found that activation of the endogenous NRF2 pathway using proelectrophilic drugs rescues photoreceptors from photo-induced oxidative stress and may therefore represent a viable treatment for oxidative stress-induced photoreceptor degeneration, which is thought to contribute to some forms of retinitis pigmentosa and age-related macular degeneration.

scholarly journals H2O2 downregulate SIRT7`s protective role of endothelial premature dysfunction via microRNA-335-5p

2022 ◽  
Author(s):  
Yixin Liu ◽  
Jinyu Yang ◽  
Xi Yang ◽  
Peng Lai ◽  
Yi Mou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Protective Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Contributing Factors ◽  
Age Related ◽  
Underlying Mechanisms ◽  
Umbilical Vein Endothelial Cells

Endothelial senescence is believed to constitute the initial pathogenesis of the atherosclerotic cardiovascular disease (ASCVD). MicroRNA-335-5p (miR-335-5p) expression is significantly upregulated in oxidative stress-induced endothelial cells (ECs). Sirtuin7 (SIRT7) is considered to prevent EC senescence, yet data on its response to ASCVD risk factors are limited. This study analyzed the elevated levels of miR-335-5p and the decreased levels of SIRT7 in human umbilical vein endothelial cells (HUVECs) , and found that high glucose, tumour necrosis factor-α (TNF-α), and H2O2 are the three contributing factors that induced cellular senescence. The current study also assessed premature endothelial senescence and decreased proliferation, adhesion, migration, and nitric oxide secretion in HUVECs with these risk factors together with SIRT7-siRNA transfection. It found that the miR-335-5p inhibitor attenuated the downregulation of SIRT7 expression induced by oxidative stress in HUVECs, and SIRT7 overexpression exerts a rescue effect against miR-335-5p induced endothelial dysfunction. Furthermore, the direct binding of miR-335-5p to SIRT7 was observed in HEK-293T. Therefore, it can be inferred that miR-335-5p downregulates the expression of SIRT7 in human cells. Current findings may provide deeper insights into the underlying mechanisms of endothelial senescence and potential therapeutic targets of ASCVD as well as other age-related diseases.

Age Effects on the Perception of Motion Illusions

Perception ◽  
10.1068/p5886 ◽  
2009 ◽  
Vol 38 (4) ◽  
pp. 508-521 ◽  
Author(s):  
Jutta Billino ◽  
Kai Hamburger ◽  
Karl R Gegenfurtner
Keyword(s):  
Age Effects ◽  
The Other ◽  
Illusory Effect ◽  
Illusory Motion ◽  
Age Related ◽  
Lower Likelihood ◽  
Underlying Mechanisms ◽  
Age Range ◽  
Processing Mechanisms ◽  
Effect Of Age

Anomalous motion illusions represent a popular class of illusions and several studies have made an effort to explain their perception. However, understanding is still inconsistent. Age-related differences in susceptibility to illusory motion may contribute to further clarification of the underlying processing mechanisms. We investigated the effect of age on the perception of four different anomalous motion illusions. The Enigma illusion, the Rotating-Snakes illusion, the Pinna illusion, and the Rotating-Tilted-Lines illusion were tested on a total of one hundred and thirty-nine participants covering an age range from 3 to 82 years. In comparison with young adults, children showed a lower likelihood of perceiving motion in all illusions with the exception of the Rotating-Tilted-Lines illusion. For adult subjects, we found significant age effects in the Rotating-Snakes illusion and the Rotating-Tilted-Lines illusion: occurrence of the illusory effect decreased with age. The other two illusions turned out to be unaffected by aging. Finally, inter-correlations between different motion illusions revealed that only the Pinna illusion and the Rotating-Tilted-Lines illusion correlated significantly with each other. The results confirm that anomalous motion illusions should not be considered as a homogeneous group. Possible links between perceptual data and neurophysiological changes related to age are discussed. Perceptual differences due to age provide the opportunity to improve our understanding of illusory motion and point to specific underlying mechanisms.

scholarly journals Factors Influencing the Accuracy of Age Estimates of Unfamiliar Faces

Perception ◽  
1995 ◽  
Vol 24 (9) ◽  
pp. 1059-1073 ◽  
Author(s):  
Patricia A George ◽  
Graham J Hole
Keyword(s):  
Single Type ◽  
Factors Affecting ◽  
Old Adults ◽  
Factors Influencing ◽  
Mirror Reversal ◽  
The Face ◽  
Necessary And Sufficient ◽  
Age Range ◽  
Unfamiliar Faces ◽  
Age Estimates

Factors affecting the accuracy with which adults could assess the age of unfamiliar male faces aged between 5 and 70 years were examined. In the first experiment twenty-five ‘young’ adult subjects, aged 16–25, and twenty-five ‘old’ adults, aged 51–60, were used. Each subject saw five versions of three different faces: these consisted of an original version of each face and four manipulated versions of it. The manipulations consisted of mirror reversal, pseudo-cardioidal strain, thresholding, and elimination of all but the internal features of the face. The second experiment was similar except that a between-subjects design was used: each subject saw three faces for each age category of target face, but was exposed to only a single type of manipulation (plus a set of ‘original’ faces which were identical for all groups, so that the comparability of the different groups in age estimation could be checked). Results from both experiments were similar. Age estimates for unmanipulated ‘original’ faces were highly accurate, although subjects were most accurate with target faces that were within their own age range. Results for the manipulated faces implied that the importance of cardioidal strain as a necessary and sufficient cue to age may have been overestimated in previous reports: subjects' age estimates were accurate when cardioidal strain was absent from the stimulus, and poor when cardioidal strain was the only cue available.

Oxidative stress and aging – the use of superoxide dismutase/catalase mimetics to extend lifespan

2003 ◽  
Vol 31 (6) ◽  
pp. 1305-1307 ◽  
Author(s):  
J.N. Sampayo ◽  
M.S. Gill ◽  
G.J. Lithgow
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Pharmacological Intervention ◽  
Protective Effects ◽  
C Elegans ◽  
Compound Libraries ◽  
Novel Drugs ◽  
The Face ◽  
Underlying Mechanisms ◽  
High Throughput Screens

To date, more than 40 genes have been identified in the nematode Caenorhabditis elegans, which, when mutated, lead to an increase in lifespan. Of those tested, all confer an increased resistance to oxidative stress. In addition, the lifespan of C. elegans can also be extended by the administration of synthetic superoxide dismutase/catalase mimetics. These compounds also appear to confer resistance to oxidative damage, since they protect against paraquat treatment. The protective effects of these compounds are apparent with treatment during either development or adulthood. These findings have demonstrated that pharmacological intervention in the aging process is possible and that these compounds can provide important information about the underlying mechanisms. To date, such interventions have targeted known processes rather than screening compound libraries because of the limitations of assessing lifespan in nematodes. However, we have recently developed a microplate-based assay that allows for a rapid and objective score of nematode survival at rates many times higher than previously possible. This system now provides the opportunity to perform high-throughput screens for compounds that affect nematode survival in the face of acute oxidative stress and will facilitate the identification of novel drugs that extend nematode lifespan.

Progressive Energy Dissipations of Human Cortical Bone in Compression

2008 ◽  
Author(s):  
Huijie Leng ◽  
Xuanliang Dong ◽  
Xiaodu Wang
Keyword(s):  
Energy Dissipation ◽  
Cortical Bone ◽  
Bone Quality ◽  
Bone Fracture ◽  
Maximum Stress ◽  
Factors Affecting ◽  
Age Related ◽  
Significant Burden ◽  
Underlying Mechanisms ◽  
Loading Modes

Bone fracture has imposed a significant burden on the health of society. The “bone quality” is used to refer to factors affecting bone fracture risk [1]. Energy dissipation till fracture, known as toughness, is a major measure of bone quality [2]. However, underlying mechanisms of energy dissipation in bone is still not clear. It has been well documented that the post-yield behavior of bone determines the major part of the toughness of bone [3, 4]. Therefore, it is important to study post-yield behaviors of human bone, especially the different pathways for energy dissipation, in order to better understand how age-related change affects bone quality. Bone behaves differently under different loading modes [5]. Different from loading in tension, after reaching the maximum stress, cortical bone in compression can continue to bear load till large deformation without brittle failure and dramatic reduction in elastic modulus [5, 6]. However, few studies of progression of post-yield behaviors of cortical bone in compression were reported in the literature.

scholarly journals Aging Leads to Elevation of O-GlcNAcylation and Disruption of Mitochondrial Homeostasis in Retina

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Lin Zhao ◽  
Zhihui Feng ◽  
Xuan Zou ◽  
Ke Cao ◽  
Jie Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxygen Consumption ◽  
Mapk Signaling ◽  
Sprague Dawley ◽  
Atp Production ◽  
Mitochondrial Homeostasis ◽  
Age Related ◽  
Chain Complexes ◽  
Effective Therapeutic Strategy ◽  
Underlying Mechanisms

Retina is particularly susceptible to aging as oxidative damage accumulates within retina, leading to age-related retinal dysfunction or even visual loss. However, the underlying mechanisms still remain obscure and effective therapeutic strategy is urgently in need. Here, we quested for the answer particularly focusing on mitochondrial homeostasis and O-GlcNAcylation in rat retina. By comparing expression of electron transfer chain complexes and key factors in mitochondrial biogenesis and dynamics in retinas of aged and young Sprague-Dawley rats, we found that mitochondrial Complex I, II, IV and V were increased in aged retina with decreased mtTFA and Mfn2. Also, we noticed that p38 and JNK of MAPK signaling were substantially more activated in aged retina, suggesting stress induction. In addition, we found that pan-O-GlcNAcylation was remarkably stronger with lower OGA expression in aged retina. To further elucidate the roles of Mfn2 and O-GlcNAcylation, we employed ARPE-19 cells and found that ATP production, oxygen consumption, and mitochondrial membrane potential were reduced and ROS level was increased by Mfn2 knockdown, while treating with PUGNAc or UDP-GlcNAc heightened oxygen consumption and reduced ROS. Our results suggest disrupted mitochondrial homeostasis may increase oxidative stress; yet enhanced O-GlcNAcylation might defend against oxidative stress and promote mitochondrial respiration in aged retina.

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