scholarly journals Vascular Ageing and Exercise: Focus on Cellular Reparative Processes

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Mark D. Ross ◽  
Eva Malone ◽  
Geraint Florida-James
Keyword(s):  
Oxidative Stress ◽  
Prolonged Exposure ◽  
The Body ◽  
Noncommunicable Diseases ◽  
Regular Exercise ◽  
Vascular Ageing ◽  
Increased Risk ◽  
And Function ◽  
Endothelial Homeostasis ◽  
Endothelial Precursors

Ageing is associated with an increased risk of developing noncommunicable diseases (NCDs), such as diabetes and cardiovascular disease (CVD). The increased risk can be attributable to increased prolonged exposure to oxidative stress. Often, CVD is preceded by endothelial dysfunction, which carries with it a proatherothrombotic phenotype. Endothelial senescence and reduced production and release of nitric oxide (NO) are associated with “vascular ageing” and are often accompanied by a reduced ability for the body to repair vascular damage, termed “reendothelialization.” Exercise has been repeatedly shown to confer protection against CVD and diabetes risk and incidence. Regular exercise promotes endothelial function and can prevent endothelial senescence, often through a reduction in oxidative stress. Recently, endothelial precursors, endothelial progenitor cells (EPC), have been shown to repair damaged endothelium, and reduced circulating number and/or function of these cells is associated with ageing. Exercise can modulate both number and function of these cells to promote endothelial homeostasis. In this review we look at the effects of advancing age on the endothelium and these endothelial precursors and how exercise appears to offset this “vascular ageing” process.

scholarly journals The Possible Role of Bifidobacterium longum BB536 and Lactobacillus rhamnosus HN001 on Locomotor Activity and Oxidative Stress in a Rotenone-Induced Zebrafish Model of Parkinson’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Ovidiu-Dumitru Ilie ◽  
Emanuela Paduraru ◽  
Madalina-Andreea Robea ◽  
Ioana-Miruna Balmus ◽  
Roxana Jijie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Locomotor Activity ◽  
Prolonged Exposure ◽  
Bifidobacterium Longum ◽  
The Body ◽  
The Other ◽  
Control Group

Background. As every organ within the body, the brain is also extremely susceptible to a plethora of noxious agents that change its chemistry. One component frequently found in current products against harmful species to crops is rotenone whose effect under prolonged exposure has been demonstrated to cause neurodegenerative disorders such as Parkinson’s disease. The latest reports have indeed revealed that rotenone promotes Parkinson’s in humans, but studies aiming to show congruent effects in zebrafish (Danio rerio) are lacking. Material and Methods. In this context, the aim of the present study was to demonstrate how chronic administration of rotenone for 3 weeks impairs the locomotor activity and sociability and induces oxidative stress in zebrafish. Results. There were no statistically significant differences following the analysis of their social interaction and locomotor tests ( p > 0.05 ). However, several exceptions have been noted in the control, rotenone, and probiotics groups when we compared their locomotor activity during the pretreatment and treatment interval ( p < 0.05 ). We further assessed the role of rotenone in disturbing the detoxifying system as represented by three enzymes known as superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA). Despite the fact that there were no statistically significant changes within SOD and GPx levels between the control group and rotenone, probiotics, and rotenone + probiotics ( p > 0.05 ), relevant changes have been observed between the analyzed groups ( p < 0.05 and p < 0.005 , respectively). On the other hand, significant differences ( p < 0.05 ) have been observed for MDA when we analyzed the data between the control group and the other three groups. Conclusions. Our results suggest that rotenone can be successfully used to trigger Parkinson’s disease-related symptomatology in zebrafish.

The effects of endometritis on the establishment of pregnancy in cattle

2012 ◽  
Vol 24 (1) ◽  
pp. 252 ◽  
Author(s):  
Robert O. Gilbert
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Inflammatory Mediators ◽  
Post Partum ◽  
Blastocyst Stage ◽  
Preimplantation Embryos ◽  
Breeding Period ◽  
Increased Risk ◽  
Factor Α ◽  
And Function

Endometritis is common in post partum dairy cows and is associated with impaired reproductive performance reflected in reduced first service conception, reduced hazard of pregnancy over the breeding period and increased risk of reproductive culling. The observed effects may be mediated directly by bacterial products, such as lipopolysaccharide (LPS, endotoxin), or indirectly by inflammatory mediators, such as cytokines, eicosanoids, nitric oxide and oxidative stress affecting sperm, ovarian, uterine and embryonic function. An inflammatory milieu in the uterus has been associated with changes in sperm motility and function as well as increased sperm phagocytosis. Zygotes resulting from fertilisation of oocytes with sperm subjected to oxidative stress are less likely to develop to the blastocyst stage. In addition, LPS and tumour necrosis factor-α (TNFα) impair follicular steroidogenesis, growth and ovulation. Oocytes exposed to LPS or prostaglandin (PG) F2α during maturation are less likely to develop to blastocyst stage after fertilisation. Embryos exposed to inflammatory mediators during development have fewer trophoectoderm cells. Nitric oxide impairs development of preimplantation embryos and TNFα increases blastomere apoptosis. Endometritis in women has been associated with higher rates of implantation failure. Extragenital inflammation (e.g. mastitis) is also associated with an increased rate of embryonic loss in cattle. These observations make it clear that direct and indirect effects of endometritis, and inflammation in general, can interrupt successful reproduction at several crucial stages.

scholarly journals Effects of Exercise-Induced ROS on the Pathophysiological Functions of Skeletal Muscle

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Fan Wang ◽  
Xin Wang ◽  
Yiping Liu ◽  
Zhenghong Zhang
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Acute Exercise ◽  
Redox System ◽  
The Body ◽  
Muscle Adaptation ◽  
Exercise Induced ◽  
And Function ◽  
Stress Fatigue

Oxidative stress is the imbalance of the redox system in the body, which produces excessive reactive oxygen species, leads to multiple cellular damages, and closely relates to some pathological conditions, such as insulin resistance and inflammation. Meanwhile, exercise as an external stimulus of oxidative stress causes the changes of pathophysiological functions in the tissues and organs, including skeletal muscle. Exercise-induced oxidative stress is considered to have different effects on the structure and function of skeletal muscle. Long-term regular or moderate exercise-induced oxidative stress is closely related to the formation of muscle adaptation, while excessive free radicals produced by strenuous or acute exercise can cause muscle oxidative stress fatigue and damage, which impacts exercise capacity and damages the body’s health. The present review systematically summarizes the relationship between exercise-induced oxidative stress and the adaptions, damage, and fatigue in skeletal muscle, in order to clarify the effects of exercise-induced oxidative stress on the pathophysiological functions of skeletal muscle.

scholarly journals Curcumin ameliorates atrophy of seminal vesicle via reduction of oxidative stress in castrated mice

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7192 ◽  
Author(s):  
Rui Li ◽  
Hao Li ◽  
Ke Rao ◽  
Kang Liu ◽  
Yan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Seminal Vesicle ◽  
Serum Testosterone ◽  
The Body ◽  
Intragastric Administration ◽  
Curcumin Treatment ◽  
Seminal Vesicle Weight ◽  
High Level ◽  
And Function

Background The growth and function of seminal vesicle are dependent on androgen. This study was conducted to investigate the role of oxidative stress in castration-induced seminal vesicle atrophy and to explore the effects of curcumin, an antioxidant extracted from rhizome of turmeric, on seminal vesicle of castrated mice. Methods C57BL/6J mice were randomly divided into three groups: control, castration, and castration with curcumin (n = 10 for each group). After surgical castration, mice in the curcumin treatment group received intragastric administration of curcumin at 100 mg/kg body weight for 4 weeks, whereas mice in the other two groups were treated with olive oil. After that, the body weight, seminal vesicle weight and serum testosterone of mice were measured. Apoptosis and oxidative stress levels in seminal vesicle were also determined. Results After castration, both the weight and size of seminal vesicle decreased dramatically. The expression of three NADPH oxidase (NOX) subtypes: NOX1, NOX2 and NOX4, increased in seminal vesicle of castrated mice, resulting in high level oxidative stress. The ratio of Bax to Bcl-2 was also elevated after castration, accompanied by enhanced caspase3 activity. Additionally, castration increased the number of apoptotic cells in seminal vesicle. Curcumin treatment could inhibit the expression of NOX1, NOX2 and NOX4, decreasing oxidative stress and apoptosis. The atrophy of seminal vesicle caused by castration was ameliorated by curcumin. Conclusion Castration could cause atrophy of seminal vesicle probably via inducing oxidative stress. Curcumin treatment could reduce the oxidative stress in seminal vesicle by decreasing the expression of NOX1, NOX2 and NOX4, thereby ameliorating apoptosis and atrophy of seminal vesicle. Oxidative stress might play a role in castration-induced seminal vesicle atrophy.

scholarly journals Coronavirus Disease-19 Pandemic and Dermatology. What to Expect?

2020 ◽  
Vol 8 (T1) ◽  
pp. 290-293
Author(s):  
Vesna Brishkoska-Boshkovski ◽  
Mirela Vasileva ◽  
Irena Dimitrovska ◽  
Vesna Grivcheva-Panovska
Keyword(s):  
Prolonged Exposure ◽  
Skin Diseases ◽  
Human Life ◽  
Well Being ◽  
Chronic Fatigue ◽  
The Body ◽  
Stressful Situation ◽  
Psychological Consequences ◽  
Increased Risk ◽  
Novel Coronavirus

The novel coronavirus (CoV), CoV disease (COVID)-19, and the ongoing pandemic, is changing every aspect of the human life. Furthermore, the COVID-19 pandemic has a profound impact on health-care worldwide, with no exception in dermatology care units. At the time of pandemic, constant fear and stress are present on the surface. Skin diseases are the most common somatic causes of psychological disorders and, conversely. During a stressful situation, the body has power to adjust and to maintain its well-being, but with prolonged exposure to stress, the first negative changes such as fear, anxiety, and depression will eventually lead to chronic fatigue and an increased risk of disease. The proportion of patients reporting emotional triggers varies with the disease, ranging from approximately 50% in acne to 90% in rosacea, alopecia areata, psoriasis, neurotic excoriations, and lichen simplex and may be 100% for patients with hyperhidrosis. In this paper, we will look at the most common psychodermatological disorders and its implication in the era of COVID-19 pandemic. According to all the pathophysiological conditions that indicate the association of skin diseases with stress, it is normal to expect their deterioration and occurrence in this pandemic period. We will be witnessing a growing number in patients’ consultations with chronic urticaria, dermographism, worsening rosacea, generalization, and relapses of psoriasis. It is needed to be prepared for as many cases as possible, because the psychological consequences will still be felt. We encourage more comprehensive studies of the implications of the COVID-19 pandemic in these patients.

scholarly journals Developmental programming of offspring adipose tissue biology and obesity risk

2021 ◽  
Author(s):  
Amanda Rodgers ◽  
Amanda N. Sferruzzi-Perri
Keyword(s):  
Adipose Tissue ◽  
Environmental Factors ◽  
Low Income ◽  
Subsequent Development ◽  
The Body ◽  
Low Income Countries ◽  
Noncommunicable Diseases ◽  
Sexually Dimorphic ◽  
Tissue Biology ◽  
And Function

AbstractObesity is reaching epidemic proportions and imposes major negative health crises and an economic burden in both high and low income countries. The multifaceted nature of obesity represents a major health challenge, with obesity affecting a variety of different organs and increases the risk of many other noncommunicable diseases, such as type 2 diabetes, fatty liver disease, dementia, cardiovascular diseases, and even cancer. The defining organ of obesity is the adipose tissue, highlighting the need to more comprehensively understand the development and biology of this tissue to understand the pathogenesis of obesity. Adipose tissue is a miscellaneous and highly plastic endocrine organ. It comes in many different sizes and shades and is distributed throughout many different locations in the body. Though its development begins prenatally, quite uniquely, it has the capacity for unlimited growth throughout adulthood. Adipose tissue is also a highly sexually dimorphic tissue, patterning men and women in different ways, which means the risks associated with obesity are also sexually dimorphic. Recent studies show that environmental factors during prenatal and early stages of postnatal development have the capacity to programme the structure and function of adipose tissue, with implications for the development of obesity. This review summarizes the evidence for a role for early environmental factors, such as maternal malnutrition, hypoxia, and exposure to excess hormones and endocrine disruptors during gestation in the programming of adipose tissue and obesity in the offspring. We will also discuss the complexity of studying adipose tissue biology and the importance of appreciating nuances in adipose tissue, such as sexual dimorphism and divergent responses to metabolic and endocrine stimuli. Given the rising levels of obesity worldwide, understanding how environmental conditions in early life affects adipose tissue phenotype and the subsequent development of obesity is of absolute importance.

scholarly journals Disparities in Obesity Prevalence in Iranian Adults: Cross-Sectional Study Using Data from the 2016 STEPS Survey

Obesity Facts ◽  
2021 ◽  
pp. 1-8
Author(s):  
Rozhin Amin ◽  
Ali-Asghar Kolahi ◽  
Mohammad-Reza Sohrabi
Keyword(s):  
Concentration Index ◽  
System Analysis ◽  
Sociodemographic Factors ◽  
Cross Sectional Study ◽  
The Body ◽  
Noncommunicable Diseases ◽  
Obesity Prevalence ◽  
Cross Sectional ◽  
Increased Risk ◽  
Steps Survey

<b><i>Introduction:</i></b> This paper outlines the prevalence, disparities, and social determinants of preobesity and obesity in Iranian adults. <b><i>Methods:</i></b> Data on 28,321 adults who participated in the 2016 National Survey of the Risk Factors of Noncommunicable Diseases (STEPS) survey were analyzed. The body mass index (BMI) was calculated from physically measured height and weight. To assess the association between sociodemographic factors and the prevalence of preobesity and obesity, a χ<sup>2</sup> test and a logistic regression model were used. Socioeconomic inequality was quantified by a concentration index. Disparities in provincial mean BMI and concentration indices were shown on the map of Iran using geographic information system analysis. <b><i>Results:</i></b> Overall, 60.3% of the participants were affected by preobesity or obesity. The preobesity prevalence was 39% in men and 35.2% in women. The obesity prevalence was 15.6% in men and 30.4% in women. The mean BMI for the country was 26.5. Higher ranges were observed across the northwestern and central territories. Female individuals in the age group 48–57 years who were married and lived in urban settings had an increased risk of being preobese or obese. The concentration index revealed a prorich inequality, with a greater magnitude among women. <b><i>Conclusion:</i></b> The findings suggest that policies aimed at reducing preobesity and obesity should remain a public health priority in Iran. However, a greater emphasis should be placed on the northwestern and central territories and on higher socioeconomic groups.

scholarly journals Profile Of Oxidative Stress Genes In Response To Obesity Treatment

2021 ◽  
Author(s):  
Amira Ahmed ◽  
Huda Farah ◽  
Omnia Ahmed ◽  
Dina Elsayegh ◽  
Abdelrahman Elgamal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Body Weight ◽  
Skeletal Muscles ◽  
Bioactive Compound ◽  
Treated Group ◽  
The Body ◽  
Tissue Samples ◽  
Increased Risk ◽  
The Impact

Background: Oxidative stress (OS) is an imbalance between free radical production and the antioxidants defense in the body. Previous studies demonstrated the correlation of OS to the increased risk of developing metabolic disorders such as obesity. Sulforaphane (SFN), a bioactive compound, can protect against inflammation and OS, thus an effective anti-obesity supplement. Aim: This study explores the impact of SNF on OS in diet induced obese (DIO) mice via profiling of OS genes and pathways in skeletal muscles related to the anti-obesity effect. Methods: Wild-type CD1 male mice and the knockout of nuclear factor (erythroid-derived 2) like 2 (NrF2) mice were fed a high-fat diet (HFD) for 16 weeks; to induce obesity. Subsequently, each group was subdivided into two subgroups and received either Vehicle (25μl) or SFN (5 mg/kg BW) for four weeks. Body weight was measured daily, and a glucose tolerance test (GTT) was performed after 21 days of treatment. Afterward, mice were decapitated, blood and tissue samples were collected and snap-frozen immediately. Total RNA was extracted from Skeletal muscle and epididymal white adipose tissue (eWAT), leptin expression was measured in (eWAT), and 84 OS genes in skeletal muscle were examined using RT-PCR. Results: Significant reduction in body weight in SFN treated WT mice, while no change in KO mice. Plasma glucose, leptin, and leptin gene expression (eWAT) were significantly reduced in the WT-DIO SFN treated group, while no changes were detected in KO mice. SFN decreases OS damage in skeletal muscles, such as lipid peroxidation and production of reactive oxygen species (ROS). Conclusion: This study demonstrated that SFN had lowered body weight in WT-DIO mice by decreasing OS damage in skeletal muscles through the NrF2 pathway and can be a potential anti-obesity drug.

scholarly journals Aging, Osteo-Sarcopenia, and Musculoskeletal Mechano-Transduction

2021 ◽  
Vol 2 ◽  
Author(s):  
Jenna M. Leser ◽  
Anicca Harriot ◽  
Heather V. Buck ◽  
Christopher W. Ward ◽  
Joseph P. Stains
Keyword(s):  
Oxidative Stress ◽  
Chronic Disease ◽  
Cellular Senescence ◽  
Healthy Aging ◽  
Mechanical Load ◽  
Low Energy ◽  
Load Sensing ◽  
Age Related ◽  
Increased Risk ◽  
And Function

The decline in the mass and function of bone and muscle is an inevitable consequence of healthy aging with early onset and accelerated decline in those with chronic disease. Termed osteo-sarcopenia, this condition predisposes the decreased activity, falls, low-energy fractures, and increased risk of co-morbid disease that leads to musculoskeletal frailty. The biology of osteo-sarcopenia is most understood in the context of systemic neuro-endocrine and immune/inflammatory alterations that drive inflammation, oxidative stress, reduced autophagy, and cellular senescence in the bone and muscle. Here we integrate these concepts to our growing understanding of how bone and muscle senses, responds and adapts to mechanical load. We propose that age-related alterations in cytoskeletal mechanics alter load-sensing and mechano-transduction in bone osteocytes and muscle fibers which underscores osteo-sarcopenia. Lastly, we examine the evidence for exercise as an effective countermeasure to osteo-sarcopenia.

scholarly journals Age and homeostasis

2020 ◽  
pp. 79-86
Author(s):  
А.А. Пальцын ◽  
Н.Б. Свиридкина
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Adaptive Response ◽  
Cold Shock ◽  
Structure And Function ◽  
The Body ◽  
Adequate Response ◽  
Response To Stress ◽  
And Function ◽  
Homeostatic Response

Гомеостаз - способность организма сохранять достаточное для жизни постоянство структуры и функции. Противоречие заключается в том, что суть жизни - это неизбежное изменение структуры и функции. Наиболее распространенный нарушитель гомеостаза - оксидативный стресс. В нейтрализации его действия участвует множество генов, включаемых транскрипционными факторами Nrf2, NFκB, TFAM, и PGC1α. Адаптивный ответ развивается не только на оксидативный стресс, но и на тепловой шок, гликемический стресс, холодовой шок, осмотический стресс, переутомление, голодание, механический стресс, антигенное воздействие, эмоциональный и психологический стресс. При стрессе в клетках накапливаются продукты неполного протеолиза - агрегаты. Гомеостатический ответ выражается увеличением содержания шаперонов, способствующих правильному свертыванию белков и протеасом, разрушающих агрегаты. Однако способность адекватно отвечать на стрессы снижается с возрастом, сужается диапазон модулирования адаптивного гомеостаза. Нарастает вероятность выхода за пределы сузившегося диапазона и гибели клетки. Homeostasis is the ability of the body to maintain sufficient for life permanence of structure and function. A contradiction is that the essence of life is inevitable changes in the structure and function. The most common homeostasis violator is oxidative stress. Numerous genes triggered by Nrf2, NFκB, TFAM, and PGC1α transcription factors are involved in neutralizing the action of oxidative stress. The adaptive response is induced not only by oxidative stress but also by heat shock, glycemic stress, cold shock, osmotic stress, exhastion, starvation, mechanical stress, antigenic impact, and emotional or psychological stress. In stress, cells accumulate products of incomplete proteolysis, aggregates. The homeostatic response is evident as increased content of chaperones that contribute to the proper folding of proteins, and proteasomes that destroy the aggregates. However, the capability for an adequate response to stress declines with age, and the range of adaptive homeostasis modulation narrows. The probability of going beyond this narrowed range and of cell death is increasing.

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