The Mechanisms and Management of Age-Related Oxidative Stress in Male Hypogonadism Associated with Non-communicable Chronic Disease

Androgens have diverse functions in muscle physiology, lean body mass, the regulation of adipose tissue, bone density, neurocognitive regulation, and spermatogenesis, the male reproductive and sexual function. Male hypogonadism, characterized by reduced testosterone, is commonly seen in ageing males, and has a complex relationship as a risk factor and a comorbidity in age-related noncommunicable chronic diseases (NCDs), such as obesity, metabolic syndrome, type 2 diabetes, and malignancy. Oxidative stress, as a significant contributor to the ageing process, is a common feature between ageing and NCDs, and the related comorbidities, including hypertension, dyslipidemia, hyperglycemia, hyperinsulinemia, and chronic inflammation. Oxidative stress may also be a mediator of hypogonadism in males. Consequently, the management of oxidative stress may represent a novel therapeutic approach in this context. Therefore, this narrative review aims to discuss the mechanisms of age-related oxidative stress in male hypogonadism associated with NCDs and discusses current and potential approaches for the clinical management of these patients, which may include conventional hormone replacement therapy, nutrition and lifestyle changes, adherence to the optimal body mass index, and dietary antioxidant supplementation and/or phytomedicines.

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Telomere Length and Oxidative Stress and Its Relation with Metabolic Syndrome Components in the Aging

Biology ◽

10.3390/biology10040253 ◽

2021 ◽

Vol 10 (4) ◽

pp. 253

Author(s):

Graciela Gavia-García ◽

Juana Rosado-Pérez ◽

Taide Laurita Arista-Ugalde ◽

Itzen Aguiñiga-Sánchez ◽

Edelmiro Santiago-Osorio ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Telomere Length ◽

Scientific Evidence ◽

Telomeric Dna ◽

Biochemical Alterations ◽

The Metabolic Syndrome ◽

Age Related ◽

And Function

A great amount of scientific evidence supports that Oxidative Stress (OxS) can contribute to telomeric attrition and also plays an important role in the development of certain age-related diseases, among them the metabolic syndrome (MetS), which is characterised by clinical and biochemical alterations such as obesity, dyslipidaemia, arterial hypertension, hyperglycaemia, and insulin resistance, all of which are considered as risk factors for type 2 diabetes mellitus (T2DM) and cardiovascular diseases, which are associated in turn with an increase of OxS. In this sense, we review scientific evidence that supports the association between OxS with telomere length (TL) dynamics and the relationship with MetS components in aging. It was analysed whether each MetS component affects the telomere length separately or if they all affect it together. Likewise, this review provides a summary of the structure and function of telomeres and telomerase, the mechanisms of telomeric DNA repair, how telomere length may influence the fate of cells or be linked to inflammation and the development of age-related diseases, and finally, how the lifestyles can affect telomere length.

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The Protective Role of Antioxidants in the Defence against ROS/RNS-Mediated Environmental Pollution

Oxidative Medicine and Cellular Longevity ◽

10.1155/2014/671539 ◽

2014 ◽

Vol 2014 ◽

pp. 1-22 ◽

Cited By ~ 78

Author(s):

Borut Poljšak ◽

Rok Fink

Keyword(s):

Oxidative Stress ◽

Nitrosative Stress ◽

Environmental Pollutants ◽

Protective Role ◽

Age Related Macular Degeneration ◽

Protective Effects ◽

Age Related ◽

Dietary Antioxidant ◽

Polycyclic Aromatic ◽

Antioxidant Supplements

Overproduction of reactive oxygen and nitrogen species can result from exposure to environmental pollutants, such as ionising and nonionising radiation, ultraviolet radiation, elevated concentrations of ozone, nitrogen oxides, sulphur dioxide, cigarette smoke, asbestos, particulate matter, pesticides, dioxins and furans, polycyclic aromatic hydrocarbons, and many other compounds present in the environment. It appears that increased oxidative/nitrosative stress is often neglected mechanism by which environmental pollutants affect human health. Oxidation of and oxidative damage to cellular components and biomolecules have been suggested to be involved in the aetiology of several chronic diseases, including cancer, cardiovascular disease, cataracts, age-related macular degeneration, and aging. Several studies have demonstrated that the human body can alleviate oxidative stress using exogenous antioxidants. However, not all dietary antioxidant supplements display protective effects, for example,β-carotene for lung cancer prevention in smokers or tocopherols for photooxidative stress. In this review, we explore the increases in oxidative stress caused by exposure to environmental pollutants and the protective effects of antioxidants.

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Anisocytosis Is Associated With High Body Mass Index and Poor Adaptation to Oxidative Stress in Obese Patients with Type 2 Diabetes Mellitus

Journal of Life Sciences ◽

10.31901/24566306.2018/10.02.232 ◽

2018 ◽

Vol 10 (02) ◽

Author(s):

Poonam Chandra Mittal

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Body Mass Index ◽

Type 2 Diabetes Mellitus ◽

Body Mass ◽

High Body Mass Index ◽

Obese Patients ◽

High Body

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Pericytopathy: Oxidative Stress and Impaired Cellular Longevity in the Pancreas and Skeletal Muscle in Metabolic Syndrome and Type 2 Diabetes

Oxidative Medicine and Cellular Longevity ◽

10.4161/oxim.3.5.13653 ◽

2010 ◽

Vol 3 (5) ◽

pp. 290-303 ◽

Cited By ~ 25

Author(s):

Melvin R. Hayden ◽

Ying Yang ◽

Javad Habibi ◽

Sarika V. Bagree ◽

James R. Sowers

Keyword(s):

Oxidative Stress ◽

Type 2 Diabetes ◽

Skeletal Muscle ◽

Metabolic Syndrome ◽

Screening Method ◽

Lifestyle Changes ◽

Pancreatic Stellate Cells ◽

Rodent Models ◽

The Metabolic Syndrome

The pericyte's role has been extensively studied in retinal tissues of diabetic retinopathy; however, little is known regarding its role in such tissues as the pancreas and skeletal muscle. This supportive microvascular mural cell plays an important and novel role in cellular and extracellular matrix remodeling in the pancreas and skeletal muscle of young rodent models representing the metabolic syndrome and type 2 diabetes mellitus (T2DM). Transmission electron microscopy can be used to evaluate these tissues from young rodent models of insulin resistance and T2DM, including the transgenic Ren2 rat, db/db obese insulin resistantߞT2DM mouse, and human islet amyloid polypeptide (HIP) rat model of T2DM. With this method, the earliest pancreatic remodeling change was widening of the islet exocrine interface and pericyte hypercellularity, followed by pericyte differentiation into islet and pancreatic stellate cells with early fibrosis involving the islet exocrine interface and interlobular interstitium. In skeletal muscle there was a unique endothelial capillary connectivity via elongated longitudinal pericyte processes in addition to pericyte to pericyte and pericyte to myocyte cellcell connections allowing for paracrine communication. Initial pericyte activation due to moderate oxidative stress signaling may be followed by hyperplasia, migration and differentiation into adult mesenchymal cells. Continued robust oxidative stress may induce pericyte apoptosis and impaired cellular longevity. Circulating antipericyte autoantibodies have recently been characterized, and may provide a screening method to detect those patients who are developing pericyte loss and are at greater risk for the development of complications of T2DM due to pericytopathy and rarefaction. Once detected, these patients may be offered more aggressive treatment strategies such as early pharmacotherapy in addition to lifestyle changes targeted to maintaining pericyte integrity. In conclusion, we have provided a review of current knowledge regarding the pericyte and novel ultrastructural findings regarding its role in metabolic syndrome and T2DM.

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Middle-Aged Indians with Type 2 Diabetes Are at Higher Risk of Biological Ageing with Special Reference to Serum CDKN2A

Journal of Diabetes Research ◽

10.1155/2020/7569259 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10

Author(s):

Joyita Banerjee ◽

Yogita Dhas ◽

Neetu Mishra

Keyword(s):

Oxidative Stress ◽

Type 2 Diabetes ◽

Special Reference ◽

Oxidized Ldl ◽

Middle Aged ◽

Biological Ageing ◽

Proinflammatory Mediators ◽

Age Related ◽

Increased Risk

Sedentary lifestyle and high visceral adiposity have elevated the risk of type 2 diabetes (T2DM) among Indians at younger age. In this study, we aimed to investigate the association of oxidative stress and chronic inflammatory mediators with ageing with special reference to the biological ageing marker cyclin-dependent kinase inhibitor 2A (CDKN2A) among middle-aged (31-50 years) Indian healthy and T2DM subjects. Malondialdehyde (MDA), oxidized LDL (oxLDL), interleukin-6 (IL-6), interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and CDKN2A were measured in T2DM patients (n=80) and controls (n=80) aged 31-50 years, further grouped into G1: 31-40 years and G2: 41-50 years. IL-6, TNF-α, MCP-1, and CDKN2A showed a significant association with ageing among both T2DM patients and controls. But the strength of the association of MCP-1 and CKDN2A with ageing was significantly stronger in T2DM patients than the controls. All the oxidative stress and proinflammatory mediators showed nonsignificant associations with CDKN2A in the controls. However, IL-6, TNF-α, and MCP-1 showed a strong association with CDKN2A in T2DM patients. An increased risk of high levels of CDKN2A was found in G1 T2DM patients (OR: 3.484 (95% CI: 1.246-9.747) p=0.017) and G2 T2DM patients (OR: 5.000 (95% CI: 1.914-13.061), p=0.001) with reference to the respective control groups. Our study reveals that the middle-aged Indians with T2DM are at higher risk of biological ageing. The development of T2DM is more common among middle-aged Indians. T2DM may exacerbate the ageing process and may subsequently predispose Indians to various age-related complications at a much early age.

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Kalpaamruthaa ameliorates myocardial and aortic damage in cardiovascular complications associated with type 2 diabetes mellitus

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2012-0292 ◽

2013 ◽

Vol 91 (2) ◽

pp. 116-123 ◽

Cited By ~ 5

Author(s):

Raja Latha ◽

Palanivelu Shanthi ◽

Panchanadham Sachdanandam

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Body Mass ◽

Protective Efficacy ◽

Cardiovascular Complications ◽

Matrix Metalloproteinase 2 ◽

Ultrastructural Changes

Myocardial and aortic damage in cardiovascular complications (CVD) associated with type 2 diabetes mellitus and the protective efficacy of Kalpaamruthaa (KA) are evaluated in this study. CVD developed in 8 weeks after type 2 diabetes mellitus was induced by the administration of a high-fat diet for 2 weeks, and then with streptozotocin (2 × 35 mg·(kg body mass)–1, by intraperitonal injection, at 24 h intervals) in male Sprague–Dawley rats. CVD-induced rats were treated with KA at 200 mg·(kg body mass)–1·(day)–1 orally for 28 days. Increased oxidative stress in CVD-induced rats lowers antioxidant defense in the aorta. Treatment with KA reduced oxidative stress by increasing antioxidant status with decreased lipid peroxides in CVD-induced rats. Histological examination of the myocardium and aorta provided support for the cytoprotective effect of KA in CVD. Ultrastructural changes in the myocardium of CVD-induced rats were improved by KA treatment. Aortic damage was observed through decreased endothelial nitric oxide synthase and increased NADPH oxidase mRNA expressions in CVD-induced rats. KA reduced the aortic damage by ameliorating these levels back to normal. KA treatment reduced the pro-inflammatory cytokines tumor necrosis factor-α and interleukin 6 in CVD-induced rats. Immunohistochemical expressions of matrix metalloproteinase-2 and -9 were observed to be elevated in the myocardium of CVD-induced rats, but these were decreased by the administration of KA. This study demonstrates the cardiovascular protective effect of KA in type 2 diabetes.

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