scholarly journals Utilizing Melatonin to Alleviate Side Effects of Chemotherapy: A Potentially Good Partner for Treating Cancer with Ageing

2020 ◽  
Vol 2020 ◽  
pp. 1-20
Author(s):  
Zhiqiang Ma ◽  
Liqun Xu ◽  
Dong Liu ◽  
Xiaoyan Zhang ◽  
Shouyin Di ◽  
...  
Keyword(s):  
Side Effects ◽  
Alkylating Agents ◽  
Protective Role ◽  
Chemotherapeutic Agents ◽  
Future Research ◽  
Drug Induced ◽  
Protective Actions ◽  
Age Related ◽  
Comprehensive Reference

Persistent senescence seems to exert detrimental effects fostering ageing and age-related disorders, such as cancer. Chemotherapy is one of the most valuable treatments for cancer, but its clinical application is limited due to adverse side effects. Melatonin is a potent antioxidant and antiageing molecule, is nontoxic, and enhances the efficacy and reduces the side effects of chemotherapy. In this review, we first summarize the mitochondrial protective role of melatonin in the context of chemotherapeutic drug-induced toxicity. Thereafter, we tabulate the protective actions of melatonin against ageing and the harmful roles induced by chemotherapy and chemotherapeutic agents, including anthracyclines, alkylating agents, platinum, antimetabolites, mitotic inhibitors, and molecular-targeted agents. Finally, we discuss several novel directions for future research in this area. The information compiled in this review will provide a comprehensive reference for the protective activities of melatonin in the context of chemotherapy drug-induced toxicity and will contribute to the design of future studies and increase the potential of melatonin as a therapeutic agent.

scholarly journals Strategies and cognitive reserve to preserve lexical production in aging

GeroScience ◽  
2021 ◽  
Author(s):  
Monica Baciu ◽  
Sonja Banjac ◽  
Elise Roger ◽  
Célise Haldin ◽  
Marcela Perrone-Bertolotti ◽  
...  
Keyword(s):  
Older Adults ◽  
Cognitive Aging ◽  
Individual Variability ◽  
Future Research ◽  
Aging Effects ◽  
Main Hypothesis ◽  
Compensatory Strategies ◽  
Age Related ◽  
Complementary Domain

AbstractIn the absence of any neuropsychiatric condition, older adults may show declining performance in several cognitive processes and among them, in retrieving and producing words, reflected in slower responses and even reduced accuracy compared to younger adults. To overcome this difficulty, healthy older adults implement compensatory strategies, which are the focus of this paper. We provide a review of mainstream findings on deficient mechanisms and possible neurocognitive strategies used by older adults to overcome the deleterious effects of age on lexical production. Moreover, we present findings on genetic and lifestyle factors that might either be protective or risk factors of cognitive impairment in advanced age. We propose that “aging-modulating factors” (AMF) can be modified, offering prevention opportunities against aging effects. Based on our review and this proposition, we introduce an integrative neurocognitive model of mechanisms and compensatory strategies for lexical production in older adults (entitled Lexical Access and Retrieval in Aging, LARA). The main hypothesis defended in LARA is that cognitive aging evolves heterogeneously and involves complementary domain-general and domain-specific mechanisms, with substantial inter-individual variability, reflected at behavioral, cognitive, and brain levels. Furthermore, we argue that the ability to compensate for the effect of cognitive aging depends on the amount of reserve specific to each individual which is, in turn, modulated by the AMF. Our conclusion is that a variety of mechanisms and compensatory strategies coexist in the same individual to oppose the effect of age. The role of reserve is pivotal for a successful coping with age-related changes and future research should continue to explore the modulating role of AMF.

scholarly journals The Protective Role of Sestrin2 in Atherosclerotic and Cardiac Diseases

2021 ◽  
Vol 22 (3) ◽  
pp. 1200
Author(s):  
Yoshimi Kishimoto ◽  
Kazuo Kondo ◽  
Yukihiko Momiyama
Keyword(s):  
Oxidative Stress ◽  
Protective Role ◽  
Chronic Inflammatory Disease ◽  
Atherosclerotic Disease ◽  
Cardiac Diseases ◽  
Compensatory Response ◽  
Age Related ◽  
Anti Oxidant ◽  
Progression Of Atherosclerosis

Atherosclerotic disease, such as coronary artery disease (CAD), is known to be a chronic inflammatory disease, as well as an age-related disease. Excessive oxidative stress produced by reactive oxygen species (ROS) contributes to the pathogenesis of atherosclerosis. Sestrin2 is an anti-oxidant protein that is induced by various stresses such as hypoxia, DNA damage, and oxidative stress. Sestrin2 is also suggested to be associated with aging. Sestrin2 is expressed and secreted mainly by macrophages, endothelial cells, and cardiomyocytes. Sestrin2 plays an important role in suppressing the production and accumulation of ROS, thus protecting cells from oxidative damage. Since sestrin2 is reported to have anti-oxidant and anti-inflammatory properties, it may play a protective role against the progression of atherosclerosis and may be a potential therapeutic target for the amelioration of atherosclerosis. Regarding the association between blood sestrin2 levels and atherosclerotic disease, the blood sestrin2 levels in patients with CAD or carotid atherosclerosis were reported to be high. High blood sestrin2 levels in patients with such atherosclerotic disease may reflect a compensatory response to increased oxidative stress and may help protect against the progression of atherosclerosis. This review describes the protective role of sestrin2 against the progression of atherosclerotic and cardiac diseases.

The Protective Role of Exercise Against Age-Related Neurodegeneration

2021 ◽  
pp. 101543
Author(s):  
Alyson L. Sujkowski ◽  
Luke Hong ◽  
R.J. Wessells ◽  
Sokol V. Todi
Keyword(s):  
Protective Role ◽  
Age Related

scholarly journals Hepato & nephro protective effects of naringenin-loaded tpgs polymeric nanosuspension against cisplatin-induced toxicity

2019 ◽  
Vol 10 (4) ◽  
pp. 2755-2764
Author(s):  
Sumathi Rajamani ◽  
Gobinath Kalyanasundaram ◽  
Tamizharasi Sengodan ◽  
Sivakumar Thangavelu ◽  
Nikhitha K Shanmukhan ◽  
...  
Keyword(s):  
Antioxidant Activities ◽  
Aqueous Solubility ◽  
Protective Role ◽  
Chemotherapeutic Agents ◽  
Glycol Succinate ◽  
High Pressure Homogenization ◽  
Protective Effects ◽  
Male Wistar Rats ◽  
Nephroprotective Effect

Cisplatin (Cis-Diammineplatinum (II) dichloride/CIS) is one of the most potent chemotherapeutic agents widely used in treatment of various cancers. Naringenin (NAR), a natural flavonoid, protect against CIS-induced injury in rats without hampering CIS beneficial cytotoxic activity. Even though NAR exhibits therapeutic potency, clinical evolution of the molecule is embarrassed because of very less aqueous solubility which corresponds to low availability at the site of the tumor. In our former analysis, nanosuspension of naringenin (NARNS) was developed by the method of high-pressure homogenization. The study had been continued to evaluate the protective role of D-α-Tocopheryl polyethylene glycol succinate (TPGS) coated NARNS, against oxidative stress-induced hepato and nephrotoxicity in male Wistar rats upon CIS treatment. Induction of acute hepato and neprotoxicity was done by intraperitoneal injection (i.p) injection of CIS (7 mg/kg of body weight) and administration of NAR and NARNS. Administration of NARNS virtually suppressed CIS-induced and liver injury evidenced by a reduction of lipid peroxidation level, blood urea nitrogen, serum uric acid, creatinine and elevated enzymatic antioxidant activities of superoxide dismutase, catalase, and glutathione peroxidase in rats liver tissue. Histological studies substantiated the biochemical parameters. The study suggests that NARNS has strong hepato and nephroprotective effect compared to NAR.

scholarly journals Mechanisms of Multidrug Resistance in Cancer Chemotherapy

2020 ◽  
Vol 21 (9) ◽  
pp. 3233 ◽  
Author(s):  
Karol Bukowski ◽  
Mateusz Kciuk ◽  
Renata Kontek
Keyword(s):  
Multidrug Resistance ◽  
Cancer Treatment ◽  
Anticancer Agents ◽  
Alkylating Agents ◽  
Gene Mutations ◽  
Resistance Mechanisms ◽  
Chemotherapeutic Agents ◽  
Future Research ◽  
Repair Capacity ◽  
Dna Repair Capacity

Cancer is one of the main causes of death worldwide. Despite the significant development of methods of cancer healing during the past decades, chemotherapy still remains the main method for cancer treatment. Depending on the mechanism of action, commonly used chemotherapeutic agents can be divided into several classes (antimetabolites, alkylating agents, mitotic spindle inhibitors, topoisomerase inhibitors, and others). Multidrug resistance (MDR) is responsible for over 90% of deaths in cancer patients receiving traditional chemotherapeutics or novel targeted drugs. The mechanisms of MDR include elevated metabolism of xenobiotics, enhanced efflux of drugs, growth factors, increased DNA repair capacity, and genetic factors (gene mutations, amplifications, and epigenetic alterations). Rapidly increasing numbers of biomedical studies are focused on designing chemotherapeutics that are able to evade or reverse MDR. The aim of this review is not only to demonstrate the latest data on the mechanisms of cellular resistance to anticancer agents currently used in clinical treatment but also to present the mechanisms of action of novel potential antitumor drugs which have been designed to overcome these resistance mechanisms. Better understanding of the mechanisms of MDR and targets of novel chemotherapy agents should provide guidance for future research concerning new effective strategies in cancer treatment.

Mo1031 PROTECTIVE ROLE OF THE PRO-RESOLVING LIPID MEDIATOR RESOLVIN D1 IN NONSTEROIDAL ANTI-INFLAMMATORY DRUG-INDUCED SMALL INTESTINAL DAMAGE

2020 ◽  
Vol 158 (6) ◽  
pp. S-762
Author(s):  
Takuya Kuzumoto ◽  
Tetsuya Tanigawa ◽  
Hiroyuki Kitamura ◽  
Akira Higashimori ◽  
Yuji Nadatani ◽  
...  
Keyword(s):  
Protective Role ◽  
Lipid Mediator ◽  
Intestinal Damage ◽  
Resolvin D1 ◽  
Drug Induced ◽  
Inflammatory Drug ◽  
Small Intestinal ◽  
Anti Inflammatory

scholarly journals α-Secretase nonsense mutation (ADAM10 Tyr167*) in familial Alzheimer’s disease

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Pablo Agüero ◽  
María José Sainz ◽  
María-Salud García-Ayllón ◽  
Javier Sáez-Valero ◽  
Raquel Téllez ◽  
...  
Keyword(s):  
Nonsense Mutation ◽  
Genetic Model ◽  
Late Onset ◽  
Future Research ◽  
Clinical Genetic ◽  
Csf Analysis ◽  
Amyloidogenic Processing ◽  
Age Related ◽  
Spanish Cohort

Abstract Background The disintegrin metalloproteinase 10 (ADAM10) is the main α-secretase acting in the non-amyloidogenic processing of APP. Some ADAM10 gene variants have been associated with higher susceptibility to develop late-onset AD, though clear clinical-genetic correlates remain elusive. Methods Clinical-genetic and biomarker study of a first family with early- and late-onset AD associated with a nonsense ADAM10 mutation (p.Tyr167*). CSF analysis included AD core biomarkers, as well as Western blot of ADAM10 species and sAPPα and sAPPβ peptides. We evaluate variant’s pathogenicity, pattern of segregation, and further screened for the p.Tyr167* mutation in 197 familial AD cases from the same cohort, 200 controls from the same background, and 274 AD cases from an independent Spanish cohort. Results The mutation was absent from public databases and segregated with the disease. CSF Aβ42, total tau, and phosphorylated tau of affected siblings were consistent with AD. The predicted haploinsufficiency effect of the nonsense mutation was supported by (a) ADAM10 isoforms in CSF decreased around 50% and (b) 70% reduction of CSF sAPPα peptide, both compared to controls, while sAPPβ levels remained unchanged. Interestingly, sporadic AD cases had a similar decrease in CSF ADAM10 levels to that of mutants, though their sAPPα and sAPPβ levels resembled those of controls. Therefore, a decreased sAPPα/sAPPβ ratio was an exclusive feature of mutant ADAM10 siblings. The p.Tyr167* mutation was not found in any of the other AD cases or controls screened. Conclusions This family illustrates the role of ADAM10 in the amyloidogenic process and the clinical development of the disease. Similarities between clinical and biomarker findings suggest that this family could represent a genetic model for sporadic late-onset AD due to age-related downregulation of α-secretase. This report encourages future research on ADAM10 enhancers.

scholarly journals Basic Concepts on the Role of Nuclear Factor Erythroid-Derived 2-Like 2 (Nrf2) in Age-Related Diseases

2019 ◽  
Vol 20 (13) ◽  
pp. 3208 ◽  
Author(s):  
Fabiane Valentini Francisqueti-Ferron ◽  
Artur Junio Togneri Ferron ◽  
Jéssica Leite Garcia ◽  
Carol Cristina Vágula de Almeida Silva ◽  
Mariane Róvero Costa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Transcriptional Factor ◽  
Future Research ◽  
Related Factor ◽  
Nuclear Factor ◽  
Nrf2 Pathway ◽  
Age Related ◽  
Basic Concepts

The transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) is one of the most important oxidative stress regulator in the human body. Once Nrf2 regulates the expression of a large number of cytoprotective genes, it plays a crucial role in the prevention of several diseases, including age-related disorders. However, the involvement of Nrf2 on these conditions is complex and needs to be clarified. Here, a brief compilation of the Nrf2 enrollment in the pathophysiology of the most common age-related diseases and bring insights for future research on the Nrf2 pathway is described. This review shows a controversial response of this transcriptional factor on the presented diseases. This reinforces the necessity of more studies to investigate modulation strategies for Nrf2, making it a possible therapeutic target in the treatment of age-related disorders.

scholarly journals Involvement of insulin resistance in D-galactose-induced age-related dementia in rats: Protective role of metformin and saxagliptin

PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0183565 ◽  
Author(s):  
Sara Kenawy ◽  
Rehab Hegazy ◽  
Azza Hassan ◽  
Siham El-Shenawy ◽  
Nawal Gomaa ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protective Role ◽  
Age Related

Hepatotoxicity of chemotherapeutic agents: current state of the problem

2016 ◽  
Vol 21 (6) ◽  
pp. 325-333
Author(s):  
M. T Vatutin ◽  
E. V Sklyannaya ◽  
Mariam A. El-Khatib ◽  
S. V Starchenko ◽  
M. V Makarova
Keyword(s):  
Kinase Inhibitors ◽  
Antitumor Agents ◽  
Opportunistic Infections ◽  
Alkylating Agents ◽  
Chemotherapeutic Agents ◽  
Protein Kinase Inhibitors ◽  
Drug Induced ◽  
Anthracycline Antibiotics ◽  
Current State ◽  
High Level

This review is devoted to the actual for the present day problem of the hepatotoxicity of chemotherapeutic agents. Liver is the most important organ essential for the maintaining of the body’s internal environment. For the present time there is observed the high level of the morbidity and mortality rate against the background of drug-induced liver lesions due to, in the first instance, the lack ofproper manner for the substitution of the liver function but transplantation. Liver deteriorations due to the administration of antitumor agents have no pathognomonic clinical or histological features that significantly embarrasses the execution of the differential diagnosis with liver disorders against the background of administration of other preparations, either associated with opportunistic infections or the progression of previously acquired pathology of the liver. In the article there is described the toxic influence on the liver of most often used in oncology chemotherapeutic agents - antimetabolites, alkylating agents, platinum compounds, epothilones, taxanes, vinca alkaloids, monoclonal antibodies, anthracycline antibiotics, topoisomerase and protein kinase inhibitors is described in this article. In the review there are summarized results of recent studies of etiology, pathogenesis, clinical features, diagnosis, prevention and treatment of chemotherapy induced hepatotoxicity. The special attention is given to recent discoveries in the area of pathogenesis of chemotherapy induced hepatotoxicity. However many moments remain to be still not studied completely, that offers perspectives for further research in this field.

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