Postępy Higieny i Medycyny Doświadczalnej
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Published By Index Copernicus International

1732-2693, 0032-5449

2021 ◽  
Vol 75 (1) ◽  
pp. 923-932
Author(s):  
Dagmara Otto-Ślusarczyk ◽  
Wojciech Graboń ◽  
Magdalena Mielczarek-Puta ◽  
Alicja Chrzanowska ◽  
Anna Barańczyk-Kuźma

Abstract Introduction Glutaminolysis, beside glycolysis, is a key metabolic pathway of a cancer cell that provides energy and substrates for the synthesis of nucleic acids, proteins, and lipids. The pathway is mediated by both mitochondrial and cytosolic enzymes. Neither expression of glutaminolysis enzymes in colon cancer cells nor the influence of various oxygen concentrations on their expression has been studied so far. Objectives The aim of the study was to determine and compare the mRNA expression of enzymes involved in glutaminolysis at various oxygen levels in human primary (SW480) and metastatic (SW620) colon cancer cells cultured in 1% O2 (hypoxia), 10% O2 (tissue normoxia), 21% O2 (atmospheric normoxia). Methods Cell viability was determined by Trypan Blue exclusion (TB) and Thiazolyl Blue Tetrazolium Bromide (MTT). The expression of HIF1α, GLUT1, GLS1, AST1, AST2, ACL, PC and GC1, GC2 at mRNA levelwas determined by RT-qPCR. Results. Correlation between increasing oxygen concentration and cell count was not observed. In both cell lines the number of viable cells was the lowest at 10% oxygen. The enzyme profile and expression of proteins involved in glutaminolysis varied depending on oxygen pressure and type of cell lines. In summary, our findings suggest differences in metabolic adaptation to oxygen availability in vivo between primary and metastatic colon cancer cells.


2021 ◽  
Vol 75 ◽  
pp. 502-510
Author(s):  
Maria Pietrzak-Nowacka ◽  
Krzysztof Safranow ◽  
Małgorzata Czechowska ◽  
Grażyna Dutkiewicz ◽  
Ewa Gątarska ◽  
...  

The aim of the follow-up study was to compare the changes of M-mode echocardiographic parameters in autosomal dominant polycystic kidney disease (ADPKD) patients and controls without renal failure during six years of observation and to explore the associations of these parameters with metabolic syndrome components and kidney function. We performed a follow-up examination in 37 ADPKD patients and 40 controls. Anthropometric parameters were measured and fasting venous blood sample from each patient was tested for glucose, insulin, C-peptide, HbA1c, creatinine, and urea concentrations. All subjects underwent standard two-dimensional M-mode echocardiography. Left ventricular hypertrophy (LVH) was diagnosed based on left ventricular mass index (LVMI) adjusted for body surface area (LVMI- -S, LVH-S) or for height (LVMI-H, LVH-H). The prevalence of LVH was significantly greater in ADPKD patients than in controls (35% vs. 10%, p=0.012) according to the ESH/ESC criteria from 2013, and (27.0% vs. 7.5%, p=0.032) according to criteria from 2017. In patients with ADPKD, no significant increase of the echocardiographic parameters was observed in the 6 years between the initial examination and the follow-up examination. Cardiac involvement in women with ADPKD occurs at an earlier stage of the disease than in men. In patients with ADPKD treated for hypertension in accordance with the 2013 ESH/ESC Guidelines the progression of LVH was not observed during the 6-year follow-up, despite the deterioration of renal function. Obesity, blood pressure and renal function do not affect LVMI changes.


2021 ◽  
Vol 75 ◽  
pp. 491-501
Author(s):  
Paweł Porzycki

Prostate cancer (PCa) is the most common type of cancer among men in Europe and this applies to almost the whole world. Current recommendations for screening and diagnosis are based on prostate specific antigen (PSA) measurements and the digital rectal examination (DRE). Both of them trigger the prostate biopsy. Limited specificity of the PSA test brings, however, a need to develop new and better diagnostic tools. In the last few years, new approaches for providing significantly better biomarkers, an alternative to PSA, have been introduced. Modern biomarkers show improvement not only as a diagnostic procedure, but also for staging, evaluating aggressiveness and managing the therapeutic process. The most promising group are molecular markers; among them microRNAs (miRNAs, miRs) are most frequent. miRNAs represent a class of about 22 nucleotides long, small non-coding RNAs, which are involved in gene expression regulation at the post-transcriptional level. This article reports a revision about the role of miRNAs in PCa including data of Adreno Receptor (AR) signaling, cell cycle, epithelial mesenchymal transition (EMT) process, cancer stem cells (CSCs) regulation and even the role of miRNAs as PCa therapeutic tool. Finding better PCa biomarkers, replacing the current PSA measurement, is firmly needed in modern oncology practice.


2021 ◽  
Vol 75 ◽  
pp. 474-490
Author(s):  
Dominika Nowak ◽  
Wojciech Słupski ◽  
Maria Rutkowska

Alzheimer’s disease (AD) described as a chronic and irreversible neurodegenerative disease remains the most common cause of dementia. Due to the aging of the population, the incurability of AD has become a growing problem of medicine in the 21stcentury. Current treatment is only symptomatic, providing minimal, temporary improvement in the patient’s cognitive function. This paper presents the latest trends in the search for effective pharmacotherapy capable of preventing or inhibiting AD progression. Since the exact pathogenesis of Alzheimer’s disease is not known, the main therapeutic strategies are based only on the following hypotheses: amyloid cascade, tau protein, oxidative stress, neuroinflammation and those associated with dysfunction of the cholinergic system as well as glutamatergic. Most of the compounds currently tested in clinical trials are targeted at pathological amyloid β (A β), which is considered the cause of neurodegeneration, according to the most widely described cascade theory. Most of the compounds currently tested in clinical trials are targeted at pathological amyloid β (Aβ), which is the main cause of neurodegeneration according to the widely described theory of the amyloid cascade. Attempts to fight the toxic Aβ are based on the following: immunotherapy (vaccines, monoclonal antibodies), compounds that inhibit its formation: γ-secretase inhibitors/modulators and β-secretase. Immunotherapy can also be us,ed to increase the clearance of hyperphosphorylated tau protein, the occurrence of which is another feature of Alzheimer’s disease. In addition to immunotherapy, anti-inflammatory, metabolic and neuroprotective compounds have been the subject of a number of studies. A range of symptomatic compounds that improve cognitive functions by compensating cholinergic, noradrenergic and glutamatergic signaling deficits have also been investigated in clinical trials.


2021 ◽  
Vol 75 ◽  
pp. 448-455
Author(s):  
Magdalena Londzin-Olesik ◽  
Beata Kos-Kudła ◽  
Aleksandra Nowak ◽  
Mariusz Nowak

Graves’ disease (GD) is a chronic autoimmune condition in which the anti-thyroid stimulating hormone receptor antibodies (TRAb) activate the thyrotropin receptor (TSHR) located on thyrocytes, leading to excessive thyroid hormone production. TSHR is also expressed in extrathyroidal tissues, in particular, within the orbit. The serum levels of TRAb correlate with the severity and activity of thyroid orbitopathy (TO). TO is the most common extrathyroidal manifestation of GD. It is an autoimmune inflammation of orbital tissues, that is, extraocular muscles, orbital adipose tissue or a lacrimal gland. Increased orbital fibroblast and adipocyte proliferation, overproduction of glycosaminoglycans, as well as extraocular muscle oedema, result in increased orbital tissue volume and trigger the onset of TO symptoms. The pathophysiology of TO is complex and has not been fully unexplained to date. Orbital fibroblasts show expression of the TSHR, which is the main target of autoimmunity. It has been hypothesised that T-cell activation induced by orbital receptor stimulation by the target antibody results in orbital tissue infiltration, triggering a cascade of events which leads to the production of cytokines, growth factors and reactive oxygen species (ROS). ROS cause damage to many components of the cell: the cell membrane through the peroxidation of lipids and proteins leading to a loss of their function and enzymatic activity. Oxidative stress leads to the activation of the antioxidant system, which operates through two mechanisms: enzymatic and non-enzymatic. Assessment of the concentration of oxidative stress markers and the concentration or activity of anti-oxidative system parameters enables the evaluation of oxidative stress severity, which in the future may be utilized to assess treatment efficacy and prognosis in patients with active OT.


2021 ◽  
Vol 75 ◽  
pp. 437-447
Author(s):  
Bożena Gabryel ◽  
Roksana Duszkiewicz

Sestrins are highly conserved proteins that regulate cell growth, metabolism, survival and proliferation under oxidative stress, genotoxic stress, hypoxia or endoplasmic reticulum stress. Sestrins affect cell signaling by inhibiting the production of reactive oxygen species, activating the AMP-activated protein kinase (AMPK), inhibiting the mTOR pathway and acting as a positive regulator of autophagy. Therefore, their protective role against cancer, metabolic disorders, cardiovascular diseases and neurodegeneration is increasingly being postulated. The article describes the mechanisms of action of sestrins and their meaning in aging and age-related diseases. The latest studies indicating their physiological significance and role in key signaling pathways controlling the cell metabolism and survival under stress conditions were also discussed.


2021 ◽  
Vol 75 ◽  
pp. 456-473
Author(s):  
Emilia Zgórzyńska ◽  
Klaudia Krawczyk ◽  
Patrycja Bełdzińska ◽  
Anna Walczewska

Neurodegenerative diseases are one of the most important medical and social problems affecting elderly people, the percentage of which is significantly increasing in the total world population. The cause of these diseases is the destruction of neurons by protein aggregates that form pathological deposits in neurons, glial cells and in the intercellular space. Proteins whose molecules are easily destabilized by point mutations or endogenous processes are alpha-synuclein (ASN), tau and TDP-43. Pathological forms of these proteins form characteristic aggregates, which accumulate in the neurons and are the cause of various forms of dementia and motor disorders. The most common causes of dementia are tauopathies. In primary tauopathies, which include progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), Pick’s disease (PiD), and frontotemporal dementia (FTD), modified tau molecules disrupt axonal transport and protein distribution in neurons. Ultimately, the helical filaments and neurofibrillary tangles of tau lead to neuron death in various structures of the brain. In Alzheimer’s disease hyperphosphorylated tau tangles along with β amyloid plaques are responsible for the degeneration of the hippocampus, entorhinal cortex and amygdala. The most prevalent synucleinopathies are Parkinson’s disease, multiple system atrophy (MSA) and dementia with Lewy bodies, where there is a degeneration of neurons in the extrapyramidal tracts or, as in MSA, autonomic nerves. TDP-43 inclusions in the cytoplasm cause the degeneration of motor neurons in amyotrophic lateral sclerosis (ALS) and in one of the frontotemporal dementia variant (FTLD-TDP). In this work ASN, tau and TDP-43 structures are described, as well as the genetic and sporadic factors that lead to the destabilization of molecules, their aggregation and incorrect distribution in neurons, which are the causes of neurodegenerative diseases.


2021 ◽  
Vol 75 ◽  
pp. 417-425
Author(s):  
Miłosz Miedziaszczyk ◽  
Patrycja Ciabach ◽  
Edmund Grześkowiak ◽  
Edyta Szałek

There is an increasing number of people who go vegetarian. Some young parents also switch to this diet. The safety of vegetarian diets, especially vegan diets, is very important, especially during pregnancy. Unfortunately, reference publications do not provide coherent data on the safety of vegetarian diets during pregnancy. On the one hand, the vegan diet has advantages because it reduces the risk of heart disease and gestational diabetes. On the other hand, vegetarians/vegans should be aware of potential deficiencies of some nutrients (iron, zinc, vitamin B12, vitamin D, omega-3 fatty acids, calcium, iodine) and the clinical consequences for the fetus. For example, iron deficiency may affect cognitive abilities, behavior, intelligence and increase the risk of preterm birth and low birth weight of infants. Plant food contains non-haem iron with variable absorption. Therefore, the vegan diet should include nutrients increasing the bioavailability of iron, e.g. ascorbic acid, carotene and retinol. Due to the fact that animal food is the main source of vitamin B12, vegans are at a very high risk of vitamin B12 deficiency, which will affect the infant’s weight at birth. Low level of vitamin D, which is prevalent in animal food, is the most common deficiency among vegans and lacto-ovo vegetarians. This vitamin prevents gestational diabetes, reduces insulin resistance and guarantees normal function of the musculoskeletal system. Zinc deficiency during pregnancy may lead to preterm birth, neural tube defects or even miscarriage. In view of the clinical consequences of potential deficiencies of nutrients, the vegetarian/vegan diet should be well balanced.


2021 ◽  
Vol 75 ◽  
pp. 426-436
Author(s):  
Małgorzata Augustyniak

The protective effect of selenium against colorectal cancer or adenoma is still a controversial issue. Although there are well-described (pato)physiological protective mechanisms of selenium against colorectal cancer, the results of the studies from 1998-2018 are inconclusive and need to be considered in the future. Neither observational nor experimental studies present consistent results. Although the Cochrane review showed that well-designed randomized clinical trials (RCTs) presented no beneficial effect of selenium supplementation on cancer incidence, well-designed RCTs confirming the protective effect of selenium supplementation against colorectal adenoma or colorectal polyp recurrence have been found in subject-related literature. In the reviewed studies, selenium concentration was measured in the blood serum/toenail or in diet. It is of great importance to highlight that blood selenium concentration depends on the concentration of this micronutrient in food, which in turn depends on selenium content in soil, bioavailability of selenium, which is different in various geographical regions, and forms of selenium. Selenium circulating in blood as a component of selenoproteins participates in oxidoreduction, thus reducing the risk of developing colorectal cancer. Despite this well-known protective mechanism against colorectal cancer occurrence, half of the reviewed studies did not confirm the protective properties of selenium. To sum up, the current state of knowledge on the association between selenium and colorectal cancer or adenoma has revealed not only inconclusive results of the studies, but has also shown that there is a need to conduct more prospective studies focused on selenium supplementation and colorectal cancer as this research is limited.


2021 ◽  
Vol 75 ◽  
pp. 398-405
Author(s):  
Marcin Kosmalski ◽  
Monika Różycka-Kosmalska ◽  
Joanna Sikora ◽  
Tadeusz Pietras

Diabetes mellitus (DM) is not a single disease, but a group of diseases that are characterized by chronic hyperglycemia and risk of damage to tissues and organs. The mechanisms of its development are different and due mainly to disorders of insulin secretion or its effects. For this reason, 4 types of DM have been distinguished. One of them is a specific type of DM, determined, inter alia, by the use of certain psychotropic medications. Chronic hyperglycemia often occurs in association with some of these drugs, but in many cases it is categorized erroneously as type 2 (T2DM) or 1 (T1DM). The relationship between DM and psychiatric disorders is bi-directional, involving two mutually independent risk factors for the development of the disease. However, not all patients with a mental illness develop carbohydrate metabolism disorders, which is due to a varied diabetogenic potential and mechanisms of action of psychotropic medications. In clinical practice, questions concerning the frequency of this type of DM, risk factors of its development and hyperglycemic mechanism of psychotropic medications arise. Therefore, the aim of this article is to attempt to answer these questions. From a practical point of view, obtaining such information should allow for the development of appropriate diagnostic and therapeutic procedures.


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