Relationship between Biochemical Pathways and Non-Coding RNAs Involved in the Progression of Diabetic Retinopathy.

Diabetic retinopathy (DR) is a progressive blinding disease, which affects the vision and quality of life of patients, and it severely impacts the society. This complication, caused by abnormal glucose metabolism, leads to structural, functional, molecular, and biochemical abnormalities in the retina. Oxidative stress and inflammation also play pivotal roles in the pathogenic process of DR, leading to mitochondrial damage and a decrease in mitochondrial function. DR causes retinal degeneration in glial and neural cells, while the disappearance of pericytes in retinal blood vessels leads to alterations in vascular regulation and stability. Clinical changes include dilatation and blood flow changes in response to the decrease in retinal perfusion in retinal blood vessels, leading to vascular leakage, neovascularization, and neurodegeneration. The loss of vascular cells in the retina results in capillary occlusion and ischemia. Thus, DR is a highly complex disease with various biological factors, which contribute to its pathogenesis. The interplay between biochemical pathways and non-coding RNAs (ncRNAs) is essential for understanding the development and progression of DR. Abnormal expression of ncRNAs has been confirmed to promote the development of DR, suggesting that ncRNAs such as miRNAs, lncRNAs, and circRNAs have potential as diagnostic biomarkers and theranostic targets in DR. This review provides an overview of the interactions between abnormal biochemical pathways and dysregulated expression of ncRNAs under the influence of hyperglycemic environment in DR.

The importance of thiamine (vitamin B1) in humans.

Thiamine (thiamin, B1) is a vitamin necessary for proper cell function. It exists in a free form as a thiamine, or as a mono-, di- or triphosphate. Thiamine plays a special role in the body as a coenzyme necessary for the metabolism of carbohydrates, fats and proteins. In addition, it participates in the cellular respiration and oxidation of fatty acids: in malnourished people, high doses of glucose result in acute thiamine deficiency. It also participates in energy production in the mitochondria and protein synthesis. In addition, it is also needed to ensure the proper functioning of the central and peripheral nervous system, where it is involved in neurotransmitter synthesis. Its deficiency leads to mitochondrial dysfunction, lactate and pyruvate accumulation, and consequently to focal thalamic degeneration, manifested as Wernicke's encephalopathy or Wernicke-Korsakoff syndrome. It can also lead to severe or even fatal neurologic and cardiovascular complications, including heart failure, neuropathy leading to ataxia and paralysis, confusion, or delirium. The most common risk factor for thiamine deficiency is alcohol abuse. This paper presents current knowledge of the biological functions of thiamine, its antioxidant properties, and the effects of its deficiency in the body.

Lutein and Zeaxanthin and Their Roles in Age-Related Macular Degeneration-Neurodegenerative Disease.

Lutein and zeaxanthin belong to the xanthophyll family of carotenoids, which are pigments produced by plants. Structurally, they are very similar, differing only slightly in the arrangement of atoms. Key sources of these carotenoids include kale, savoy cabbage, spinach, broccoli, peas, parsley, corn, and egg yolks. The recommended daily intake of lutein is approximately 10.0 mg and that of zeaxanthin is 2 mg. Lutein intake in adults varies, with average intakes being 1-2 mg/day. Due to the lack of synthesis of consumption of these compounds in humans, these substances are extremely important for the proper functioning of certain organs of the body (eye, skin, heart, intestines). Eating a lot of dark leafy vegetables and some fruits can help to prevent our bodies from developing diseases. The protective effects of carotenoids are mainly related to their defense against oxidative stress and their ability to scavenge free radicals. Lutein and zeaxanthin are the only dietary carotenoids that accumulate in the retina, specifically the macula, and are called macular pigments. These carotenoids are concentrated by the action of specific binding proteins such as StARD3, which binds lutein, and GSTP1, which binds zeaxanthin and its dietary metabolite, mesozeaxanthin. It has been shown that supportive therapy with lutein and zeaxanthin can have a beneficial effect in delaying the progression of eye diseases such as age-related macular degeneration (AMD) and cataracts. This article presents the current state of knowledge on the role of lutein and zeaxanthin, especially from human studies targeting their metabolism and bioavailability, with recommendations to consume xanthophyll-rich foods.

Assessment of DNA damage profile and oxidative /antioxidative biomarker level in patients with inflammatory bowel disease.

<b>Aim:</b> The purpose of this study was to investigate the oxidative DNA damage, pro-antioxidant status in Polish patients with inflammatory bowel disease (IBD). <br><b>Methods:</b> Oxidative DNA damage was measured by comet assay techniques; nitric oxide (NO) and plasmatic lipid peroxidation (MDA) as oxidative stress were valuated by colometric methods; superoxide dismutase (SOD1), catalase (CAT) and glutathione peroxidase (GPx1) as antioxidative defense were determined by spectrophotometric methods. <br><b>Results:</b> The level of oxidative DNA damage in IBD patients was significantly higher in relation to controls (P = 0.01). Alike, in control subject as well as in patients with IBD, lymphocytes are characterized by complete repair of DNA damage. A significant decrease of SOD (P = 0.031), CAT (P = 0.006), GPx1 (P = 0.001) activity was seen in IBD patients vs control. MDA (P = 0.001) and NO (P = 0.001) concentrations were significantly increased in IBD patients as compared to healthy subjects. <br><b>Conclusions:</b> Our results may be due to the induction of DNA repair genes which may occur at the stage of the pathological changes (IBD) that may be caused by excessive oxidative stress. However, the cause of this relationship, and whether it is direct or indirect, remains to be explored.

Environmental factors increasing the risk of activation and development of inflammatory bowel diseases / Czynniki srodowiskowe zwiekszajace ryzyko aktywacji i rozwoju chorób zapalnych jelit.

Inflammatory bowel disease (IBD) is a particularly troublesome disease that has a huge impact on the human digestive tract, mainly the intestine. These diseases manifest themselves as chronic, uncontrolled inflammation of the intestines, difficult to control, with periods of spontaneous exacerbations and remissions. Depending on the variety of symptoms present and their location in the human gastrointestinal tract, these diseases can occur in various forms. The most common: ulcerative colitis (UC) and Crohn's disease (CD). The underlying cause of activation as well as subsequent development is not clearly defined, but it is known that these disorders are autoimmune. The pathogenesis of IBD is associated with chronic idiopathic, recurrent gastrointestinal inflammation. Exposure to many environmental factors, which are partially discussed in the following work, especially in people genetically predisposed to the development of these diseases, can activate the chronic inflammatory process of the intestine.

Association between SOD1, CAT, GSHPX1 polymorphisms and the risk of inflammatory bowel disease in the Polish population.

PURPOSE: The main aim of this study was investigate the association between the genetic polymorphism of antioxidant enzyme genes: SOD1, CAT and GSHPX1 and the risk of inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis in the Polish population. METHODS: A total of 445 subjects including 200 patients with IBD and 245 controls were allowed in this study. We determined activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx1) and examination their association with the SNPs of respective genes (SOD1 +35A/C, CAT C-262T and GSHPX1 Pro197Leu). RFLP technique was used to determine the selected genes polymorphisms. Antioxidant enzymes activity were evaluated in erythrocyte hemolysate of 23 patients with non-active IBD and 30 healthy participants. RESULTS: The A/C genotype and the C allele frequencies of A/C polymorphism of SOD1 gene were significantly associated with the reduced risk of IBD (OR=0.43; 95% CI 0.23; 0.83). Alike, C/T (OR=0.45; 95% CI= 0.29; 0.70) and T/T genotype (OR=0.43; 95% CI= 0.21; 0.87) of GSHPX1 gene polymorphism diminished the susceptibility to IBD. A significant decrease of CAT (P=0.028) and increase of GPx1 (P=0.025) enzyme activities were seen in IBD patients compared to control. CONCLUSIONS: Our data confirm dysregulated antioxidant capacity in patients suffering from IBD. Both, the SOD1 A/C genotype as well as GSHPX1 C/T and T/T genotypes may be associated with a reduction risk of IBD in the Polish population.

Analysis of antioxidative factors related to AMD risk development in the polish patients.

PURPOSE: Age-related macular degeneration (AMD) is a major cause of blindness in developed countries. Oxidative mechanisms may play a key role in the aetiology of AMD. The main aim of this study was to investigate antioxidative markers in the pathogenesis of AMD. METHODS: A total of 510 subjects including 240 patients with AMD (mean age 77.9 ± 8.5 year) and 270 controls (mean age 74.0 ± 10.4 year) were allowed in this study. We measured activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and examined their association with the SNPs of respective genes (SOD1 + 35A/C, CAT C-262T and GPx Pro197Leu). Restriction fragment length polymorphism (RFLP) technique was used to determine the selected gene polymorphisms. Sixty subjects including 30 patients with AMD (mean age 69.4 ± 9.3) and 30 controls (mean age 64.6 ± 8.2) were enrolled to determine the activity of antioxidant enzymes by spectrometry method. RESULTS: A significant decrease in enzymes, SOD (p = 0.011), CAT (p = 0.002) and GPx (p ≤ 0.001) in AMD patients compared to controls, was indicated. The risk of susceptibility to AMD was significantly higher in patients with AMD who had Pro197Leu C/T genotype of GPx (OR = 2.78; 95% CI = 1.78-4.35). The A/C genotype and the C allele frequencies of A/C polymorphism of SOD1 gene significantly reduce the risk of AMD (OR=0.48; 95% CI 0.27; 0.85). CONCLUSION: In conclusion, our data showed that insufficient antioxidant capacity may have an important role in age-related macular degeneration. The polymorphism of GPx Pro197Leu may reduce the ability to scavenge free radicals in retina and contribute to the development of AMD.

Evaluation of Effect CAT -262C/T, SOD + 35A/C, GPx1 Pro197Leu Polymorphisms in Patients with IBD in the Polish Population.

Inflammatory bowel disease (IBD) are a heterogeneous group of disorders in the course dominated by chronic, recurrent gastrointestinal inflammation. It is believed that the activation of IBD occurs in patients with a genetic predisposition to their development. Chronic inflammation develops as a result of an excessive reaction of the immune system principally under the influence of environmental risk factors. Among them, it has been shown that the mechanism of oxidative stress is associated with the pathophysiology of inflammatory bowel disease, responsible for the commencement and progress of these diseases. The aim of the study was the relationship between single nucleotide polymorphisms (SNPs) of individual antioxidant enzymes, and the prevalence of inflammatory bowel disease that may be associated with increased levels of oxidative stress. MATERIAL AND METHODS: A total of 111 IBD patients, including 65 patients with ulcerative colitis (UC) and 46 with Crohn's disease (CD) and 125 healthy controls recruited from the Polish population, were genotyped for CAT -262C / T (rs1001179), SOD + 35A / C (rs2234694), GPx Pro 197 Leu polymorphisms. Genotyping of CAT, SOD, GPx gene polymorphism was performed by a RFLP-PCR. RESULTS: The performed analysis of genetic polymorphisms of antioxidant enzymes showed that polymorphic variant of the CAT -262 C / T may have protective effects in patients with ulcerative colitis in the range of genotype C / T; OR = 0.49 (0.25-0.99), p = 0.044. Trend protective, but statistically unrelated, it was also observed for genotype T / T and T allele of the same polymorphism and genotypes and alleles + 35A / C SOD1 in UC as well as polymorphic variants CAT -262 C / T, Pro197Leu of GPx1, + 35A / C SOD1 in CD. The results were compared with a control group of potentially healthy individuals without such diseases. CONCLUSIONS: It has been shown that the polymorphism of antioxidant enzymes CAT gene -262 C / T may have protective effects in patients who are carriers of a genotype C / T at the UC. The potential protective effect without statistical relationships were also observed for other genotypes and alleles studied polymorphic variants of antioxidant enzymes in CD and CAT- 262C / T and + 35 A / C SOD1 in UC. Conducted our audit should be extended to more group of patients in order to assess whether or not to confirm the observed during analysis, the protective effect of CAT-262 C / T in ulcerative colitis and other trends observed for other polymorphic variants tested genes.

Evaluation pro/antioxidant balance in patients with wet form of age-related macular degeneration. / [Ocena równowagi proantyoksydacyjnej u chorych na wysiekowa postac zwyrodnienia plamki zwiazanego z wiekiem].

Objective: The aim of study was to evaluate the ability of the enzymatic antioxidant barrier to protect against peroxidation in patients with wet age-related macular degeneration, as compared to healthy subjects. Material and methods: Hemolysate blood samples collected from 25 patients with wet form age-related macular degeneration and 25 healthy controls were analysed to determine the activity of superoxide dismutase (using Misra and Fridovich method), catalase (using Beers and Sizer method), glutathione peroxidase (using Sedlak and Lindsay method modified by Little and O'Brien), and malondialdehyde concentration (using Placer method). Results: We observed a statistically significant decrease in the activity of following enzymes in patients with wet age-related macular degeneration, as compared to controls: superoxide dismutase (2086.3 vs. 2348.5 U/gHb/100 ml; p ≤ .05), catalase (6.9 vs. 7.6 BU/gHb, p ≤ .05) and glutathione peroxidase (36.3 vs. 45.8 U/gHb; p ≤ .05). At the same time, an increase in age-related macular degeneration thiobarbituric acid reactive substance concentration was demonstrated in patients with wet age-related macular degeneration, as compared to healthy subjects (.119 vs. .286 µmol/gHb; p ≤ .001). Conclusion: The obtained results indicate inefficient enzymatic antioxidant system which manifests as intense peroxidation in patients with age-related macular degeneration.

Evaluation of selected indicators of antioxidant status in patients with head and neck cancer.

INTRODUCTION: The aim of the study was to evaluate lipid peroxidation (TBARS) and the antioxidant enzymatic barrier in patients with head and neck cancer and in healthy controls. MATERIAL AND METHODS: Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA) were measured by spectrometry in red blood cells of 22 patients and healthy controls. RESULTS: Decreased activity of SOD, CAT, and GPx as well as an increased concentration of MDA was found in cancer patients in comparison to healthy controls. DISCUSSION: Increased lipid peroxidation in red blood cells of cancer patients indicates an intensification of oxidative stress reactions. Measurements of the activity of the antioxidant enzymes point unambiguously to a reduced antioxidant capacity in head and neck cancer patients. However, this was a pilot study with a low number of participants. Moreover, future research should take into account genetic and extragenetic factors.

Evaluation of oxidative DNA damage and antioxidant defense in patients with nasal polyps.

OBJECTIVES: The presence of inflammatory cells indicates the development of epithelial cell injury in nasal polyposis (NP) and the potential for production of high levels of reactive oxygen and nitrogen species. The aim of our study was to clarify the role of oxidative stress and antioxidant status in the deterioration accompanying NP. METHODS: Twenty patients (11 men) aged 47.2 ± 17.0 years with nasal polyps were included in the study. Twenty healthy subjects (7 men) aged 48.2 ± 15.3 years formed the control group. The erythrocyte activities of antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), and plasma nitric oxide (NO) concentrations were measured. An alkaline comet assay was used to determine the extent of blood lymphocyte DNA damage of oxidized purines as glicosylo-formamidoglicosylase (Fpg) sites, and oxidized pyrimidines as endonuclease III (Nth) sites. RESULTS: A significant increase of NO (P < 0.05) and non-significant decreases of SOD (P > 0.05), CAT (P > 0.05), and GPx (P > 0.05) were seen in NP patients compared to healthy controls. The level of blood lymphocyte oxidative DNA damage in NP patients was significantly higher compared to the control group (P = 0.01). DISCUSSION: The blood lymphocyte DNA damage level increased in patients with NP. Elevated DNA damage may be related to overproduction of reactive oxygen and nitrogen species and/or decreased antioxidant protection.

DNA damage and oxidant-antioxidant status in blood of patients with head and neck cancer.

Oxidative stress induces a cellular redox imbalance that has been found to be present in various cancer cells, and overproduction of free radicals may be related to oncogenic stimulation. We investigated the activity of the following antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA) concentrations in blood of patients with head and neck squamous cell carcinoma (HNSCC) compared with the control group. A comet assay was used to assess DNA damage. A nonsignificant increase of MDA and a decrease of SOD, CAT, and GPx (p>0.05) were seen in HNSCC patients compared with controls. It was found that the level of oxidative DNA damage in HNSCC patients was significantly higher compared with the control group (p ≤ 0.001). Our observations suggest that HNSSC patients may represent an impaired antioxidant defense system, resulting in DNA damage and genome instability. It has to be also considered that an oxidant/antioxidant imbalance may be connected to the complex mechanism leading to the DNA damage indicated in the blood of patients with head and neck cancer.

Association of IL1ß and IL4 gene polymorphisms with nasal polyps in a Polish population.

Imbalance between proinflammatory and anti-inflammatory cytokines may regulate the inflammatory reaction in the nasal polyps. Polymorphisms in the regulatory regions of the cytokines genes may influence their expression. The aim of this study was to investigate the relationship between an IL-1ß and IL-4 promoter polymorphisms and nasal polyps. The C-511T promoter polymorphism of the IL-1ß gene and C-590T promoter polymorphism of the IL-4 gene were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis in 208 Polish patients with nasal polyps and 200 healthy Polish subjects. The risk of susceptibility to NP was significantly higher in patients with NP who had -511 T/T genotype of IL1ß than in controls (OR 3.07; 95 % CI 1.18-7.99). No statistically significant differences were found between NP patients and the control group with regard to genotype distribution and allele frequencies of C/T polymorphism of IL4 gene. Our study demonstrated that the TT genotype for C-511T mutation associated with the risk of developing NP in a Polish population.

Evaluation of oxidative stress markers in pathogenesis of diabetic neuropathy.

Experimental evidences suggest that hyperglycaemia-induced overproduction of reactive oxygen species and subsequent damage to proteins, lipids and DNA may play a key role in the development of distal symmetric polyneuropathy (DSPN)-the most common complication of diabetes mellitus. The study population consisted of 51 individuals aged 52-82 years classified into 3 groups: 16 patients diagnosed with type 2 diabetes mellitus (T2DM) with DSPN, 16 T2DM patients without DSPN and 19 control subjects without diabetes and neuropathy. The study was conducted to determine the activity of antioxidant enzymes: catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX) and total antioxidant status (TAS) in the examined groups. An alkaline comet assay was used to determine the extent of DNA damage of oxidized purines as glicosylo-formamidoglicosylase (Fpg) sites, and oxidized pyrimidines as endonuclease III (Nth) sites. A significant decrease of SOD (P < 0.05), GPX (P < 0.05) and nonsignificant decrease of CAT (P > 0.05), and TAS status (P > 0.05) were seen in T2DM patients with neuropathy compared to T2DM patients as well as controls. T2DM patients with or without neuropathy revealed significantly lower (P < 0.05) plasma concentration of nitrous oxide compared to the control subjects. Endogenous level of oxidative DNA damage in T2DM patients with DSPN was significantly higher compared both to the controls and T2DM patients without DSPN (P < 0.001). Moreover, lymphocytes isolated from T2DM patients with DSPN were more susceptible to oxidative DNA lesions induced by hydrogen peroxide than from T2DM patients without DSPN (P < 0.001). Our results confirm hypothesis that oxidative stress may play a substantial role in the development and progression of diabetic distal symmetric polyneuropathy.

[The effects of whole-body cryotherapy and melatonin supplementation on total antioxidative status and some antioxidative enzymes in multiple sclerosis patients]. / Wplyw krioterapii ogólnoustrojowej i suplementacji melatonina na calkowity potencjal antyoksydacyjny w osoczu oraz aktywnosc wybranych enzymów antyoksydacyjnych w erytrocytach chorych na stwardnlenie rozsiane.

Oxidative stress is an important factor which contribute to the pathogenesis of lesions in multiple sclerosis (MS). Whole body cryotherapy (WBCT) is often used in treatment neurological and orthopedic diseases. THE AIM, MATERIAL AND METHODS: The aim of this study was to determinate the level of total antioxidative status (TAS) in plasma and activity of superoxide dismutase (SOD) and catalase (CAT) in erythrocytes of MS patients (n = 28) before and after 10 exposures of WBCT (-120 degrees C/3 minutes/day). 16 MS patients during 10 exposures of WBCT additionally were supplemented by 10 mg of melatonin. RESULTS: Increasing of TAS level in plasma as well as supplemented with melatonin and non-supplemented MS patients was observed after 10 exposures of WBCT Melatonin statistically significant increased activity of SOD and CAT in erythrocytes of MS patients treated with WBCT. CONCLUSIONS: Results of our study indicate significant increase of TAS level in plasma of MS patients of WBCT treatment. This indicate that WBCT might be a therapy which suppress oxidative stress in MS patients.

[The role of disorders of the prooxidant-antioxidant system in diabetes etiopathology]. / Znaczenie zaburzen ukladu prooksydacyjno-antyoksydacyjnego dla etiopatologii cukrzycy.

Chronic hyperglycemia is believed to play a pivotal role in the development of diabetic complications. It was found that hyperglycemia triggered a number of mechanisms that evoke overproduction of reactive oxygen species (ROS). Diabetes mellitus is associated with an increased level of free radicals, disturbances of the enzymatic antioxidant defense system and lower concentration of exogenous antioxidants. In consequence, these abnormalities lead to a redox imbalance called oxidative stress. The aim of the present study is to summarize the role of reactive oxygen species and changes in the antioxidant defense system in the development of diabetic complications.

The level of isoprostanes as a non-invasive marker for in vivo lipid peroxidation in secondary progressive multiple sclerosis.

Oxidative stress leads to lipid peroxidation and may contribute to the pathogenesis of lesions in multiple sclerosis (MS), an autoimmune disease characterized by inflammatory as well as degenerative phenomena. Isoprostanes are prostaglandin-like compounds which are formed by free radical catalysed peroxidation of arachidonic acid esterified in membrane phospholipids. They are a new class of sensitive specific markers for in vivo lipid peroxidation. In this study 26 patients (15 females and 11 males; mean age 48.2 ± 15.2 year; mean disease duration 10.0 ± 6.5 year) with secondary progressive MS (SPMS) and 12 healthy controls were enrolled. In patients with multiple sclerosis the lipid peroxidation as the level of urine isoprostanes and the level of thiobarbituric acid reactive species (TBARS) in plasma were estimated. Moreover, we estimated the total antioxidative status (TAS) in plasma. It was found that the urine isoprostanes level was over 6-fold elevated in patients with SPMS than in control (P < 0.001). In SPMS patients TBARS level was also statistically higher than in controls (P < 0.01). However, we did not observed any difference of TAS level in serum between SPMS patients and controls (P > 0.05). In patients with SPMS the lipid peroxidation and oxidative stress measured as the increased level of isoprostanes was observed. Thus, we suggest that the level of isoprostanes may be used as non-invasive marker for a determination of oxidative stress what in turn, together with clinical symptoms, may determine an specific antioxidative therapy in SPMS patients.

Effects of whole-body cryotherapy on a total antioxidative status and activities of antioxidative enzymes in blood of depressive multiple sclerosis patients.

OBJECTIVES: Oxidative stress (OS) plays an important role in the pathogenesis of multiple sclerosis (MS). In MS patients depression is often observed. Cryotherapy might have an effect on OS. The aim of this study was to compare the effects of whole body cryotherapy (WBCT) on changes in total antioxidative status (TAS) of plasma and activities of antioxidative enzymes in erythrocytes from depressive and non depressive MS patients. METHODS: Twenty-two MS patients with secondary progressive disease course (12 depressive and 10 non depressive) were treated with 10 exposures in a cryochamber. Before and after WBCT the plasma TAS and the activities of superoxide dismutase (SOD) and catalase (CAT) in the erythrocytes were measured. RESULTS: The level of TAS in depressive MS group was significantly lower than in non depressive MS (P < 0.0003). WBCT increased the level of TAS in depressive (P < 0.002) more than in non depressive MS patients (P < 0.01). WBCT treatment of MS patients resulted in the significant increase of TAS level in plasma but had no effects on activities of SOD and CAT. CONCLUSIONS: Our results indicate that WBCT suppresses OS in MS patients, especially in depressive patients.

[Effect of melatonin on activity of superoxide dismutase (CuZn-SOD) in erythrocytes of patients during short- and long-term hypokinesis]. / Wplyw melatoniny na aktywnosc dysmutazy ponadtlenkowej (CuZn-SOD) w krwinkach czerwonych chorych w okresie hipokinezji krótko- i dlugoterminowej.

INTRODUCTION: Short- or long-lasting hypokinesis is to a large degree the consequence of negative habits of human beings towards a comfortable and more sedentary lifestyle. The period of decreased physical activity can cause disturbance in the balance between systemic processes of the oxidation and reduction, which leads to an increase in reactive oxygen species (ROS) and oxidative stress generation. The aim of the study was to determine the effect of melatonin administration on the cellular superoxide dismutase (CuZn-SOD) activity in red blood cells of patients with short- and long-term hypokinesis as compared to the group of subjects with normal physical activity. MATERIAL AND METHODS: The study included 33 subjects with immobilization. The study group was divided into two subgroups (depending on hypokinesis duration): group A: 15 subjects classified for total hip alloplasty (a short-lasting decrease in physical activity); group B: 18 subjects suffering from multiple sclerosis or the stroke of brain (the long-term hypokinesis). The control group (group C) comprised 17 subjects with normal physical activity. Melatonin was applied at a dose of 5 mg daily, one hour before sleep. The CuZn-SOD activity in red blood cells was determined, according to the Misra and Fridovich method, in two periods: 1) on the first day, 2) on the 10th day (group A), and 30 days (group B) after melatonin administration. RESULTS: A slight increase in CuZn-SOD activity (+3.1%) was observed in group A 10 days after alloplasty and melatonin administration as compared to group B, where a considerable rise in the enzyme activity (+23.3%) was found 30 days after rehabilitation and melatonin supplementation. The average CuZn-SOD activity in both investigative groups was lower than that in the controls (group C). CONCLUSIONS: It was estimated that the short- and long-lasting hypokinesis leads to an increase in ROS generation, what is confirmed by the increase in CuZn-SOD activity. The results of the study on superoxide dismutase activity indicate that oral administration of melatonin for the period of 30 days has a more favorable influence on antioxidative processes than 10-day's melatonin intake.

Effects of the whole-body cryotherapy on a total antioxidative status and activities of some antioxidative enzymes in blood of patients with multiple sclerosis-preliminary study.

OBJECTIVE: There is evidence that multiple sclerosis (MS) is not only characterized by immune mediated inflammatory reactions but also by neurodegenerative processes. Neutralization of oxidative stress and excitotoxicity, might represent a therapeutic approach to provide neuroprotection in MS. The purpose of this study was to compare changes in total antioxidative status and activities of chosen antioxidative enzymes, such as: SOD, CAT in erythrocytes of patients with MS before and after using WBCT with control group. MATERIALS AND METHODS: 32 patients with multiple sclerosis (ICD10-G35) and 20 healthy subjects were recruited for the study. The examined MS group (n=16) was treated with a series of 10 daily exposures in a cryogenic chamber (2-3 min, from -120 degrees C to -110 degrees C) and program of exercises. The control MS group (n=16) had only exercises. Plasma TAS as well as SOD and CAT activities in erythrocytes were measured. RESULTS: The level of TAS in MS patients was distinctly reduced compared to healthy subjects. After two weeks of WBCT treatment an increase of TAS in the whole examined group (p>0.01) were observed in relation to control MS group. There was not increase of CuZnSOD and CAT activities. CONCLUSION: Our results suggest positive antioxidant effects of WBCT as a short-term adjuvant treatment for patients suffered due to MS.