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.

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.

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.

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.

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.

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.

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.

[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 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.

[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.

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.

[Oxidative stress in multiple sclerosis]. / Stres oksydacyjny w stwardnieniu rozsianym.

Accumulating data indicate that oxidative stress (OS) plays a major role in the pathogenesis of multiple sclerosis (MS). Reactive oxygen species (ROS), leading to OS, generated in excess primarily by macrophages, have been implicated as mediators of demyelization and axonal damage in MS. ROS cause damage to main cellular components such as lipids, proteins and nucleic acids (e.g., RNA, DNA), resulting in cell death by necrosis or apoptosis. In addition, weakened cellular antioxidant defense systems in the central nervous system (CNS) in MS, and its vulnerability to ROS effects may augmented damage. Thus, treatment with antioxidants might theoretically prevent propagation of tissue damage and improve both survival and neurological outcome. Central nervous system is particularly susceptible to ROS-induced damage due to the high oxygen demands of the brain and low concentration of endogenous antioxidants. Its refer both enzymatic antioxidants: catalase, glutathione peroxidase, glutathione reductase, superoxide dismutase and nonenzymatic antioxidants glutathione, vitamins A,C,D, coenzym Q, uric acid etc. Enzymatic and non enzymatic antioxidants like vitamins, micro and macro elements could regulate progress and function different immunologic cells. Modulation of immunologic processes by this components could be an effective method in decreased risk of incidence of disease and(or) treatment of MS or other immunologic diseases.

[Total antioxidant status concentration in blood plasma of professional sportsmen after dosed physical exercise]. / Calkowity potencjal antyoksydacyjny w osoczu sportowców po dozowanym wysilku fizycznym.

UNLABELLED: The mechanism of functioning of the well-balanced protection system against free radicals is based on the mutual and synergistic activity of its all elements. One of the first organism reactions to physical effort is an elevated oxygen requirement due to an increased rate of metabolism, particularly in the skeletal muscles involved in performing physical work. In case of insufficient antioxidative system of blood plasma, free radicals attack the erythrocytic membrane externally and internally, leading to formation of considerable amounts of reactive oxygen species (ROS). The aim of this study was to evaluate the influence of dosed submaximal and maximal physical exercise on the plasma total antioxidant status (TAS) concentration in professional sportsmen and in subjects of normal physical activity. MATERIAL AND METHODS: 41 rugby players (junior and senior group) and 20 men of normal physical activity (control group) were the subject of the study. The plasma TAS concentration was determined: before an effort in the control group, and after 30-minute restitution period in sportsmen. RESULTS: The concentration of TAS values in subjects of normal physical activity before exercises were on average 0.65 +/- 0.15 mmol/l. In the junior group after the dosed submaximal physical exercise, the mean TAS concentration was 0.69 +/- 0.29 mmol/l, but the dosed maximal exercise lead to an increase in TAS values - 0.73 +/- 0.34 mmol/l. The higher plasma TAS concentration after the dosed submaximal physical exercise was observed in the senior group as compared to the junior group, and was on average 0.93 +/- 0.22 mmol/l. However, after the maximal exercise, the TAS concentration decreased and its average value was 0.66 +/- 0.26 mmol/l. CONCLUSIONS: The results of the study indicate that the intensity of performed exercises affects the plasma TAS concentration during a single physical activity. The plasma TAS concentration was higher in sportsmen regardless of the type of effort as compared to the control group. Supplementation of micromolecular antioxidants present in nutrients ingested by the sportsmen might have influenced the study outcomes.

[Influence of complex compounds on the activity of antioxidant enzymes in neoplastic diseases of the digestive tract]. / Wplyw zwiazków koordynacyjnych na aktywnosé enzymów antyoksydacyjnych w chorobach nowotworowych przewodu pokarmowego.

UNLABELLED: Chemotherapy is an important field of clinical medicine and pharmacology Chemotherapy is the main method of treating the neoplasm. It involves treating the neoplastic disease with the use of natural or synthetic anticancer drugs commonly known as the cytostatics. The cancer therapy involving the cytostatics is a difficult and not always effective process, which requires taking into consideration the mechanisms of action, pharmacokinetics and the dosage schemas. The complexity of the chemotherapy is influenced by: still incomplete knowledge of causes of neoplasm formation, slight biological differences between the cancer cells and the regular cells, very small selectivity of cytostatics' action, narrow therapeutic index of the anticancer drugs, high toxicity for healthy cells and unsatisfactory anticancer activity. The aim of the study was to obtain the complex compounds of copper (II), and especially of dinitrate (V) di (3,4, 5-trimethyl-N1-pyrazol-kappaN2) copper (II), and its subsequent testing for pro- and antioxidative activity in people suffering from neoplastic diseases of the digestive tract (colorectal and gastric carcinoma). Material and methods. The activity of catalase was determined in erythrocytes patients suffering from colorectal and gastric carcinoma and in control group (hernia, chronic gastric ulcer disease and haemorrhoids) using the method of Beers and Sizer at 240 nm on the Beckman spectrophotometer. RESULTS: The results of the test on catalase in patients suffering from colorectal and gastric carcinoma indicate that the addition to the blood of the complex compound of Cu(II) significantly influences the activity of the enzyme in comparison with the control group in which the substance tested was not used. In the tests a marked statistical difference was observed between the studied and the control group. CONCLUSION: The results reveal that chemical compounds, that is, dinitrate (V) di (3,4,5-trimethyl-N1-pyrazol-kappaN2) copper (II), has a significant influence on the activity of catalase, the antioxidant enzyme.

[In vitro biological activity of new platinum(II) and palladium(II) complex compounds]. / Aktywnoss biologiczna--in vitro nowych zwiazków koordynacyjnych platyny(II) i palladu(II).

UNLABELLED: A nitrogen ring is present in many biological molecules, which play an important part in cell division as well as in genetic information transfer. It is also a part of the purine system, which builds DNA and has potential places/spots of platinum drug co-ordination. Therefore, it may be hoped, that platinum(II) complexes with diazol ligands will have considerable affinity for DNA binding sites. The work was aimed at assessment of biological activity and especially of cytotoxic activity, of new complex connections of the selected diazols with Pt(II) and Pd(II) ions. MATERIALS AND METHODS: The MTT test is aimed at the assessment of cytotoxicity of chemical compounds. It consists in the colorimetric determination of a product--farmazon, formed after adding MTT (bromide 3[4,5-dimetylo-2-ilo]-2,5-difenylotetrazolu) to the culture suspension in the presence of the compound subject to the test. All the tested Pt(II) complexes before adding to the cell cultures were dilluted in DMF. MTT tests for individual complexes were conducted on two cell lines L1210 and P388. RESULTS: Compounds 13, 21 and 25 on P388 neoplastic cell revealed about three times smaller in-vitro cytotoxicity, whereas platinum(II) and palladium(II) complexes 13, 21, 25, 43, 46, revealed cytotoxicity being about 3-4 times smaller than the reference cisplatin. Complex 45 revealed eight times smaller activity and complex 44 revealed significantly small, about two hundred smaller activity. CONCLUSION: Based on the MTT tests it may be concluded that compounds 13, 21 and 25 reveal selective cytotoxicity to P388 neoplastic cells.

[Testing antineoplastic activity of new platinum(II) and palladium(II) complex compounds]. / Badanie aktywnosci przeciwnowotworowej nowych zwiazków koordynacyjnych platyny(II) i palladu(II).

UNLABELLED: A pyrazole system is incorporated in many biological molecules which play an important part in genetic processes. It seems that co-ordinating biological molecules, which would serve as carriers, should contribute to minimising the toxic effects of the potential platinic drugs. AIM OF THE STUDY: Assessment of in vivo biological activity, and in particular of antineoplastic activity of new platinum(II) and palladium(II) complexes. MATERIAL AND METHODS: The assessment of toxicity of the compounds was made with the Deichmann and Le Blanck method. The antineoplastic activity of the new complex compounds--pyrazole derivatives with Pt(II) and Pd(II) ions was tested on mouse L1210 leukemia cell culture and on lymphatic leukemia P388. BDF1 or CDF1 mice divided into groups of 5-9 animals were subject to the tests. RESULTS: Complexes 13, 21, 25, 16, 24 and 28 did not reveal any antineoplastic activity to the mouse L1210 leukemia, whereas complexes 13, 21 and 25 revealed in-vivo antineoplastic activity to the P388 leukemia, extending the mouse's survival time by about 50%. The control group consisted of mice which were administered a 14% methylcellulose solution. CONCLUSIONS: As a result of the tests conducted to asses the in-vivo antineoplastic activity it was found that the 25 complex demonstrates the strongest activity to the P388 leukemia. It may be presumed that it is caused by trans configuration of the complex predisposing to the creation of interstrand cross-links. It may be also caused by the presence of the chloromethyl substituents, located on N1 nitrogen atom of the ligand, which increases the capacity of nitrogen N7 guanine alkylation in DNA.

[Role of free radicals in the physiological processes]. / Wolne rodniki tlenu i azotu w fizjologii.

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are produced during variety of biological processes. Low concentration of these molecules influences cell growth, differentiation or proliferation. Above derivatives of oxygen and nitrogen take part in physiological processes such as signal transduction, regulation of protein kinases or transcription factors. ROS and RNS regulate redox balance, regulate immune responses, activate macrophages and neutrophils. Under theirs' control is cell adhesion and relaxation of smooth muscles. These molecules are very important for correct function and life of the cell.

[Chosen non-enzymatic substances that participate in a protection against overproduction of free radicals]. / Wybrane substancje nieenzymatyczne uczestniczace w procesie obrony przed nadmiernym wytwarzaniem wolnych rodników.

Free radicals are substantial elements that take part in proper function of metabolic pathways of human cells and tissues in hydrophobic as well as in hydrophilic environment. Nevertheless overproduction of above molecules causes oxidative stress, a process which is very harmful for lipids, proteins, and others molecules what reduces their normal function. To protect against adverse effects of free radicals and theirs derivatives to human body there is a group of antioxidants divided into enzymatic and non-enzymatic substances. Enzymatic antioxidants are represented mainly by enzymes such as: copper-zinc superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR). Glutathione (GSH), thioredoxin (Trx), vitamins, melatonin, polyphenols, trace elements, albumin, and others function as non-enzymatic free radicals scavengers. This work in a brief way describes properties of chosen representants of non-enzymatic antioxidant system.

[The influence of degenerative changes on the production of free radicals and the lipid peroxidation at the patients after alloplasty of the hip joint]. / Wplyw zmian zwyrodnieniowych na generacje wolnych rodników tlenowych i peroksydacje lipidów u chorych po przebytej alloplastyce stawu biodrowego.

UNLABELLED: Since now researches claimed that rheumatoid arthritis was not characterized with an inflammatory process due to the lack of vessel in the cartilaginous tissue. Nevertheless, an inflammation of synovial membrane and a reduction of activity of articulation co-exist with rheumatoid arthritis. Recent results have proved that the above disease is connected with an oxidative stress. AIM OF THE STUDY: The aim of this investigation was to estimate changes of nitric oxide (NO) in plasma and malondialdehyd (MDA) concentration in red blood cells of patients suffering from an alloplastic of the hip joint. We also measured how physical activity in a reduced motor activity influences the NO and MDA concentration. MATERIAL AND METHODS: Malonyl dialdehyde (MDA) concentration in RBCs was assayed with Placer method, nitrogen concentration in blood plasma was determined using the Griess indirect method. Biochemical tests have been performed on a group of 36 patients with osteoarthritis hospitalised at the Traumatic-Orthopaedic Department of the Ministry of Internal Affairs and Administration Hospital in Lodz, Poland. A control group included 21 subjects with normal physical activity. RESULTS: The concentration of nitric oxide in plasma of patients that were operated was lower than in a healthy control group. Ten days after the operation it decreased, but after a month it was higher than before the operation. The concentration of MDA in red blood cells was higher before and after the alloplastic than in the healthy control group. Ten days after operation the concentration of MDA was lower about 15.8% but after 30 days it lowered up to about 26.3% in comparison to the concentration before the operation. CONCLUSIONS: Our results are not the same as those shown by other researches which suggest increased production of nitric oxide. Reduction of the motor activity due to degenerative joint disease and alloplastic causes reduction in lipid peroxidation of red blood cells.