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Main goal of this research was investigation the protective effects of coenzyme Q10 on methotrexate-induced liver damage. Study was performed on 32 Wistar rats divided in 4 groups, whereas first group received normal saline, second received coenzyme Q10, third received methotrexate alone and fourth group received concomitantly coenzyme Q10 and methotrexate. Morphological and functional changes in liver tissue were performed by biochemical analysis of serum, histopathological analysis of liver tissue sections and determination of parameters of oxidative stress in liver tissue. Administration of methotrexate in rats caused a significant increase of the concentrations of AST, ALT and γ-GT and significant decrease of amount of total proteins in the serum compared with C group of animals. Also, methotrexate significantly increased MDA and AOPP levels in and decreased catalase activity in hepatic tissue. Histopathological analysis showed pronounced liver damage with cellular derangement of hepatic cordons and significant cell swelling, vacuolar degeneration and signs of inflammatory response after methotrexate administration. In group of rats that received coenzyme Q10 8 days after methotrexate administration, injury of liver tissue was significantly decreased with mild disorder of normal radial arrangement of the hepatocytes and only discretely uneven distribution of hepatic glycogen content. In same group, biochemical analysis showed significantly decreased concentrations of serum parameters of liver injury and changes of parameters of oxidative stress were statistically significantly ameliorated compared with results in group that received methotrexate alone. Our results confirmed coenzyme Q10 as a protective agent in methotrexate-induced hepatotoxicity probably due to its antioxidant effects. [ABSTRACT FROM AUTHOR]

Oxidative stress (OS), termed as the imbalance between antioxidants and pro-oxidants in favor of the latter, is highly prevalent in chronic kidney disease (CKD) even at early stages and is gradually increased, in parallel to deterioration of kidney function. In end-stage kidney disease (ESKD), OS is further aggravated and associated with various adverse outcomes, including atherosclerosis and cardiovascular disease. In this review, we aim to present the clinical implications of OS, the pathogenetic causative mechanisms and the potential therapeutic interventions in both hemodialysis and peritoneal dialysis patients. [ABSTRACT FROM AUTHOR]

Carbon tetrachloride (CCl4) is a potent oxidative agent, used in animal models for the induction of liver and neuronal damage. In this study, we tracked the changes in the concentration of malondialdehyde (MDA) and the activity of catalase (CAT) in the brain tissue of Wistar rats exposed to CCl4. The animals were divided into two groups of six rats each. The control group was treated with vehicle olive oil (10 ml/kg) and the experimental group included CCl4-treated animals (1 ml/kg). The level of oxidative stress was determined in a 10% homogenate of whole encephalitic mass (WEM). The levels of MDA in the experimental group were significantly increased (p = 0.0009), while CAT activity was significantly decreased (p = 0.0143) in the CCl4-treated group compared to the control group. The results confirmed the theory about the CCl4-induced oxidative damage on the brain tissue in rats and may be a basis for further research related to potentially protective substances in this animal model. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is one of the main reasons for the mortality connected with tumor diseases. There is still a shortage of examination including the influence of urate pathway enzymes in the progressiveness and invasion of CRC, so the present study investigated the role of xanthine oxidase (XO), adenosine deaminase (ADA) and 5'-nucleotidase (5'-NT) activity, concerning TBA-reactive substances (TBARS) as an oxidative stress (OS) marker in progression, also an invasion of human colorectal cancer. We took tissue specimens from 50 patients with colon cancer, in all four TNM clinical stages of the disease. They were divided into 3 groups: cancer tissue, tissue surrounding the tumor and healthy control tissue group. We made 10% homogenates in which we conducted the study with proper methods. The activity of ADA and XO in tumor tissue and tissue adjacent to the tumor is statistically higher in comparison to healthy colon tissue. The 5'-NT is not significantly higher in carcinoma tissue. The highest activity of ADA and XO is in T2 and T3 tumor stages. TBARS has the highest concentration in T3 and T4 stages of the tumor. Presented results suggest that the possible cause of OS in colon carcinoma is high XO and ADA activity. It may include those enzymes in the transformation of the colon tissue, as well as in the progression of CRC. So, the ADA and XO activity might be helpful in determing the margins of colon resection. They can have significance in diagnosis, but in the prognosis of the disease as well. [ABSTRACT FROM AUTHOR]

The aim of this study was to examine the relationship of inflammatory parameters, lipid peroxidation and oxidative modification of proteins with ultrasound findings of biliary tract in patients with choledocholithiasis. The study included 70 subjects divided into two groups: the choledocholithiasis group (CHDL)-40 patients with obstructive jaundice caused by choledocholithiasis and the control group-30 healthy individuals. All the patients were anamnestically and clinically observed at the Internal Department of Military Hospital in Niš, Serbia. The values of MDA were not significantly correlated with the degree of dilatation of intrahepatic and extrahepatic bile ducts, while the values of carbonyl groups showed a significant correlation with the degree of dilatation of intrahepatic bile ducts (p < 0.05). Dilatation of bile ducts was not significantly associated with inflammation and lipid peroxidation, however, oxidative modification of the protein showed a significant positive correlation with dilatation of the intrahepatic bile ducts. [ABSTRACT FROM AUTHOR]

Aluminium forms about 8% of the earth’s crust. It is most commonly found as bauxite ore, which is used for extraction of this metal. Aluminium has a high reactivity and forms compounds such as aluminium oxide, aluminium hydroxide, and potassium aluminium sulfate. Exposure of these compounds to oxidants leads to the formation of a superficial coating of aluminium oxide, which is highly resistant to corrosion and insoluble in water. However, acid rains have allowed the dissolution of these compounds and the entry of aluminium into biological systems. It can enter in human body through water, food, drugs, and inhalation of polluted air. Once when accumulates in the body aluminium exhibits toxic effects on different organ systems: central nervous, respiratory, skeletal, hematopoietic, reproductive, digestive (liver), and integumentary system. Toxic systemic effects of aluminium are first observed in patients with kidney failure treated with medicines containing aluminium compounds which manifest as: dialysis encephalopathy syndrome, osteomalacia with osteodystrophy and microcytic anaemia. Aluminium is on the top of a surprisingly short list of neurotoxic inorganic elements and their compounds. It is linked with development of neurodegenerative diseases, including autism, attention deficit disorders, amyotrophic lateral sclerosis, Alzheimer's disease, dementia, Gulf war syndrome, and Parkinsonism. Clinical and experimental studies suggest several possible mechanisms of toxic aluminium action on cells. Those are: increased production of oxidative stress, alteration of membrane function, disruption of intracellular signaling, and alteration or inhibition of enzyme functions. [ABSTRACT FROM AUTHOR]

There is a lot of evidence pertaining to the ethiopathogenetic importance of oxidative stress in a number of autoimmune diseases, including some immune-mediated neurological diseases such as multiple sclerosis. However, the role of oxidative stress and oxidative status in patients with myasthenia gravis is still an under-researched area. The aim of our research was to compare serum total and direct bilirubin, albumin, total proteins and creatinine levels in myasthenia gravis (MG) patients with healthy controls, and patients with multiple sclerosis (MS). The subjects were divided into three groups (92 MG patients, 68 healthy controls and 74 MS patients). All MG patients were newly diagnosed, classified with MGFA Clinical Classification, and divided into two groups regarding onset age (early < 50 years, late ≥50 years), sex (male, female), thymus pathology (present, absent). Serum antioxidant status was significantly lower in MG and MS group compared to the healthy controls (p < 0.05). There was no significant difference in serum antioxidant status between patients with MG and those with MS. Regarding MGFA Classification we have not found any correlation with serum levels of measured parameters. Our findings suggested that there was a potential role of oxidative process in MG pathology. Among the analyzed parameters, direct bilirubin showed significantly lower value in women, the elderly and in the group of MG patients with pathologically altered thymus gland. [ABSTRACT FROM AUTHOR]

Impaired glucose tolerance is a state characterized by hyperglycemia, but with the levels of blood glucose between normal and diabetic values. Diabetic retinopathy is a complication of diabetes the pathogenesis of which is associated with oxidative stress. Metformin is currently the drug of first choice in the treatment of diabetes mellitus type 2. The objective was to determine whether there is oxidative damage to the retina in an animal model using the analysis of oxidative damage parameters, TBA reactive substances (TBARS) and advanced oxidative protein products (AOPP), and whether this damage can be mitigated by metformin tratment. The experiment was performed on 10 weeks old Wistar rats randomized into 4 groups. Impaired glucose tolerance was induced by intraperitoneal injection of streptozotocin (STZ), administered 15 minutes after an intraperitoneal injection of nicotinamide. After 4 weeks, metformin was introduced (100 mg/kg, per os). After 2 weeks, the animals were sacrificed under deep anesthesia. The concentrations of TBARS and AOPP in retinal homogenates were significantly higher in animals with impaired glucose tolerance compared to controls (TBARS: 4.09 ± 0.39 vs. 2.98 ± 0.26; p < 0.001 and AOPP: 34.49 ± 3.21 vs. 26.26 ± 3.16; p < 0.001). A strong positive correlation between serum glucose level and level of TBARS (r = 0.757, p < 0.01) and AOPP levels (r = 0.683, p < 0.01) was found. Metformin did not show any significant effects on the examined parameters. Values of the examined parameters indicate that impaired glucose tolerance causes a strong oxidative stress in the retina, which is the first step in the onset of diabetic retinopathy. Metformin therapy at a dose of 100 mg/kg, showed no significant beneficial effect on the process of lipid peroxidation and oxidation of proteins in the tissues of the retina in animals with impaired glucose tolerance. [ABSTRACT FROM AUTHOR]

In a series of 50 type 1 diabetes participants, mean age 18.9±2.8 years, disease duration longer than five years, each with proven incipient diabetic nephropathy, our goal was to determine the potential impact of oxidative stress on the development of diabetic nephropathy. We determined the antioxidant activity of thiol compounds (SH groups), lipid peroxidation by measuring malondialdehyde (MDA), and advanced oxidation protein products (AOPP). Insufficient antioxidant defense was proven in the diabetic nephropathy group, with a dramatic drop in the activity of thiol compounds compared to controls (132.32±36.60 μmol/L vs 189.22±42.90 μmol/l, p <0.001). This may explain the increase in oxidative stress, or increased lipid peroxidation characterized by the production MDA in the diabetic nephropathy group compared to controls (51.28±12.76 μmol/L vs 17.54±6.35 μmol/L, p <0.001), and the increase in AOPP in patients compared to controls (48.82±13.84 vs 18:45±1.73 μmol/l, p <0.001). Correlation analysis showed a correlation between MDA and SH (r=-0.451, p <0.001), and between SH and AOPP (r=-0.487, p <0.001). However, only MDA is a statistically significant risk factor for the development of diabetic nephropathy. Univariate logistic regression analysis showed that MDA is an independent risk factor. An increase in MDA by 1μmol increases the risk of the development of diabetic nephropathy by 32.4%. Reducing SH concentration by 1μmol/L increases the risk of developing diabetic nephropathy by 4%. We conclude that the lower the antioxidant effect of thiol compounds, the more intensive the lipid peroxidation (MDA) will be, thereby increasing the risk for the development of diabetic nephropathy. Acta Medica Medianae 2017;56(3):94-100. [ABSTRACT FROM AUTHOR]

Reduced systemic antioxidant defence is considered to play an important mediating role in the pathogenesis of diabetic neuropathy. The aim of this study was to determine superoxide dismutase (SOD) and catalase (CAT) levels in the erythrocytes of patients with type 2 diabetes mellitus (DM) and diabetic distal symmetrical polyneuropathy (DDSP), and to analyze the connection between the activity of these antioxidative enzymes and peripheral nerve function. This study involved 100 patients with type 2 DM and signs of DDSP, as well as the control group of 50 healthy subjects and 40 diabetic patients without DDSP. The evaluation of DDSP was based on physical examination and nerve conduction studies. The degree of peripheral nerve dysfunction was estimated by analyzing and scoring sensory and motor nerve conduction parameters. Laboratory analyses involved erythrocyte SOD and CAT values. SOD values were significantly lower in the patients in comparison with the control group (p<0.0001) and diabetic patients without DDSP. The values of erythrocyte CAT were also reduced in diabetic neuropathy patients compared with the controls and patients without DN, although the reduction was not statistically significant. A number of electroneurographic parameters correlated significantly with SOD and CAT levels in the studied patients. Erythrocyte SOD and CAT values were reduced in patients with type 2 DM and DDSP and they correlated with certain electroneurographic parameters of peripheral nerve conduction, which suggested that oxidative stress was potentially implicated in the development of diabetic neuropathy. [ABSTRACT FROM AUTHOR]

As one of the most widespread illnesses today, depression has a big social and economical significance. Therefore, enormous efforts are made in getting deeper insights into its etiology and pathogenesis, which are still unknown to us. Owing to the fast technological development, neurosciences have started to develop intensively. Neuroimaging technologies and new sensitive laboratory tests enable the discovery of active molecules that take part in pathophysiological processes so that they can be considered as potential biomarkers. Although the biomarker which would be specific for depression has not been isolated yet, there are a lot of studies that confirm the existence of changes of the level of active substances in depressive patients with the regard to control ones. In this paper, we will take a look into potential biomarkers that ere in the centre of the research: the factors of growth, that is, brain-derived neurophic factor (BDNF), inflammatory and neuroendocrine biomarkers, as well as potential indicators of the oxidative and nitrosative stress. This kind of the possibility of the insight into biological bases of the depressive processes would enable new ranges in diagnostics, therapies and prognosis of this disorder and would contribute to the better quality of life of patients and their families. [ABSTRACT FROM AUTHOR]

Mutations in genes encoding antioxidant enzymes may reduce their activity and make organism more prone to oxidative damage. The objective of this study was to determine the distribution of glutathione peroxidase 1 (GPX1) Pro200Leu gene polymorphism in renal transplant recipients and healthy volunteers, as well as the association between investigated gene polymorphism and erythrocytes' antioxidative status and estimated GFR (eGFR) within a two-year follow-up after renal transplantation. A total of 85 patients with transplanted kidney and 110 healthy volunteers were genotyped for GPX1 Pro200Leu gene polymorphisms using the polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) method. Of all patients enrolled in genotyping analysis, only 72 patients on tacrolimus went into oxidative stress parameters research. We measured the erythrocytes' concentration of reduced glutathione (GSH) and the activities of GPX and glutathione reductase (GR). GFR was estimated by MDRD formula for creatinine clearance. There was no statistical difference in the distribution of GPX1 gene polymorphism between patients and controls. The obtained results demonstrated that renal transplant recipients with Leu/Leu genotype of tested GPX1 polymorphism had higher erythrocytes' activity of GR compared to the carries of Pro/Pro genotype, but there were no differences in other oxidative stress parameters. The carriers of at least one Leu allele (Pro/Leu + Leu/Leu genotype) had significant decline in eGFR between the first and second year post-transplant. Genotyping of tested polymorphism in clinical practice may represent significant predictor of renal function decline and may provide identification of patients at high risk of graft loss. [ABSTRACT FROM AUTHOR]

Periodontal disease is a chronic inflammatory disease caused by gram-negative bacteria, characterized by gingival inflammation and alveolar bone resorption. In the pathogenesis of periodontal disease free radicals and oxidative stress play a significant role. Free radicals are frequently formed as metabolic by-products and their overproduction leads to cell damage and the development of oxidative stress. Antioxidants are substances that reduce the effects of free radicals and represent a specific defense that protects the organism from their harmful effects. Polymorphonuclear leukocytes (PMNL) are the main immune cells in oral tissue, protecting it from the damaging effects of bacteria. Interactions of leukocytes with bacteria initiate various defensive biochemical and physiological processes that lead to the destruction of the pathogen, but also leading to the respiratory burst in PMNL, with consequential production of free radicals and local tissues damage. Free radicals cause lipid peroxidation in a tissue, DNA and protein damage, enzyme oxidation, stimulation of pro-inflammatory cytokines. Antioxidants play an important role in the protection of oral tissues from the damaging effects of free radicals. The group of enzymatic antioxidants includes superoxide dismutase, oral peroxidase, catalase and glutathione peroxidase; while nonenzymic antioxidants include uric acid, albumin, vitamin C and glutathione. Free radicals play an important role in the pathogenesis of systemic diseases and diseases localized in the oral tissues as well. An imbalance between the production of free radicals and salivary antioxidants may trigger oxidative stress the onset of which is suggested as a basis for the development of periodontal disease. [ABSTRACT FROM AUTHOR]

Naši rezultati ukazuju da oksidativni produkti lipidne peroksidacije imaju značajnu ulogu u nastanku i hroničnom toku sistemskog lupus eritematodesa. Ćelijsko oštećenje izazvano kiseoničnim radikalima nastalim zbog intenzivne lipidne peroksidacije i smanjene antioksidantne zaštite može biti zaustavljeno kortikosteroidnim lekom. Terapija kortikosteroidom je jedna od mogućnosti za bolesnike koji imaju zapaljensku autoimunu bolest. Na taj način se omogućava velikom broju bolesnika da izbegnu nastanak najtežih štetnih efekata tih autoimunih bolesti (bubrežna insuficijencija, ankiloza, prevremena ateroskleroza). Primena vitamina C ne pojačava efekat smanjenja koncentracije MDA kod bolesnika sa SLE koji se leče metilprednizolonom.

Colorectal cancer is one of the most frequent human malignant diseases and one of the most common causes of malignant diseases death. Oxidative and nitrosative stress have an important role in cancer initiation and propagation. That is why this study is focused on the determination of oxidative and nitrosative stress markers in tumor, adjacent and health tissue, which are important for the estimation of tumor proliferative and angiogenic potential. The study encompassed 50 patients who underwent surgery due to colorectal cancer. In the tissue samples from resected colon preparation (tumor, adjacent and healthy tissue, at least 10 cm distant from tumor), oxidative and nitrosative stress markers, malondialdehyde (MDA) and nitric oxide (NO) were determined. The obtained results prove the presence of oxidative stress in tumor tissue. Highly significantly (p<0.001) increased MDA concentrations in both tumor and adjacent tissue (12.43±9.39 and 11.57±5.56 nmol/mg proteins) compared to healthy one (7.25±5.52) reflect higher tumor aggressiveness and metastatic capacity. Higher NO concentrations in adjacent tissue (85.100±37.972 nmol/mg prot.) compared to the tumor one (58.608±22.789) point out high angiogenic potential of tumor surrounding tissue, which could have the clinical importance in the assessment of tumor invasiveness and the probability of local recurrence. In conclusion, the determination of the intensity of reactive oxygen and nitrogen species generation in tumor and adjacent colon tissue of patients with colorectal carcinoma could be useful in the estimation of the cancer invasive and metastatic capacity related to the prognosis of the disease and the choice of adjuvant therapy. [ABSTRACT FROM AUTHOR]

Our results suggest that oxidative products of lipid peroxidation have a significant role in the onset and chronic course of systemic lupus erythematodes (SLE). Cellular damage, caused by reactive oxygen species generated due to intensive lipid peroxidation and lowered antioxidative defenses, may be attenuated by corticosteroid drugs. Corticosteroid therapy is one of the possible therapeutic choices for the patients with an inflammatory autoimmune disease. Such an approach enables a large number of patients to avoid the development of the most serious complications of autoimmune diseases (renal failure, ankylosis, premature atherosclerosis). Vitamin C supplementation does not enhance the malondialdehyde concentration lowering effect of methylprednisolone in patients with SLE. [ABSTRACT FROM AUTHOR]

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