The aim of the study was to evaluate parameters of oxidative and nitrosative stress as well as antioxidative parameters in a group of renal transplant recipients with stable graft function and no ...clinical signs of cardiovascular disease. We also aimed to determine the correlations among these parameters and to evaluate potential differences in all the biomarkers with regard to the immunosuppression protocol.
We enrolled 57 renal transplant recipients and 31 controls who were age and sex matched with the renal transplant recipients. All of the patients included in this study had post-renal transplant surgery at least 12 months earlier and were on standard immunosuppressive therapy. In this study, we determined thiobarbituric acid-reactive substances in plasma and red blood cells and advanced oxidation protein products, nitrosative stress parameters (asymmetric and symmetric dimethylarginine - ADMA and SDMA), and antioxidative parameters (total SH groups and catalase activity).
The results of our study demonstrated that the levels of oxidative and nitrosative stress were significantly increased compared to the healthy population (p<0.01 except for plasma catalase activity p<0.05). Correlation analysis showed significant positive correlations between: ADMA and SDMA (p<0.01); ADMA and nitrates (p<0.05); SDMA and nitrates (p<0.05); between OS parameters in the experimental group; AOPP and SH groups (p<0.05) and TBARS in plasma and SH groups (p<0.01), SDMA and AOPP (p< 0.05); SDMA and TBARS in plasma (p<0.05); SDMA and SH groups (p<0.01); nitrates and SH groups (p<0.05).
There was no significant difference in oxidative and nitrosative stress parameters with respect to the immunosuppressive protocol.
Oxidative stress plays a role in the pathogenesis of many chronic diseases. It is recognized in overt hypothyroidism while its existence in subclinical hypothyroidism (SCH) is not well established. ...The aim of this study was to determine whether there was increased oxidation of lipids and proteins in SCH, and examine their association with lipids and thyroid hormones.
Methods: Male adults (35-59 years) with SCH (n=467) and euthyroid controls (n=190) were studied. Anthropometric measurements, plasma lipids, thyroid stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), total antioxidant capacity (T-AOC), lipid peroxidation products, malondialdehyde (MDA), advanced oxidation protein products (AOPP) and dityrosine concentrations were measured.
Results: Plasma concentrations of MDA were significantly higher (p<0.05) in SCH (8.11±1.39 nmol/mL) compared with euthyroid controls (7.34±1.31 nmol/mL) while AOPP, dityrosine and T-AOC levels were not different. MDA was not associated with TSH (β=-0.019, P=0.759), FT4 (β=-0.062, P=0.323) and FT3 (β=-0.018, P=0.780) in SCH while levels increased with elevated total cholesterol (β=0.229, P=0.001), LDL (β=0.203, P=0.009) and triglycerides (β=0.159, P=0.036) after adjustment for ageand body mass index. T-AOC reduced (β=-0.327, P=0.030) with increased MDA in euthyroid controls and not in SCH (β=-0.068, P=0.349), while levels increased with elevated triglycerides in both groups.
Conclusion: Oxidative stress was increased in subclinical hypothyroidism as evidenced by the elevated lipid peroxidation product, malondialdehyde, while protein oxidation was absent. Thus, reduction of oxidative stress may be beneficial in patients with subclinical hypothyroidism
Uvod: Oksidativni stres učestvuje u patogenezi mnogih hroničnih oboljenja. Ima ulogu u manifestnoj hipotireozi, dok njegovo prisustvo u subkliničkoj hipotireozi (SH) nije sasvim razjašnjeno. Cilj ove studije bio je da se odredi da li postoji povišena oksidacija lipida i proteina u SH i da se istraži njihova povezanost sa lipidima i tireoidnim hormonima.
Metode: Ispitivani su odrasli muškarci (35-59 godina) sa SH (n=467) i eutireoidne kontrolne osobe (n=190). Izmereni su antropometrijski parametri, koncentracije lipida u plazmi, tireostimulišućeg hormona (TSH), slobodnog tiro- ksina (FT4), slobodnog trijodtironina (FT3), ukupni antioksidantni kapacitet (T-AOC), proizvodi lipidne peroksidacije, malondialdehid (MDA), uznapredovali proizvodi proteinske oksidacije (AOPP) i ditirozin.
Rezultati: Koncentracije MDA u plazmi bile su značajno povisene (p<0,05) u SH (8,11 ±1,39 nmol/mL) u poredenju sa eutireoidnim kontrolnim osobama (7,34±1,31 nmol/mL) dok se nivoi AOPFJ ditirozina i T-AOC nisu raz- likovali. MDA nije bio povezan sa TSH (p =-0,019, P=0,759), FT4(p=-0,062, P=0,323) i FT3 (p=-0,018, P=0,780) u SH dok su nivoi rasli s povisenim vrednostima ukupnog holesterola (p = 0,229, P=0,001), LDL(p = 0,203, P= 0,009) i triglicerida (P = 0,159, P= 0,036) posle prila-gocfavanja za starost i indeks telesne mase. Porast nivoa MDA bio je pracen snizenjem nivoa T-AOC (P=-0,327, P=0,030) kod eutireoidnih kontrolnih osoba, ali ne i u SH (P=-0,068, P=0,349), dok su u obe grupe nivoi rasli s porastom triglicerida.
Zaključak: Oksidativni stres bio je povišen u subkliničkoj hipotireozi, što su pokazali i povišeni nivoi proizvoda lipidne peroksidacije, malondialdehida, dok je oksidacija proteina bila odsutna. Stoga, snižavanje oksidativnog stresa može biti korisno kod pacijenata sa subkliničkom hipotireozom
Background: Chronic obstructive pulmonary disease (COPD) is a complex disorder characterized by increased oxidative stress. Functional genetic variants of phase I and II genes are implicated in ...oxidants-antioxidants imbalance and may be involved in COPD development. In this study, we aimed to investigate the role of cytochrome P450 (CYP), glutathione S-transferase (GST) and microsomal epoxide hydrolase (mEH) functional variants in the pathogenesis of COPD in a Serbian population.
Methods: The genotypes of 122 COPD patients and 100 controls with normal lung function were determined for CYP1A1 *1A/*2A, CYP2E1 *1A/*5B, GSTM1 null, GSTT1 null GSTP1 Ile105Val, mEH Tyr113His and mEH His139Arg gene variants.
Results: Results obtained showed that GSTM1 null variant was significantly more represented in COPD patients than in controls (61.5% vs. 47.0%; OR=1.80; p=0.042). Also, a significant difference was observed for combinations of GSTM1 null and GSTP1 105Val/(Val) (38.5% vs. 24.0%; OR=1.98; p=0.029), as well as for CYP1A1 *1A/*2A, GSTM1 null and mEH 113His/(His) genotypes (7.4% vs. 1.0%; OR=7.88; p=0.025).
Conclusions: These are the first data concerning the analysis of the variants of phase I and II genes in the pathogenesis of COPD in a Serbian population. Results obtained in this study open up the possibility for thorough analyses of the role of genetic factors in COPD on larger cohorts. Also, they implicate the importance of previously described genetic associations with COPD in our population, as well as reveal a new one, not reported so far.
Uvod: Hronična opstruktivna bolest pluća (HOBP) jeste složeno oboljenje koje karakteriše povišen oksidativni stres. Funkcionalne varijante gena faze I i II ksenobiotičkog meta- bolizma mogu uticati na ravnotežu oksidanti-antioksidanti i mogu dovesti do razvoja HOBR Cilj ove studije je bio ispi- tivanje uloge funkcionalnih genskih varijanti u genima za citohrom P450 (CYP), glutation S-transferazu (GST) i mi- krozomalnu epoksidnu hidrolazu (mEH) u patogenezi HOBP u srpskoj populaciji.
Metode: U ovoj studiji analizirane su genske varijante CYP1A1 *W*2A, CYP2E1 *W*5B, GSTM1 null, GSTT1 null, GSTP1 lle105Val, mEH Tyr113His i mEH His139Arg u grupi obolelih od HOBP koja je obuhvatala 122 ispita- nika i kontrolnoj grupi koja je obuhvatala 100 ispitanika sa normalnom funkcijom pluća.
Rezultati: Dobijeni rezultati su pokazali da je GSTM1 null varijanta statistički značajno povišena u grupi obolelih od НОВР u poređenju sa kontrolnom grupom (61,5% i 47,0%; OR=1,80; p=0,042). Takođe, uočena je značajna razlika u zastupljenosti kombinacije genotipova GSTM1 null i GSTP1 105Val/(Val) (38,5% i 24,0%; OR=1,98; p=0,029), kao i kombinacije СУР1А1 *1A/*2A, GSTM1 null i mEH 113His/(His) (7,4% i 1,0%; OR=7,88; p=0,025).
Zaključak: Ovo su prvi podaci o ulozi genskih varijanti gena faze I i II u patogenezi HOBP u srpskoj populaciji. Rezultati dobij|eni u ovoj studiji otvaraju mogućnostza detaljniju ana- lizu uloge genetičkih faktora u HOBP na većim grupama ispitanika. Pored toga, podaci dobijeni u našoj studiji po- tvrđuju važnost genetičkih determinanti povezanih sa HOBP u prethodnim studijama, ali takođe otkrivaju nove genetičke faktore, koji nisu objavljeni do sada.
Antioxidant activity of the ethanolic extract and fractions from the stem bark of T. catigua was investigated. IC50 (for DPPH scavenging) by T. catigua varied from 9.17 ± 0.63 to 76.42 ± 5.87 mg mL-1 ...and total phenolic content varied from 345.63 ± 41.08 to 601.27 ± 42.59 mg GAE g-1 of dry extract. Fe2+-induced lipid peroxidation was significantly reduced by the ethanolic extract and fractions. Mitochondrial Ca2+-induced dichlorofluorescein oxidation was significantly reduced by the ethanolic extract in a concentration-dependent manner. Ethanolic extract reduced mitochondrial Dym only at high concentrations (40-100 mg mL-1), which indicates that its toxicity does not overlap with its antioxidant effects. Results suggest involvement of antioxidant activities of T. catigua in its pharmacological properties.
U radu je opisano ispitivanje antioksidativnog u~inka etanolnog ekstrakta i pojedinih frakcija kore stabljike T. catigua. IC50 (za DPPH test) varirao je izme|u 9,17 ± 0,63 i 76,42 ± 5,87 mg mL-1, a ukupni sadr`aj fenola od 345,63 ± 41,08 i 601,27 ± 42,59 mg GAE po gramu suhog ekstrakta. Etanolni ekstrakt i frakcije zna~ajno su reducirale Fe2+-induciranu lipidnu peroksidaciju. Nadalje, reducirana je oksidacija diklorfluoresceina inducirana ionima kalcija u mitohondrijima, a redukcija je ovisila o dozi etanolnog ekstrakta. Etanolni ekstrakt smanjio je mitohondrijsku Dym samo pri visokim koncentracijama (40 ± 100 mg mL-1), {to ukazuje da se toksi~nost ne preklapa s antioksidativnim u~inkom. Rezultati pokazuju da u farmakolo{ko djelovanje T. catigua treba uklju~iti i antioksidativni u~inak.
Earlier research has evidenced the oxidative and neurotoxic potential of imidacloprid, a neonicotinoid insecticide, in different animal species. The primary aim of this study was to determine how ...metabolic modulators piperonyl butoxide and menadione affect imidacloprid’s adverse action in the liver and kidney of Sprague-Dawley rats of both sexes. The animals were exposed to imidacloprid alone (170 mg kg-1) or in combination with piperonyl butoxide (100 mg kg-1) or menadione (25 mg kg-1) for 12 and 24 h. Their liver and kidney homogenates were analysed spectrophotometrically for glutathione peroxidase, glutathione S-transferase, catalase, total cholinesterase specific activities, total glutathione, total protein content, and lipid peroxidation levels. Imidacloprid displayed its prooxidative and neurotoxic effects predominantly in the kidney of male rats after 24 h of exposure. Our findings suggest that the observed differences in prooxidative and neurotoxic potential of imidacloprid could be related to differences in its metabolism between the sexes. Co-exposure (90-min pre-treatment) with piperonyl butoxide or menadione revealed tissue-specific effect of imidacloprid on total cholinesterase activity. Increased cholinesterase activity in the kidney could be an adaptive response to imidacloprid-induced oxidative stress. In the male rat liver, co-exposure with piperonyl butoxide or menadione exacerbated imidacloprid toxicity. In female rats, imidacloprid+menadione co-exposure caused prooxidative effects, while no such effects were observed with imidacloprid alone or menadione alone. In conclusion, sex-, tissue-, and duration-specific effects of imidacloprid are remarkable points in its toxicity
Rezultati ranijih istraživanja pokazali su oksidativni i neurotoksični potencijal imidakloprida, neonikotinoidnog insekticida, u različitih životinjskih vrsta. Primarni je cilj ovog istraživanja bio utvrditi kako modulatori metabolizma piperonil butoksid i menadion utječu na nepovoljne učinke imidakloprida na jetra i bubrege muških i ženskih štakora soja Sprague-Dawley. Životinje su 12 h odnosno 24 h bile izložene samo imidaklopridu (170 mg kg-1) ili njegovoj kombinaciji s piperonil butoksidom (100 mg kg-1) odnosno menadionom (25 mg kg-1). U homogenatima jetara i bubrega spektrofotometrijski su utvrđene razine glutation peroksidaze, glutation S-transferaze, katalaze, specifične aktivnosti ukupne kolinesteraze, ukupni glutation, ukupni proteini te razine lipidne peroksidacije. Imidakloprid se pokazao prooksidativnim i neurotoksičnim uglavnom u bubrezima muških štakora nakon 24-satne izloženosti. Naši rezultati upućuju na to da su razlike u prooksidativnom i neurotoksičnom djelovanju imidakloprida povezane sa spolnim razlikama. Predtretmanom piperonil butoksidom odnosno menadionom (90 min prije davanja imidakloprida) otkriveno je da imidakloprid djeluje na ukupnu aktivnost kolinesteraze specifično za pojedina tkiva. Povišena aktivnost kolinesteraza u bubrezima mogla bi odražavati prilagodbu na oksidativni stres uzrokovan imidaklopridom. Piperonil butoksid odnosno menadion u jetrima muških štakora samo su pogoršali toksičnost imidakloprida. U ženki je djelovanje imidakloprida s menadionom bilo prooksidativno; takvo se djelovanje nije vidjelo nakon primjene samo imidakloprida odnosno samo menadiona. Vjerujemo da je promjenjivo djelovanje imidakloprida s obzirom na spol, tkivo i trajanje izloženosti važno za daljnja istraživanja njegove toksičnosti
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