Elektromagnetsko se zračenje emitira iz prirodnog okruženja, ali i uporabom industrijskih i svakodnevnih uređaja za bežičnu komunikaciju, stoga su ljudski i životinjski organizmi stalno izloženi ...zračenju. Tijekom posljednjih godina, zbog brzog tehnološkog napretka, elektromagnetsko zračenje iz umjetnih izvora premašilo je vrijednosti zračenja prirodnog podrijetla. Opća zabrinutost svih nas, zbog sve
većeg broja uređaja (mobilnih telefona, prijenosnih računala, Wi-Fi-ja i mikrovalnih pećnica), koji koriste radiofrekvencijsko elektromagnetsko zračenje (RF-EMZ) opravdana je zbog sve brojnijih dokaza o njihovoj štetnosti na žive organizme. Suvremeni uređaji moderne tehnologije emitiraju radiofrekvencijske elektromagnetske valove malih frekvencija koje ljudsko i životinjsko tijelo apsorbira što može imati potencijalne štetne učinke na: mozak, srce, endokrini sustav i reproduktivnu funkciju. Muški je reproduktivni sustav jedno od najosjetljivijih tkiva na RF-EMZ-e. Tako je primjerice, iz trenutno dostupnih studija provedenih in vitro i in vivo, jasno da RF-EMZ-e ima štetne učinke na spermatogenezu, odnosno kakvoću ejakulata ljudi i životinja – broj spermija u ejakulatu, preživljavanje, morfologiju i gibljivost spermija - utječe na stanični metabolizam i endokrini sustav i može prouzročiti genotoksičnost, genomsku nestabilnost i oksidativni stres, a to može prouzročiti neplodnost. Štetni učinci RFEMZ-a dijele se na toplinske i netoplinske. Većinanegativnih bioloških učinaka pripisuje se netoplinskim učincima, a toplinski se učinci nastali RF-EMZ mobilnog telefona, smatraju manje štetnima. Zbog stvaranja prevelike količine reaktivnih kisikovih spojeva u muškom spolnom sustavu hipertermija skrotuma i povećani oksidativni stres mogu biti ključni mehanizmi putem kojih RF-EMZ-e utječe na plodnost muškaraca. Navedeni su i negativni učinci povezani s vremenom korištenja, ponajprije mobilnog telefona. Stoga je cilj ovoga preglednog rada opisati neke od učinaka RF-EMZ-a na muški spolni sustav.
Za održavanje fizioloških procesa sper- matogeneze i steroidogeneze u testisima te povoljnih mikorookolišnih uvjeta u tkivima epididimisa tijekom sazrijevanja, prolaska i pohrane spermija nužno je ...primjereno djelo- vanje antioksidansa radi održavanja fiziološ- ke razine reaktivnih kisikovih spojeva (ROS). Stanje oksidacijskog stresa, koje nastaje naru- šavanjem ravnoteže između oksidansa (ROS i dr.) i prooksidansa (antioksidansi) u korist ok- sidansa, može za posljedicu imati narušavanje spermatogeneze i steroidogeneze. Tkiva testisa i epididimisa sa spermijima različitog stupnja zrelosti podložna su lipidnoj peroksidaciji, od- nosno oksidacijskom stresu. Narušene funkcije testisa mogu se odraziti i na sposobnost stvara- nja gibljivih, vijabilnih i morfološki normalnih spermija koji imaju sposobnost oploditi jajne stanice te održati rast i razvoj zametka. Visoka je aktivnost antioksidacijskih enzima u testi- sima nužna za primjerenu zaštitu spermija i stanica tkiva testisa od oksidacijskih oštećenja. Nadalje, stjecanje gibljivosti i oplodne sposob- nosti spermija tijekom njihovog prolaska kroz epididimis povezano je s različitim biokemij- skim promjenama osobito u svojstvima njiho-
vih membrana. Tijekom prolaska kroz epidi- dimis spermiji su podvrgnuti stalnoj promjeni mikrookoliša u lumenu, koje je modificirano zbog sekrecijskih i endocitotičkih aktivnosti stanica sluznice epitela. U konačnici, usklađena aktivnost u sekreciji različitih tvari kao i endo- citozi u epitelnim stanicama duž kanala, utje- če na konačno sazrijevanje spermija, njihovu koncentraciju, zaštitu, pohranu i oplodnu spo- sobnost. Navedene uzastopne promjene prati i promjena osobitosti spermija tijekom njihovog prolaska kroz epididimis, a osobito promjene u svojstvima njihovih membrana. No, mijenja se i sastav bjelančevina, lipida i ostalih tvari u ra- zličitim dijelovima epididimisa, koje sudjeluju u procesima sazrijevanja spermija, a čije funk- cije nisu u potpunosti razjašnjene. Međutim, ni sposobnost testisa i epididimisa u zaštiti sper- mija od štetnih učinka oksidacijskih procesa koji se zbivaju tijekom njihove tvorbe, pohrane i sazrijevanja u epididimisima pomoću lokalno sintetiziranih antioksidansa, nije do sada u pot- punosti istražena.
Nitric oxide (NO) is oxidative stress biomarker which is regarded as one of the key determinants of energy metabolism and vascular tone. Considering the controversial reports on the association ...between nitric oxide products (NOx) and metabolic syndrome (MetS), the aim of the current study was to examine that potential relationship. Additionally, we aimed to evaluate a broad spectrum of other oxidative stress biomarkers i.e., malondialdehyde (MDA), advanced oxidation protein products (AOPP), xanthine oxidoreductase (XOD), xanthine oxidase (XO) xanthine dehydrogenase (XDH) in relation with MetS.
A total of 109 volunteers (46.8% of them with MetS) were included in this cross-sectional study. Biohemical and anthropometric parameters, as well as blood pressure, were obtained. The MetS was diagnosed according to the International Diabetes Federation criteria.
Multivariate logistic regression analysis showed that XOD (OR=1.011; 95% CI 1.002-1.019; p=0.016), XO (OR=1.014; 95% CI 1.003-1.026; p=0.016), MDA (OR=1.113; 95% CI 1.038-1.192; p=0.003) and AOPP (OR=1.022; 95% CI 1.005-1.039; p=0.012) were the independent predictors of MetS, whereas no association between NOx and MetS was found. As XOD rose for 1 U/L, XO for 1 U/L, MDA for 1 μmol/L and AOPP for 1 T/L, probability for MetS rose for 1.1%, 1.4%, 11.3% and 2.2%, respectively. Adjusted R
for the Model was 0.531, which means that 53.1% of variation in MetS could be explained with this Model.
Unlike XOD, MDA and AOPP, NOx is not associated with MetS.
Coronary artery disease (CAD) is one of the most important causes of mortality and morbidity in wide world population. Dyslipidemia, inflammation and oxidative stress may contribute to disruption of ...endothelium structure and function, atherosclerosis and CAD. Our study was aimed to determine whether Cu/Zn superoxide dismutase (Cu/Zn SOD) and Mn superoxide dismutase (Mn SOD) gene expression could be modulated by oxidative stress in CAD patients.
This study included 77 CAD patients and 31 apparently healthy persons. Serum lipid levels, high sensitivity C-reactive protein (hsCRP), total antioxidant status (TAS) and thiobarbituric acid-reacting substances (TBARS) were measured. SOD isoenzymes gene expression was determined in peripheral blood mononuclear cells using quantitative polymerase chain reaction.
Mn SOD messenger ribonucleic acid (mRNA) levels were significantly lower in CAD patients than in controls (p=0.011), while Cu/Zn SOD mRNA levels did not change significantly between tested groups (p=0.091). We found significantly lower high-density lipoprotein-cholesterol (HDL-c) (p<0.001) and TAS (p<0.001) levels and significantly higher hsCRP (p=0.002) and TBARS (p<0.001) in CAD patients than in controls. There were significant positive correlations between TAS and Mn SOD mRNA (ρ=0.243, p=0.020) and TAS and Cu/Zn SOD mRNA (r=0.359, p<0.001). TBARS negatively correlated only with Cu/Zn SOD mRNA (ρ=-0.215, p=0.040). TAS levels remained independent predictor for Mn SOD mRNA levels (OR=2.995, p=0.034).
Results of this study showed that Mn SOD gene expression were decreased in CAD patients compared to controls and can be modulated by non-enzymatic antioxidant status in blood.
Isoniazid is one of the most commonly used drugs to treat tuberculosis. Its administration is associated with a high incidence of hepatotoxicity. The aim of this study was to establish the protective ...effects of taurine against cytotoxicity induced by isoniazid and its suspected toxic metabolite hydrazine in isolated rat hepatocytes by measuring reactive oxygen species (ROS) formation, lipid peroxidation, mitochondrial depolarisation, reduced glutathione (GSH), and oxidised glutathione (GSSG). Isoniazid caused no significant ROS formation in normal hepatocytes, but in glutathione-depleted cells it was considerable. Hydrazine caused ROS formation and lipid peroxidation in both intact and glutathione-depleted cells. Both isoniazid and hydrazine caused mitochondrial membrane depolarisation. Hydrazine lowered cellular GSH reserve and increased GSSG. Taurine (200 μmol L
) and N-acetylcysteine (200 μmol L-1) effectively countered the toxic effects of isoniazid and/or hydrazine by decreasing ROS formation, lipid peroxidation, and mitochondrial damage. Taurine prevented depletion of GSH and lowered GSSG levels in hydrazine-treated cells. This study suggests that the protective effects of taurine against isoniazid and its intermediary metabolite hydrazine cytotoxicity in rat hepatocytes could be attributed to antioxidative action.
Izoniazid je jedan od najčešćih lijekova za tuberkulozu, ali se njegova primjena povezuje s veoma učestalom hepatotoksičnosti. Cilj je ovog istraživanja bio ocijeniti djelotvornost taurina u zaštiti izoliranih hepatocita štakora od citotoksičnosti izazvane izoniazidom i njegovim toksičnim metabolitom hidrazinom. U tu smo svrhu utvrdili razine reaktivnih kisikovih spojeva (ROS), lipidnu peroksidaciju, depolarizaciju mitohondrija, reducirani glutation (GSH) te oksidirani glutation (GSSG). Izoniazid nije doveo do značajnoga nastanka ROS-a u normalnih hepatocita, ali je zato bio značajan u stanica osiromašenih glutationom. I izoniazid i hidrazine doveli su do depolarizacije membrane mitohondrija. Hidrazin je smanjio staničnu rezervu GSH i povećao razinu GSSG. Taurin (200 μmol L-1) i N-acetilcistein (200 μmol L
) uspješno su zaštitili od toksičnoga djelovanja izoniazida i/ili hidrazina, smanjivši nastanak ROS-a, lipidnu peroksidaciju i oštećenje mitohondrija. Taurin je spriječio potpuni gubitak GSH-a te snizio razine GSSG-a u stanica tretiranih hidrazinom. Rezultati našeg istraživanje upućuju na to da se zaštitno djelovanje taurina od stanične toksičnosti izoniazida i hidrazina može pripisati njegovu andioksidacijskome djelovanju.
Ćelije stalno proizvode slobodne radikale i reaktivne vrste kiseonika kao dio metaboličkih procesa. Povećani aerobni metabolizam tokom fizičke aktivnosti potencijalni je izvor oksidativnog stresa. ...Takođe, anaerobna fizička aktivnost i oksidativni stres međusobno su povezani jer intenzivna anaerobna aktivnost vodi ka oštećenjima proteina, lipida i nukleinskih kiselina u mišićnim ćelijama i krvi. Složeni sistem antioksidantne odbrane, koji ima enzimski i neenzimski dio, ima ulogu u zaštiti tkiva od prevelikih oksidativnih oštećenja. Većina do sada sprovedenih istraživanja o uticaju različitih oblika fizičke aktivnosti na nivo oksidativnog stresa potvrđuje promjene u biomarkerima koji ukazuju na lipidnu peroksidaciju i modifikacije na proteinima. Osobe koje ne treniraju, za razliku od onih koji treniraju, podložnije su većim promjenama u organizmu uzrokovanim oksidativnim stresom pri fizičkoj aktivnosti. Rezultati ciljanih istraživanja su pokazali da nema bitnih razlika između polova u nivou oksidativnog stresa pri fizičkoj aktivnosti i odgovoru organizma na eventualno primjenjenu antioksidantnu suplementaciju. Interesantno je da i pored brojnih studija, tačna lokacija nastanka oksidativnog stresa pri fizičkoj aktivnosti još uvijek nije pouzdano utvrđena. Uz navedeno, rezultati sprovedenih istraživanja pružaju nedovoljno dokaza o efektivnosti upotrebe antioksidantne suplementacije u cilju povećanja odbrane od oksidativnog stresa. Neophodno je detaljnije istražiti redoks status i oksidativni stres pri fizičkoj aktivnosti i kod sportista adolescenata.
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.
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.
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 age and 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.
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.
The aim of the study was to investigate the association of paraoxonase 1 (PON1) polymorphism, PON1/arylesterase (ARE) activity and oxidative stress index (OSI) in breast cancer (BC) patients with ...type 2 diabetes (DM).
Our study group consisted of 30 healthy women (HV group) and 66 female BC patients. The BC patients were divided into two groups: those with (n=37) and without DM (n=29) (BDM and NBDM group). Genotyping of PON1 Q192R and L55M polymorphisms were done by polymerase chain reaction (PCR) - restriction fragment length polymorphism (RFLP) method. Serum PON1/ARE enzyme activities, total oxidant status (TOS) and total antioxidant status (TAS) were analysed by spectrophotometric method. The ratio of TOS to TAS was accepted as the oxidative stress index (OSI).
PON1 Q192R genotype frequency distribution was significantly different in the BDM group compared to the NBDM group (p=0.021). When alleles distribution was examined, R and L alleles were significantly lower, Q and M alleles were significantly higher in the BDM group than in the NBDM group (p<0.001). TOS and OSI were statistically higher in BC patients than HV group (p<0.001).
Our results suggest that PON1 gene Q and M alleles may be the risk factors predisposing formation of BC due to increased oxidant damage seen in DM. However, these statements require further confirmation with screening PON1 polymorphism in a greater number of patients with DM, and also wide range follow-up studies are necessary for the same purpose.
Asthma is a chronic disorder of the airways. Oxidative stress is an important part of asthma pathogenesis. It plays a crucial role in exacerbating the disease, as well as an important consequence of ...airways inflammation.
Aim: The present study was undertaken to investigate the lipid peroxidation and catalase activity in serum and antioxidant level in plasma of asthmatic patients and their association with lifestyle and severity of the disease.
Methods: A total of 210 subjects, 120 asthmatics and 90 healthy controls matched in respect to age, sex, lifestyle and socioeconomic status, were chosen randomly for the present study. The samples were analyzed for MDA concentration and catalase activity in serum and ferric reducing ability of plasma (FRAP). Statistical analysis was done using unpaired Student’s t-test, ANOVA with Duncan post hoc test and Pearson coefficient of correlation.
Results: The serum MDA was found to be significantly higher in the asthmatics as compared to healthy individuals (p<0.01) while catalase activity in serum and antioxidant level of the plasma were markedly lower in the asthmatics as compared to healthy individuals (p<0.01). A significant difference was observed in serum MDA, catalase activity and plasma antioxidant level among the patients in relation to the severity of disease. There was a marked increase in the serum MDA in the patients with longer duration of the disease (p<0.05).
Conclusion: The oxidant-antioxidant imbalance occurs in asthma leading to oxidative stress and is an important part of the asthma pathogenesis.
Uvod: Astma je hronično oboljenje disajnih puteva. Oksi- dativni stres čini važan deo u patogenezi astme. Ima presudnu ulogu u pogoršanju bolesti i predstavlja važnu posle- dicu upale disajnih puteva.
Ova studija je preduzeta kako bi se istražili lipidna peroksi- dacija i aktivnost katalaze u serumu i nivo antioksidanasa u plazmi kod bolesnika sa astmom i njihova povezanost sa životnim stilom i težinom bolesti.
Metode: Ukupno 210 ispitanika, 12|0 astmatičara i 90 zdravih kontrolnih ispitanika odgovarajuće starosti, pola, životnog stila i socioekonomskog statusa, nasumično je izabrano za ovu studiju. Analizom uzoraka određene su koncentracija MDA i aktivnost katalaze u serumu i primenjena je metoda FRAP (ferric reducing ability of plasma). Statistička analiza je izvršena pomoću Studentovog t testa, testa ANOVA sa Duncan post hoc testom i Pearsonove korelacije koeficijenta.
Rezultati: MDA u serumu bio je značajno viši kod astmatičara u poređenju sa zdravim ispitanicima (p<0,01), dok su aktivnost katalaze u serumu i nivo antioksidanasa u plazmi bili upadljivo niži kod astmatičara u poređenju sa zdravim ispitanicima (p<0,01). Između pacijenata je uočena značajna razlika u nivoima MDA u serumu, aktivnosti katalaze i nivoima antioksidanasa u plazmi u odnosu na težinu oboljenja. Postojao je upadljiv porast nivoa MDA u serumu kod pacijenata povezan sa dužinom bolesti (p<0,05).
Zaključak: U astmi se javlja poremećaj oksidantne-antiok- sidantne ravnoteže, što dovodi do oksidativnog stresa i čini važan deo patogeneze astme.
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