This study investigated the effects of a nutritionally relevant intake of eicosapentaenoic (EPA) and docosahexaenoic (DHA) fatty acids derived from oily fish or a fish oil supplement on selected ...cardiovascular risk factors in average middle-aged individuals.
Thirty-three participants were randomized to receive salmon (oily fish) providing 274 mg EPA + 671 mg DHA/day or a commercial fish oil supplement providing 396 mg EPA + 250 mg DHA/day in a cross-over trial over an 8-week period separated by a 6-month washout period. Blood samples were collected before and after each intervention and lipids, inflammatory and oxidative stress parameters were determined.
Plasma levels of EPA, DHA and total n-3 fatty acids significantly increased after both interventions. A decreasing trend in triglycerides was more pronounced with salmon than with the fish oil supplement, but the changes noticed were not significant. Although there were no relevant changes in inflammatory marker concentrations at the end of both interventions, significant negative correlations were noticed between total plasma n-3 fatty acids and soluble intercellular adhesion molecule and C-reactive protein throughout the whole intervention period (p<0.05). Among the oxidative stress parameters, intervention with salmon showed a prooxidative effect through a superoxide anion increase (p=0.025). A relevant positive correlation was also found between its concentration and total plasma n-3 fatty acids (p<0.05). Other oxidative stress markers were not significantly influenced by the dietary interventions applied.
Following two sets of recommendations for n-3 fatty acids intake aimed at the general public had only a moderate effect on the selected cardiovascular risk factors in average healthy middle-aged subjects over a short-term period.
The primary goal of this study was to evaluate the influence of cytochrome P450 (CYP) 3A5 (6986A>G) and ABCB1 (3435C>T) polymorphisms on tacrolimus (TAC) dosage regimen and exposure. Second, we ...evaluated the influence of TAC dosage regimen and the tested polymorphisms on renal oxidative injury, as well as the urinary activities of tubular ectoenzymes in a long-term period after transplantation. Also, we aimed to determine the association between renal oxidative stress and tubular damage markers in the renal transplant patients.
The study included 72 patients who were on TAC based immunosuppression. Allele-specific PCR was used for polymorphism determination. We measured the urinary thiobarbituric acid reactive substances (TBARS) and reactive carbonyl derivates (RCD) in order to evaluate oxidative injury, as well as the urinary activities of ectoenzymes (N-acetyl-β-D-glucosaminidase, aminopeptidase N and dipeptidyl peptidase IV) to evaluate tubular damage.
The carriers of CYP 3A5*1 allele required statistically higher daily doses of TAC than CYP *3/*3 carriers, as well as the carriers of C allele of ABCB1 gene compared to those with TT genotype. Also, there were no differences in TBARS, RCD and the activities of ectoenzymes between the patients’ genotypes. Our results showed significant correlations between urinary TBARS and RCD and the ectoenzymes’ activities.
Our findings suggest that CYP 3A5 and ABCB1 3435 polymorphism may affect TAC daily doses, but not the drug’s tubular toxicity. Furthermore, tubular damage may be associated with increased renal oxidative stress.
Statins are potent cholesterol-lowering drugs that can have serious adverse effects on the muscles and liver. The aim of our in vitro study was to establish the protective effect of coenzyme Q
(CoQ
, ...in its optimal dose of 200 μmol L
) against cytotoxicity induced by atorvastatin, simvastatin, and lovastatin in isolated rat hepatocytes by observing parameters such as cell death, reactive oxygen species formation, lipid peroxidation, mitochondrial membrane potential, and cellular reduced and oxidised glutathione content. Our findings have shown that pretreatment with CoQ
was effective in reducing the toxic effects of statins in rat hepatocytes. This work demonstrates that the addition of CoQ
to statin treatment regimens may protect hepatocytes (and also other types of cells) from statin-induced injuries and alleviate their side effects.
Statini su snažni lijekovi za snižavanje kolesterola, koji mogu izazvati ozbiljne nuspojave u mišićima i jetrima. Svrha je ovog in vitro istraživanja bila utvrditi zaštitno djelovanje koenzima Q
(CoQ
, u optimalnoj dozi od 200 μmol L
) protiv citotoksičnosti atorvastatina, simvastatina i lovastatina u izoliranih štakorskih hepatocita kroz parametre poput vijabilnosti, nastanka reaktivnih kisikovih čestica, lipidne peroksidacije, potencijala mitohondrijske membrane te reduciranog i oksidiranog glutationa. Rezultati su pokazali da predtretman štakorskih hepatocita CoQ
djelotvorno ublažava toksične učinke statina te da bi njegovo kombiniranje sa statinima moglo zaštititi hepatocite (i druge vrste stanica) od oštećenja izazvanih statinima te ublažiti nuspojave povezane s ovim lijekovima.
Background: This study investigated the effects of a nutritionally relevant intake of eicosapentaenoic (EPA) and docosahexaenoic (DHA) fatty acids derived from oily fish or a fish oil supplement on ...selected cardiovascular risk factors in average middle-aged individuals.
Methods: Thirty-three participants were randomized to receive salmon (oily fish) providing 274 mg EPA + 671 mg DHA/day or a commercial fish oil supplement providing 396 mg EPA + 250 mg DHA/day in a cross-over trial over an 8-week period separated by a 6-month washout period. Blood samples were collected before and after each intervention and lipids, inflammatory and oxidative stress parameters were determined.
Results: Plasma levels of EPA, DHA and total n-3 fatty acids significantly increased after both interventions. A decreasing trend in triglycerides was more pronounced with salmon than with the fish oil supplement, but the changes noticed were not significant. Although there were no relevant changes in inflammatory marker concentrations at the end of both interventions, significant negative correlations were noticed between total plasma n-3 fatty acids and soluble intercellular adhesion molecule and Creactive proteinconcenthroughout the whole intervention period (p<0.05). Among the oxidative stress parameters, intervention with salmon showed a prooxidative effect through a superoxide anion increase (p=0.025). A relevant positive correlation was also found between its concentration and total plasma n-3 fatty acids (p<0.05). Other oxidative stress markers were not significantly influenced by the dietary interventions applied.
Conclusion: Following two sets of recommendations for n- 3 fatty acids intake aimed at the general public had only a moderate effect on the selected cardiovascular risk factors in average healthy middle-aged subjects over a short-term period
Uvod: U ovoj studiji praćeni su efekti preporuka za unos eikozapentaenske (EPA) i dokozoheksaenske kiseline (DHA), iz dva razlicita izvora, lososa i suplementa sa ribljim uljem, na odabrane faktore kardiovaskularnog rizika u prosečnoj populaciji srednjih godina.
Metode: Trideset i tri ispitanika su po slučajnom izboru konzumirali losos koji je obezbeđivao 274 mg EPA +671 mg DHA/dan ili komercijalni suplement ribljeg ulja koji je obezbeđivao dnevno 396 mg EPA + 250 mg DHA tokom 8 nedelja. Nakon perioda od 6 meseci ispitanicima su zamenjene intervencije (ukrštena studija). Uzorci krvi su sakupljani pre i posle svake intervencije, a zatim su određivani lipidni, inflamatorni parametri kao i markeri oksidativnog stresa.
Rezultati: Koncentracije EPA, DHA i ukupnih n-3 masnih kiselina u plazmi su značajno povećane posle obe intervencije. Nije bilo statistički značajnnih promena u lipidnim parametrima, iako je zabelezeno vece smanjenje nivoa triglicerida posle intervencije lososom u poredenju sa suplementom. Nisu uočene značajne promene u koncentraciji inflamatornih markera, ali je utvrđena značajna negativna korelacija između ukupnih n-3 masnih kiselina plazme i rastvorljivog intracelularnog adhezionog molekula i C-reaktivnog proteina tokom ukupnog trajanja studije (p<0,05). Od parametara oksidativnog stresa, intervencija lososom je imala umeren prooksidativni efekat usled povecanja superoksidnog anjona (p= 0,025). Između ovog parametra i ukupnih n-3 masnih kiselina nađena je statistički značajna pozitivna korelacija. Ostali marked oksidativnog stresa nisu se značajno menjali.
Zaključak: Preporučene vrednosti za unos n-3 masnih kiselina pokazale su umeren efekat na parametre kardiovaskularnog rizika u prosečnoj populaciji srednjih godina u kratkom periodu trajanja studije
This work responds to the need to find, in a sole document, the affect of oxidative stress at different levels, as well as treatment with antioxidants to revert and diminish the damage. Oxidative ...Stress and Chronic Degenerative Diseases - a Role for Antioxidants is written for health professionals by researchers at diverse educative institutions (Mexico, Brazil, USA, Spain, Australia, and Slovenia). I would like to underscore that of the 19 chapters, 14 are by Mexican researchers, which demonstrates the commitment of Mexican institutions to academic life and to the prevention and treatment of chronic degenerative diseases.
Acetaminophen (N-acetyl para amino phenol, APAP) is a widely used antipyretic and analgesic drug responsible for various drug-induced liver injuries. This study evaluated APAP-induced toxicity in ...isolated rat hepatocytes alongside the protective effects of silafibrate and N-acetyl cysteine (NAC). Hepatocytes were isolated from male Sprague-Dawley rats by collagenase enzyme perfusion via the portal vein. This technique is based on liver perfusion with collagenase after removing calcium ions (Ca
) with a chelator. Cells were treated with different concentrations of APAP, silafibrate, and NAC. Cell death, reactive oxygen species (ROS) formation, lipid peroxidation, and mitochondrial depolarisation were measured as toxicity markers. ROS formation and lipid peroxidation occurred after APAP administration to rat hepatocytes. APAP caused mitochondrial depolarisation in isolated cells
Administration of silafibrate (200 μmol L
) and/or NAC (200 μmol L
) reduced the ROS formation, lipid peroxidation, and mitochondrial depolarisation caused by APAP
Cytotoxicity induced by APAP in rat hepatocytes was mediated by oxidative stress. In addition, APAP seemed to target cellular mitochondria during hepatocyte damage. The protective properties of silafibrate and/or NAC against APAP‑induced hepatic injury may have involved the induction of antioxidant enzymes, protection against oxidative stress and inflammatory responses, and alteration in cellular glutathione content.
Acetaminofen (N-acetil-para-aminofenol, APAP) često je korišteni antipiretik i analgetik koji može izazvati oštećenja jetara. Na modelu izoliranih hepatocita štakora istražili smo toksične učinke APAP-a i protektivne učinke silafibrata i N-acetilcisteina (NAC). Hepatociti su izolirani iz mužjaka štakora soja Sprague-Dawley perfuzijom jetara i uvođenjem enzima kolagenaze putem portalne vene. Ta se tehnika zasniva na perfuziji jetara kolagenazom nakon uklanjanja kalcijevih iona (Ca
) kelatorom. Stanice su tretirane različitim koncentracijama APAP-a, silafibrata i NAC-a. Kao markeri toksičnosti mjereni su smrt stanica, stvaranje reaktivnih kisikovih vrsta (ROS), lipidna peroksidacija i depolarizacija mitohondrija. Primjena APAP-a u štakora izazvala je stvaranje ROS-ova i lipidnu peroksidaciju. APAP je uzrokovao depolarizaciju mitohondrija u izoliranim stanicama. Primjena silafibrata (200 μmol L
) i/ili NAC-a (200 μmol L
) smanjila je stvaranje ROS-a, lipidnu peroksidaciju i depolarizaciju mitohondrija uzrokovanu APAP-om. Utvrdili smo da je citotoksičnost APAP-a posredovana oksidativnim stresom. Nadalje, čini se da su mitohondriji ciljni stanični organeli za oštećenja hepatocita izazvanih APAP-om. Moguće je da su protektivna svojstva silafibrata i/ili NAC-a protiv APAP‑om induciranog oštećenja jetara uključivala i indukciju antioksidacijskih enzima, zaštitu od oksidativnog stresa i upalnih odgovora te promjenu razine staničnoga glutationa.
Oxidative stress may be involved in the pathogenesis of every human disease. To understand its possible role in benign prostatic hyperplasia (BPH), we measured the overall oxidative status of ...patients with BPH and the serum activity of the high density lipoprotein (HDL)-related antioxidant enzymes paraoxonase 1 (PON1) and arylesterase (ARE).
Fifty-six urology outpatient clinic patients with BPH (mean age 64±8.6 years) were prospectively included in the study. Forty volunteer healthy controls from the laboratory staff (mean age 62±10 years) were enrolled for comparison. Serum total antioxidant status (TAS), total oxidant status (TOS), PON1, ARE, and HDL levels were measured by commercially available, ready-to-use kits.
Serum TAS and HDL levels were significantly lower in the BPH group than in the control group (P=0.004 and P=0.02, respectively). No significant between-group differences were observed for TOS levels or PON1 and ARE enzyme activities (P=0.30, P=0.89, and P=0.74, respectively). In the BPH group, the calculated parameters PON1/HDL and ARE/HDL were significantly higher (P=0.02 and P=0.04, respectively).
Our findings agree with the previous reports of impaired oxidant/antioxidant balance in BPH patients. The activities of HDL-related enzymes between groups with significantly different HDL levels may be deceptive; adjusted values may help to reach more accurate conclusions.
PDF
