Search

Aging is closely related to the main aspects of multiple sclerosis (MS). The average age of the MS population is increasing and the number of elderly MS patients is expected to increase. In addition to neurons, N-methyl-D-aspartate receptors (NMDARs) are also expressed on non-neuronal cells, such as immune cells. The aim of this study was to investigate the role of NMDARs in experimental autoimmune encephalomyelitis (EAE) in young and aged rats. Memantine, a non-competitive NMDAR antagonist, was administered to young and aged Dark Agouti rats from day 7 after immunization. Antagonizing NMDARs had a more favourable effect on clinical disease, reactivation, and apoptosis of CD4+ T cells in the target organ of aged EAE rats. The expression of the fractalkine receptor CX3CR1 was increased in memantine-treated rats, but to a greater extent in aged rats. Additionally, memantine increased Nrf2 and Nrf2-regulated enzymes’ mRNA expression in brain tissue. The concentrations of superoxide anion radicals, malondialdehyde, and advanced oxidation protein products in brain tissue were consistent with previous results. Overall, our results suggest that NMDARs play a more important role in the pathogenesis of EAE in aged than in young rats.

Aging is closely related to the main aspects of multiple sclerosis (MS). The average age ofthe MS population is increasing and the number of elderly MS patients is expected to increase. Inaddition to neurons,N-methyl-D-aspartate receptors (NMDARs) are also expressed on non-neuronalcells, such as immune cells. The aim of this study was to investigate the role of NMDARs inexperimental autoimmune encephalomyelitis (EAE) in young and aged rats. Memantine, a non-competitive NMDAR antagonist, was administered to young and agedDark Agoutirats from day7 after immunization. Antagonizing NMDARs had a more favourable effect on clinical disease,reactivation, and apoptosis of CD4+T cells in the target organ of aged EAE rats. The expression ofthe fractalkine receptor CX3CR1 was increased in memantine-treated rats, but to a greater extent inaged rats. Additionally, memantine increased Nrf2 and Nrf2-regulated enzymes’ mRNA expressionin brain tissue. The concentrations of superoxide anion radicals, malondialdehyde, and advancedoxidation protein products in brain tissue were consistent with previous results. Overall, our resultssuggest that NMDARs play a more important role in the pathogenesis of EAE in aged than in young rats.

Gojaznost je jedno od najznačajnjih oboljenja savremene medicine u grupi hroničnih nezaraznih bolesti. Posebno je važan uticaj uvećane masne mase tela u patogenezi kardiovaskularnih bolesti, sa mogućim posledicama za nastanak insuficijencije srca, koronarne insuficijencije, poremećaja ritma. Disproporcija u efektima agresivnih faktora, mehaničkih faktora zbog uvećanja telesne mase, i funkcionalnih zbog poremećaja adipokinske sekrecije i prisutnih faktora rizika, otežavaju prevenciju poremećaja na ciljnim organima. Sama činjenica da gojaznost kao hronična bolest dovodi do nastanka komorbiditeta na srcu, uz prisutne tradicionalne faktore rizika, stavlja u fokus interakciju proinflamatornih adipokina disfunkcionalnog masnog tkiva i poremećaj geometrije miokarada leve komore na prvo mesto. CILJ: Ispitati povezanost veličine subkutanih i visceralnih abdominalnih masnih depoa, cirkulišućih koncentracija hemerina i SFRP-5 i geometrije miokarda leve komore kod gojaznih bolesnika sa kardiometaboličkim sindromom, kao i utvrditi da li porast stepena kardiometaboličkog sindroma doprinosi većoj učestalosti poremećaja geometrije miokarda leve komore kod gojaznih ispitanika. MATERIJAL I METODE: Istraživanje je uključivalo gojazne ispitanike, bez pridruženih komorbiditeta, kao i zdrave normalno uhranjene ispitanike usklađene po godinama života i polu koji su činili kontrolnu grupu. Dodatno, ispitivana grupa je podeljena na tri podgrupe u odnosu na kriterijume za postojanje kardiometaboličkog sindroma. Svim ispitanicima su urađena antropometrijska merenja, analiza komponenata telesne kompozicije, laboratorijska analiza uzoraka krvi na automatizovanim analizatorskim sistemima, sa određivanjem parametara metabolizma glikoze (bazalno i 2 h u toku oralnog glukoza tolerans testa), lipida i lipoproteina i parametara inflamacije. Serumske koncentracije proinflamatornih adipokina, hemerina i rezistina, odnosno antiinflamatornog adipokina SFRP-5, su određivane ELISA tehnikom, Enzyme-linked i, Obesity is one of the most important diseases of modern medicine in the group of chronic non-communicable diseases. The influence of increased body fat mass is especially important in the pathogenesis of cardiovascular diseases, with possible consequences for the occurrence of heart failure, coronary insufficiency and rhythm disorders. Disproportion in the effects of aggressive factors, mechanical factors due to weight gain, and functional factors due to disorders of adipokine secretion and present risk factors, make it difficult to prevent disorders on target organs. The very fact that obesity as a chronic disease leads to comorbidities in the heart, with the presence of traditional risk factors, focuses on the interaction of proinflammatory adipokines of dysfunctional adipose tissue and left ventricular myocardial geometry disorder in the first place. OBJECTIVE: To examine the relationship between the size of subcutaneous and visceral abdominal fat depots, circulating concentrations of chemerin and SFRP-5 and left ventricular myocardial geometry in obese patients with cardiometabolic syndrome, as well as to determine whether the increase in cardiometabolic syndrome contributes to higher frequency of geometric disorders in obese subjects. MATERIAL AND METHODS: The study included obese subjects, without any associated comorbidities, as well as healthy normally fed subjects matched by age and gender who made up the control group. Additionally, the examined group was divided into three subgroups according to the criteria for the existence of cardiometabolic syndrome. All subjects underwent anthropometric measurements, analysis of body composition components, laboratory analysis of blood samples on automated analytical systems, with determination of glucose metabolism parameters (basal and 2 hours during oral glucose tolerance test), lipids and lipoproteins and inflammation parameters. Serum concentrations of proinflammatory adipokine, chemerin, and resistin, and the a

Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver diseases in the general population. NAFLD consists of three major entities including steatosis, nonalcoholic steatohepatitis (NASH) and cirrhosis. The principal causes of steatosis are insulin resistance and hyperinsulinemia, which lead to increased lipolysis in adipose tissue with subsequent inflow of free fatty acids (FFA) to the liver and stimulation of hepatic de novo lipogenesis. Lipotoxic effects of FFAs cause mitochondrial dysfunction and oxidative stress that lead to the activation of inflammatory response and progression of steatosis to NASH. Autophagy is impaired in NAFLD and contributes to the accumulation of damaged organelles and proteins in hepatocytes, ultimately leading to apoptosis. Chronic liver injury and inflammation stimulate fibrogenic pathways and ultimately may result in liver cirrhosis. Hepatic stellate cells (HSCs) play a central role in hepatic fibrogenesis and are a major source of collagen and other extracellular matrix proteins. Transforming growth factor beta (TGF-β) induces a transdifferentiation of HSCs into myofibroblast-like cells which express collagen I gene and alpha-smooth muscle actin. Neuregulin-1 (NRG-1) belongs to epidermal growth factor family and is involved in cell differentiation, proliferation, growth and survival. Recombinant human NRG-1 (rhNRG-1) exerts antifibrotic effects in the heart, lungs, kidneys and skin. However, the exact role of NRG-1 in liver fibrogenesis has not been elucidated. Betaine, 3-methyl glycine is a nontoxic amino acid, a methyl-group donor and exerts antioxidative effects by increasing the amount of sulfur-containing amino acids. Additionally, betaine may induce epigenetic silencing of genes involved in lipogenesis contributing to alleviation of steatosis. On the other hand, the effects of betaine on inflammation, autophagy and apoptosis, as well as on signaling pathways involved in NAFLD pathogenesis are, od najčešćih uzročnika hroničnih oboljenja jetre u razvijenim zemljama, s obzirom na sve veću učestalost gojaznosti i dijabetes melitusa tipa 2 pre svega u mlađoj populaciji. NAFLD predstavlja hepatičnu manifestaciju metaboličkog sindroma, koja se može ispoljiti u tri oblika: kao masna promena jetre, nealkoholni steatohepatitis (eng. non-alcoholic steatohepatitis; NASH) ili ciroza jetre, sa mogućnošću progresije u hepatocelularni karcinom. Patogeneza NAFLD je kompleksna i još uvek nedovoljno rasvetljena. Savremena teorija ukazuje na značaj interakcije brojnih mehanizama na ćelijskom i molekularnom nivou u patogenezi NAFLD, tzv.teorija višestrukih udara. Smatra se da centralnu ulogu u njenom razvoju ima insulinska rezistencija, što uslovljava povećanje de novo lipogeneze u jetri, povećanje lipolize u masnom tkivu, povećan priliv masnih kiselina u jetru i nastanak steatoze. Slobodne masne kiseline ispoljavaju lipotoksično dejstvo i uzrokuju mitohondrijsku disfunkciju, oksidativni stres, kao i stres endoplazmatskog retikuluma. Usled povećanja permeabilnosti sluznice u digestivnom traktu i prolaska endotoksina bakterija crevne flore u cirkulaciju, dolazi do pokretanja zapaljenskog odgovora i oslobađanja proinflamatornih citokina, kao što su interleukini (IL-1, IL-6, IL-8) i faktor tumorske nekroze alfa (TNF-α). Oštećenja ćelija usled zapaljenja i oksidativnog strresa dovode do apoptoze i nekroze hepatocita. Ovi mehanizmi dovode do pogoršanja steatoze usled oksidativne modifikacije apoB100 i smanjenog efluksa lipoproteina veoma male gustine (eng. very low density lipoprotein; VLDL), kao i do progresije steatoze u NASH kod genetski predisponiranih osoba.Skorašnje studije ukazuju da su izmenjeni procesi apoptoze i autofagije verovatno uključeni u patogenezu NAFLD. Hronično oštećenje jetre i inflamacija podstiču razvoj fibroze posredstvom brojnih proinflamatornih citokina, faktora rasta i slobodnih kiseoničnih radikala...

Nealkoholna masna bolest jetre (NAFLD) obuhvata širok spektar bolesti jetre, od inicijalne steatoze do steatohepatitisa, koji može dalje da progredira do fibroze i ciroze jetre, uz mogućnost razvoja hepatocelularnog karcinoma. Ključnu ulogu u patogenezi NAFLD, na samom početku, ima insulinska rezistencija (IR) u masnom tkivu, koja povećava lipolizu i dopremanje masnih kiselina (MK) u jetru, a takođe utiče i na posrast de novo sinteze MK u heptocitima. Tako, najpre dolazi do razvoja steatoze, koja povećava osetljivost hepatocita na oštećenje dejstvom faktora aktivacije inflamatorne kaskade i fibrogeneze, dovodeći do dalje progresije bolesti u steatohepatitis i fibrozu jetre. Među ovim faktorima najznačajniji su oksidativni/nitrozativni stres, mitohondrijalna disfunkcija, lipotoksičnost, proinflamatorni citokini, kao i disbalans produkcije adipokina. Dosadašnja eksperimentalna i klinička istraživanja ukazala su na značajnu ulogu endokanabinoidnog sistema (ES) u razvoju NAFLD. U našoj studiji korišćena je dijeta bogata mastima (HFD, engl. high fat diet), koja izaziva strukturne, funkcionalne i metaboličke promene u jetri miševa slične ispoljavanjima NAFLD i metaboličkog sindroma u ljudi (porast nivoa oksidativnog i nitrozativnog stresa u hepatocitima, razvoj dislipidemije, IR, hepatičke steatoze, inflamacije i fibroze). Ciljevi ove disertacije su bili: da se ispita uloga kanabinoidnih CB1 receptora u patogenezi NAFLD sa posebnim osvrtom na ulogu u razvoju oksidativnog/nitrozativnog stresa, uticaj na kapacitet antioksidativne zaštite, kao i koncentraciju Zn, Cu, Mn i Fe u tkivu jetre; da se ispita uticaj CB1 receptora na lipidni status, profil MK u jetri (palmitinska, stearinska, oleinska, linoleinska i arahidonska kiselina), kao i adipokine (leptin, apelin, rezistin i visfatin) i proinflamatorne citokine (IL-6 i IFN-γ) u masnom tkivu i jetri; da se ispita uticaj blokade CB1 receptora na glikemiju, koncentraciju insulina i HOMA indeks. NAFLD je izazvana mužjacima miševa, Non alcoholic fatty liver disease (NAFLD) encompasses a wide range of liver diseases from initial steatosis to steatohepatitis, which may further progress to liver fibrosis or cirrhosis and potentially develop hepatocellular carcinoma. At the very beginning, insulin resistance (IR) in adipose tissue has the key role in the NAFLD pathogenesis, increasing lipolysis and supply of fatty acids (FA) to liver and also affecting the increase of de novo synthesis of FA in hepatocytes. In this manner steatosis occurs first, increasing the sensitivity to the damage occurred due to the factors which activate inflammatory cascade and fibrogenesis and lead to further progression of the disease towards steatohepatitis and liver fibrosis. The most significant among these factors are oxidative/nitrosative stress, mitochondrial dysfunction, lipotoxicity, proinflammatory cytokines, as well as the adipokine production imbalance. Previous experimental and clinical research has emphasized the considerable role of the endocannabinoid system (ECS) in the development of NAFLD. In our study we used high fat diet (HFD) which causes structural, functional and metabolic changes in mouse liver similar to the manifestations of NAFLD and metabolic syndrome in humans (increased level of oxidative and nitrosative stress in hepatocytes, development of dyslipidemia, IR, hepatic steatosis, inflammation and fibrosis). The goals of this thesis were: to test the role of cannabinoid CB1 receptors in the pathogenesis of NAFLD with particular overview of their role in the development of oxidative/nitrosative stress, impact on the capacity of antioxidative protection, as well as Zn, Cu, Mn and Fe concentrations in liver tissue; to test the impact of CB1 receptors on the lipid profile, FA profile in liver (palmitic, stearic, oleic, linoleic and arachidonic), as well as adipokines (leptin, apelin, resistin and visfatin) and proinflammatory cytokines (IL-6 and IFN- γ) in adipose tissue and liver; to test the imp

We used rimonabant to investigate the role of CB1 receptor on hepatic FFAs profile during NAFLD. Male mice C57BL/6 were divided into: control group fed with control diet 20 weeks (C; n = 6); group fed with HFD 20 weeks (HF; n = 6); group fed with control diet and treated with rimonabant after 18 weeks (R; n = 9); group fed with HFD and treated with rimonabant after 18 weeks (HFR; n = 10). Rimonabant (10 mg/kg) was administered daily to HFR and R group by oral gavage. Rimonabant decreased liver palmitic acid proportion in HFR group compared to HF group (p lt 0.05). Liver stearic and oleic acid proportions were decreased in R group compared to control (p lt 0.01 respectively). Rimonabant increased liver linoleic and arachidonic acid proportions in HFR group compared to HF group (p lt 0.01 respectively). CB1 blockade may be useful in the treatment of HFD-induced NAFLD due to modulation of plasma lipid and hepatic FFA profile.

Structure and functions of Na+/K+-ATPase and SERCA are described with details on their subunits, isoforms, and intracellular localization. Main regulatory mechanisms are summarized. Molecular mechanisms of cell death and heart failure are explained with the analysis of the role of Na+/K+-ATPase and SERCA in these processes. Facts are considered from a cytological, pathological, and clinical perspective with an accent to new therapeutic strategies. The aim of this contribution is an overview of functional results in a structural context.

Osnovna terapija kod pacijenata sa diferentovanim karcinomom štitaste žlezde (DTC) je totalna ili skoro totalna tireoidektomija i primena radioaktivnog joda (131-I). Cilj terapije radioaktivnim 131-I je eliminacija postoperativno zaostalog tireoidnog tkiva i jodavidnih metastaza. Primena 131-I indukuje jonizaciju materije praćenu oksidativnim stresom i oslobađanjem pojedinih citokina, kao i oštećenje ćelija uz povećanje frekvence mikronukleusa i moguću indukciju apoptoze limfocita periferne krvi. Osnovni cilj ovog istraživanja je da se ispitaju celularne i biohemijske promene u perifernoj krvi pacijenata sa DTC pre i sedam dana nakon aplikacije radioaktivnog 131-I. Istraživanje je dizajnirano kao komparativna kliničko-eksperimentalna studija tokom koje su upoređivani testirani parametri u eksperimentalnoj i kontrolnoj grupi ispitanika. U kliničkom ispitivanju ukupno je učestvovalo 24 pacijenta (16 žena i 8 muškaraca), prosečne starosti 50.83±13.22 godina. Četiri do šest nedelja posle totalne tireoidektomije, i 10 dana nakon dijete siromašne jodom, pacijentima je aplikovana ablaciona doza radioktivnog natrijum jodida (131-I), i to 3.7 GBq (100 mCi) (13 pacijenata) ili 5.5 GBq (150 mCi) (11 pacijenata). Kriterijumi za uključivanje u studiju bili su: histopatološki postavljena dijagnoza papilarnog ili folikularnog karcinoma štitaste žlezde nakon totalne tireoidektomije, konzilijarno doneta odluka o aplikaciji radioaktivnog 131-I, hipotireoidno stanje pacijenta (TSH>30 mIU/L) i potpisan formular informisanog pristanka saglasno Helsinškoj deklaraciji. Kliničkim ispitivanjem nisu obuhvaćeni pacijenti mlađi od 18 godina, pacijenti sa akutnim infekcijama (do mesec dana pre aplikacije 131-I), sa ranije dijagnostifikovanim i/ili lečenim autoimunskim bolestima, ranije dijagnostifikovanim i/ili lečenim hroničnim inflamatornim bolestima i ranije dijagnostifikovanim i/ili lečenim drugim tumorima, odnosno osobe kod kojih je primenjena zračna ili hemioterapija. Sve posmatrane varij, The initial treatment in patients with differentiated thyroid carcinoma (DTC) includes total or near total thyroidectomy and radioactive iodine (131-I) therapy. The propose of 131-I therapy is to ablate remnant thyroid tissue and treat iodine-avid metastases. 131-I induces whole body irradiation followed by oxidative stress and the release of some cytokines, as well as the cellular damage with an increase of micronucleus frequency and potential apoptosis of peripheral blood lymphocytes. The aim of this study was to investigate the cellular and biochemical changes in the peripheral blood of DTC patients before and seven days after administration of radioactive 131-I. The investigation was designed as a comparative clinical-experimental study in which we compared tested parameters in the experimental and control group of subjects. The study population included 24 well-differentiated thyroid cancer patients (16 females and 8 males), with a mean age of 50.83±13.22 years. Four to six weeks after total thyreoidectomy and 10 days after a low iodine diet, the patients were treated with fixed nominal activities of 3.7 GBq (100 mCi)(13 patients) or 5.5 GBq (150 mCi)(11 patients) of orally administrated sodium iodide (131-I). Inclusion criteria were: histopathological confirmed diagnosis of papillary or follicular thyroid carcinoma after total thyroidectomy, consultative decision about the application of radioactive 131-I, hypothyroid condition (TSH>30 mIU/L), and written informed consent according to the Declaration of Helsinki. Patients younger than 18 years, those with acute infections (one month before the application of 131-I), and previously established and/or treated autoimmune diseases, chronic inflammatory diseases and other type of tumors, as persons who underwent the radio- or chemotherapy were not included in the study. The control group consisted of 24 healthy subjects, 19 females and 5 males, with a mean age of 46.37±12.79 who had never diagnosed tumors or chroni

Hepatiĉna encefalopatija (HE) predstavlja neuropsihijatrijski sindrom, koji se razvija kao posledica akutne ili hroniĉne insuficijencije jetre. Za ispitivanje patogeneze HE koriste se razliĉiti eksperimentalni modeli, ukljuĉujući model izazvan portno-kavnim šantom, stenozom portne vene, modele izazvane hepatotoksiĉnim agensima (tioacetamid, D-galaktozamin, paracetamol, azoksimetan, ugljen-tetrahlorid) i modele ciroze jetre. U razvoju HE kljuĉnu ulogu ima hiperamonijemija, a mehanizmi ukljuĉeni u patogenezu HE ukljuĉuju: citotoksiĉni edem mozga, poremećaje neurotransmisije (preteţno glutamatergiĉke i GABA-ergiĉke), energetske poremećaje, oksidacijski stres, mitohondrijsku disfunkciju i neuroinflamaciju. U HE povećava se sinteza neurosteroida, koji pozitivnom alosternom modulacijom receptora za gama-aminobuternu kiselinu (GABAA receptora) pojaĉavaju efekte GABA u centralnom nervnom sistemu. Finasterid, inhibitor 5α-reduktaze i sinteze neurosteroida, potencijalno moţe menjati tok HE. Ciljevi ove disertacije su bili: da se ispitaju bihejvioralne i elektroencefalografske (EEG) promene u HE izazvanoj tioacetamidom kod pacova; da se odrede parametri oksidacijskog stresa i antioksidacijske zaštite, aktivnost acetilholinesteraze (AchE) i ekspresiju ćelijskih markera u razliĉitim moţdanim regionima u intoksikaciji tioacetamidom; da se ispita uticaj finasterida na bihejvioralne, EEG i ćelijske promene u HE izazvanoj tioacetamidom kod pacova. U cilju ispitivanja efekata tioacetamida (TAA) na ponašanje, EEG i ćelijske promene muţjaci Wistar pacova su podeljeni u sledeće grupe: 1. kontrolna grupa (n=8); 2. eksperimentalna grupa tretirana TAA na dozno zavisan naĉin: TAA300 (300 mg/kg, n=8), TAA600 (600 mg/kg, n=10) i TAA900 (900 mg/kg, n=18). Dnevne doze TAA (300 mg/kg) su primenjene tokom jednog (TAA300), dva (TAA600) ili tri uzastopna dana (TAA900). U cilju ispitivanja uticaja finasterida na HE izazvanu TAA-om, ţivotinje su podeljene u sledeće grupe: 1. kontrolna grupa (n=8); 2., Hepatic encephalopathy (HE) represents a neuropsychiatric syndrome, that appears as a consequence of acute or chronic liver failure. Various experimental models are used for the investigation of the pathogenesis of HE, including porto-caval shunt, portal vein stricture, models induced by hepatotoxic agents (thioacetamide, D-galactosamine, acetaminophen, azoxymethane, carbon tetrachloride) and models of liver cirrhosis. Hyperammonemia has a pivotal role in the development of HE, and mechanisms involved in the pathogenesis of HE include: cytotoxic brain edema, alterations in neurotransmission (especially glutamatergic and GABAergic), energy disturbances, oxidative stress, mitochondrial dysfunction and neuroinflammation. The synthesis of neurosteroids is increased in HE and by positive allosteric modulation of gamma-aminobutyric acid (GABAA) receptors they potentiate the effects og GABA in the central nervous system. Finasteride, 5α-reductase and neurosteroid synthesis inhibitor, may potentially modulate the course of HE. The aims of this dissertation were: to investigate the behavioral and electroencephalographic (EEG) changes in thioacetamide-induced HE in rats; to determine the parameters of oxidative stress and antioxidative protection, the activity of acetylcholinesterase (AchE) and cellular marker expression in various brain regions; to investigate the effects of finasteride on behavioral, EEG and cellular changes in thioacetamide-induced HE in rats. In order to investigate the effects of thioacetamide (TAA) on the behavior, EEG and cellular changes male Wistar rats were divided into the following groups: 1. control; 2. experimental group treated with TAA in a dose-dependent manner: TAA300 (300 mg/kg; n=8), TAA600 (600 mg/kg; n=10) and TAA900 (900 mg/kg; n=18). Daily doses of TAA (300 mg/kg) were administered once (TAA300), twice (TAA600) or three times (TAA900) in subsequent days. In order to investigate the effects of finasteride on TAA-induced HE, the animals

Development of nonalcoholic fatty liver disease (NAFLD) occurs through initial steatosis and subsequent oxidative stress. The aim of this study was to examine the effects of -lipoic acid (LA) on methionine-choline deficient (MCD) diet-induced NAFLD in mice. Male C57BL/6 mice (n=21) were divided into three groups (n=7 per group): (1) control fed with standard chow, (2) MCD2 groupfed with MCD diet for 2 weeks, and (3) MCD2+LA group2 weeks on MCD receiving LA i.p. 100mg/kg/day. After the treatment, liver samples were taken for pathohistology, oxidative stress parameters, antioxidative enzymes, and liver free fatty acid (FFA) composition. Mild microvesicular hepatic steatosis was found in MCD2 group, while it was reduced to single fat droplets evident in MCD2+LA group. Lipid peroxidation and nitrosative stress were increased by MCD diet, while LA administration induced a decrease in liver malondialdehyde and nitrates+nitrites level. Similary, LA improved liver antioxidative capacity by increasing total superoxide dismutase (tSOD), manganese SOD (MnSOD), and copper/zinc-SOD (Cu/ZnSOD) activity as well as glutathione (GSH) content. Liver FFA profile has shown a significant decrease in saturated acids, arachidonic, and docosahexaenoic acid (DHA), while LA treatment increased their proportions. It can be concluded that LA ameliorates lipid peroxidation and nitrosative stress in MCD diet-induced hepatic steatosis through an increase in SOD activity and GSH level. In addition, LA increases the proportion of palmitic, stearic, arachidonic, and DHA in the fatty liver. An increase in DHA may be a potential mechanism of anti-inflammatory and antioxidant effects of LA in MCD diet-induced NAFLD.