GSH Levels In Rats Research Articles

Antioxidant effect of omega-3 fatty acids on exercise-induced oxidative stress in rats.

The aim of this study is to examine the effects of omega-3 supplementation on Catalase (CAT) activity, Malondialdehyde (MDA), advanced oxidation protein products (AOPP) and reduced glutathione (GSH) levels in long-term aerobic exercises in rats. 28 male Wistar albino rats (8 weeks old, 220-350 g body weight) were included in the study. The rats were given treadmill exercise for 20 minutes at an average speed of 15 cm/s, 5 days a week, for 8 weeks. The experiment was terminated at the end of the eighth week. Blood samples were taken. CAT, MDA, AOPP and GSH analyses were performed. SPSS v. 21 package program was used in the analysis of the data. The distribution of the data was examined with the normality homogeneity test, and it was determined that it was a normal distribution. As a result, the One-Way ANOVA test, one of the parametric tests, was used. Tukey test was used to determine the difference between groups. Significance levels were evaluated as (p < 0.05). Statistical analysis showed a statistically significant difference between groups in CAT, MDA and GSH levels (p < 0.05), while there were no differences between the groups in AOPP levels (p > 0.05). In the conclusion of the study, it was determined that omega-3 supplementation caused a decrease in MDA level, an increase in CAT activity and GSH level in rats exposed to chronic long-term exercise. Thus, it can be said that omega-3 supplementation in chronic long-term exercise will provide antioxidant protection against potential oxidative damage.

Eel Oil Attenuates Acetaminophen-Induced Acute Liver Injury Through Inhibition of Oxidative Stress in Rats

Health practitioners all over the world have studied liver injury caused by drug side effects. Excessive production of free radicals causes cell damage, which has implications for pathological conditions in both humans and animals. Omega-3 fatty acids are a component of fish that can work as hepatoprotective agents. Eel (Anguilla bicolor) is known to contain omega-3 including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). This study aimed to evaluate the hepatoprotective activity of eel oil on rats via inhibiting oxidative stress. Methods: Acetaminophen-induced male Wistar rats were used as liver injury experimental models. Rats were divided into 5 groups, namely normal control, negative control, positive control (silymarin, 100 mg/kg), and two groups of eel oil dose (2000 mg/kg and 4000 mg/kg). The study was conducted for 14 days. The levels of serum glutamic pyruvic transaminase (SGPT), serum glutamic pyruvic transaminase (SGOT), alkaline phosphatase (ALP), total bilirubin, albumin, Malondialdehyde (MDA), and glutathione (GSH) levels of the liver organ were measured. The data were analyzed using statistics and analysis of variance. Results: The study showed that eel fish oil can reduce SGPT and total bilirubin levels of male Wistar rats induced by acetaminophen. Eel oil at a dose of 4000 mg/kg could significantly reduce SGPT and liver bilirubin levels in male Wistar rats (p&lt;0.05). Eel oil is effective in reducing malondialdehyde (MDA) levels and increasing glutathione (GSH) levels at a dose of 2000 mg/kg. Conclusion: Eel oil has hepatoprotective activity by inhibiting SGPT, total bilirubin, MDA, and increasing GSH levels in rats.

Glutathione in the nucleus accumbens regulates motivation to exert reward-incentivized effort.

Emerging evidence is implicating mitochondrial function and metabolism in the nucleus accumbens in motivated performance. However, the brain is vulnerable to excessive oxidative insults resulting from neurometabolic processes, and whether antioxidant levels in the nucleus accumbens contribute to motivated performance is not known. Here, we identify a critical role for glutathione (GSH), the most important endogenous antioxidant in the brain, in motivation. Using proton magnetic resonance spectroscopy at ultra-high field in both male humans and rodent populations, we establish that higher accumbal GSH levels are highly predictive of better, and particularly, steady performance over time in effort-related tasks. Causality was established in <i>in vivo</i> experiments in rats that, first, showed that downregulating GSH levels through micro-injections of the GSH synthesis inhibitor buthionine sulfoximine in the nucleus accumbens impaired effort-based reward-incentivized performance. In addition, systemic treatment with the GSH precursor N-acetyl-cysteine increased accumbal GSH levels in rats and led to improved performance, potentially mediated by a cell-type-specific shift in glutamatergic inputs to accumbal medium spiny neurons. Our data indicate a close association between accumbal GSH levels and an individual's capacity to exert reward-incentivized effort over time. They also suggest that improvement of accumbal antioxidant function may be a feasible approach to boost motivation.

Effect of Hydroalcoholic Extract of Stem Bark of &amp;lt;i&amp;gt;Bridelia ferruginea&amp;lt;/i&amp;gt; on Blood Coagulation

<i>Bridelia ferruginea</i> is a plant commonly used in several regions of the world for its various properties. It is offered to certain patients with cerebrovascular accidents. It is with this in mind that this study is undertaken in order to verify whether <i>B. ferruginea</i> has an activity on blood coagulation. <i>Materiel and method:</i> Stem bark of <i>B. ferruginea</i> was collected at Noepe (24 km northwest of Lome). Hydroalcoholic extract (50/50) was obtained by evaporation. Male Wistar rats were used for the tests. Qualitative screening was done according to conventional methods and total phenols were quantified. Some parameters of coagulation (blood platelets, aPTT, PR and fibrinogen) were determined. Oxidative stress was induced by Fe-NTA. Results were analysed by GraphPad®Prism 8.4.2. Analysis of variance (ANOVA) was used to compare several groups. The difference between groups was determined by Tukeyʼs test and considered significant at p<0.05. <i>Results:</i> Hydroalcoholic extract of <i>B. ferruginea</i> increased aPTT and decreased PR. Compared to the negative control (distilled water), oxidative stress was responsible in vivo for an increase in platelets blood number and PR and a decrease in aPTT and fibrinogen. The hydroalcoholic extract of <i>B. ferruginea</i> caused a decrease in platelets blood number (at low concentration), PR and fibrinogen level and an increase in the platelets blood number (at high concentration) and aPTT. Hydroalcoholic extract of <i>B. ferruginea</i> decreased MDA levels and increased GSH levels in rats subjected to oxidative stress. <i>Conclusion:</i> The present study proved existence of antioxidant and anticoagulant activities of <i>B. ferruginea</i> stem bark. There is a link between oxidative stress and coagulation. Future studies may better elucidate interaction between oxidative stress and coagulation mechanisms involved.

Superior Properties of N-Acetylcysteine Ethyl Ester over N-Acetyl Cysteine to Prevent Retinal Pigment Epithelial Cells Oxidative Damage.

Oxidative stress plays a key role in the pathophysiology of retinal diseases, including age-related macular degeneration (AMD) and diabetic retinopathy, which are the major causes of irreversible blindness in developed countries. An excess of reactive oxygen species (ROS) can directly cause functional and morphological impairments in retinal pigment epithelium (RPE), endothelial cells, and retinal ganglion cells. Antioxidants may represent a preventive/therapeutic strategy and reduce the risk of progression of AMD. Among antioxidants, N-acetyl-L-cysteine (NAC) is widely studied and has been proposed to have therapeutic benefit in treating AMD by mitigating oxidative damage in RPE. Here, we demonstrate that N-acetyl-L-cysteine ethyl ester (NACET), a lipophilic cell-permeable cysteine derivative, increases the viability in oxidative stressed RPE cells more efficiently than NAC by reacting directly and more rapidly with oxidizing agents, and that NACET, but not NAC, pretreatment predisposes RPE cells to oxidative stress resistance and increases the intracellular reduced glutathione (GSH) pool available to act as natural antioxidant defense. Moreover, we demonstrate the ability of NACET to increase GSH levels in rats’ eyes after oral administration. In conclusion, even if experiments in AMD animal models are still needed, our data suggest that NACET may play an important role in preventing and treating retinal diseases associated with oxidative stress, and may represent a valid and more efficient alternative to NAC in therapeutic protocols in which NAC has already shown promising results.

Oxido-inflammatory responses and histological alterations in rat lungs exposed to petroleum product fumes.

Petroleum products-petrol, kerosene, and diesel-composed of volatile organic constituents contribute to air pollution. Exposure of gas station attendants (GSAs) to petroleum products fumes (PPFs) may account for occupation-related predisposition to respiratory toxicity and disease pathogenesis. We simulated GSA exposure to PPF inhalation and examined their effect on oxido-inflammatory responses, toxicity, and histopathological alterations in rat lungs, following 8-hours daily exposure for 60 and 90 days. Reactive oxygen and nitrogen species (RONS), oxidative stress and inflammatory biomarkers, namely: superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione-S-transferase (GST), TNF-α, IL-1β, xanthine oxidase (XO), nitric oxide (NO) activity were evaluated. Besides, histopathological examination of the lungs and trachea of exposed rats, PPF exposure resulted in significant (P < .05) increases in RONS, biomarkers of oxidative stress, pro-inflammation cytokines, and reduced (P < .05) GSH levels in rats, secondary to histopathological alteration in lungs and trachea cytoarchitecture examined in an exposure-duration-dependent manner. We conclude, therefore, that the observed biochemical and histological changes create a microenvironment that is permissive to diseases pathogenesis of the respiratory system via oxido-inflammatory mechanistic pathways.

Antioxidant Effect of Bilberry on Oxidative Stress Caused by Acute Exercise in Rats

This research is supported by Atatürk University Scientific Research Commission. Abstract This study, it was aimed to determine the antioxidant effect of bilberry extract in decreasing the oxidative stress caused by acute exhaustive exercises in rats' blood and liver tissues. 27 Spraque-Dawley type male rats were divided into four groups (control, exercise, bilberry and bilberry+exercise groups). Bilberry extract was administered using gavage once daily. Before blood and liver tissues were taken, the rats ran in a treadmill at a speed of 25 m/min (1.5 km / h) at a slope of 0 for about 1 hour or until exhaustion. Compared to the control group, serum GSH levels and GPx activities did not have a significant change in the bilberry, acute exercise and bilberry + acute exercise groups; while serum MDA levels decreased significantly. When compared to the control group, liver GPx activity significantly increased in the bilberry and bilberry+acute exercise groups. Again, it was determined that liver GSH level significantly increased in bilberry+acute exercise group.The results of this study demonstrate that bilberry extract may provide antioxidant protection against a potential oxidative damage as it causes an increase in hepatic GPx activity and GSH levels in rats exposed to acute exhaustive exercise. Keywords: Antioxidants, acute exhaustive exercise, bilberry, glutathione, glutathione peroxidase, malondialdehy DOI: 10.7176/JMPB/65-04 Publication date: April 30 th 2020

The role of oxymatrine in regulating TGF-β1 in rats with hepatic fibrosis.

To investigate whether oxymatrine (OMT) prevents hepatic fibrosis in rats by regulating liver transforming growth factor β1 (TGF-β1) level. Hepatic fibrosis was induced in rats by thioacetamide (TAA). Blood was collected at the end of week 12 to determine the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and glutathione (GSH). Changes in liver tissue were observed after hematoxylin-eosin (HE) staining. Fibrosis was confirmed by Masson's collagen staining. Liver TGF-β1 level was determined by ELISA. OMT significantly reduced serum ALT and AST but increased GSH levels in rats with hepatic fibrosis. Moreover, it significantly improved liver histology in rats with TAA-induced hepatic fibrosis. It significantly decreased liver TGF-β1 level compared to that in the untreated group. It also significantly reduced collagen deposition in rats. Oxymatrine is effective in protecting rats from thioacetamide-induced hepatic fibrosis by regulating TGF-β1 expression.

Protective effects of Aristolochia longa and Aquilaria malaccensis against lead induced acute liver injury in rats

Objective: To investigate the protective effects of Aristolochia longa (A. longa) and Aquilaria malaccensis (A. malaccensis) on acute hepatotoxicity induced by lead in female albino rats. Methods: Twenty five (25) apparently healthy female Wistar rats were randomly divided into five groups of five rats in each: control, Pb, Pb + A. longa (Ar), Pb+ A. malaccensis (Aq), and Pb+ A. longa (Ar) + A. malaccensis (Aq) lead (100 mg/kg b.w.) as Pb (C2H3O2)2 added in their drinking water for 75 days. A. longa (rhizome powder at a dose of 10 g/kg of diet) and A. malaccensis (heartwood powder at a dose 10 g/kg of diet) were added to the feed during the last 15 days of lead exposed in the animals. Results: Obtained results revealed that lead treatment caused a significant increase in serum GOT, GPT and ALP activities and in liver of MDA level and CAT activity. In contrast, it led to an decrease in the liver GOT, GPT and GST activities and in GSH level in rats. Also, the results clearly showed that lead causes alterations of hepatic tissue in comparison with controls. Our results showed that treatment with A. malaccensis and A. longa a partial correction of the previous parameters. The histological observations confirmed the hepatoprotection results by the biochemical parameters. Conclusions: Results demonstrated beneficial effects of A. longa and A. malaccensis treatment in Pb-induced oxidative stress and tissue damage in liver.

Amelioration of energy metabolism by melatonin in skeletal muscle of rats with LPS induced endotoxemia.

In the literature, few studies have investigated the effects of melatonin on energy metabolism in skeletal muscle in endotoxemia. We investigated the effects of melatonin on tissue structure, energy metabolism in skeletal muscle, and antioxidant level of rats with endotoxemia. We divided rats into 4 groups, control, lipopolysaccharide (LPS) (20 mg/kg, i.p., single dose), melatonin (10 mg/kg, i.p., three times), and melatonin + LPS. Melatonin was injected i.p. 30 min before and after the 2nd and 4th hours of LPS injection. Antioxidant status was determined by glutathione (GSH) measurement in the blood. Muscle tissue was stained using modified Gomori trichrome (MGT), succinic dehydrogenase (SDH), and cytochrome oxidase (COX) and histological scored. Also the sections were then stained with hematoxylin and eosin. The stained sections were visualized and photographed. Creatine, creatine phosphate, adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) levels were investigated using high performance liquid chromatography (HPLC) in muscle tissue. In the Melatonin + LPS group, blood GSH levels were increased compared with the LPS group (P<0.01). Melatonin reduced myopathic changes in the LPS group according to the histopathologic findings. In addition, ATP values were increased compared with the LPS group (P<0.05). Our findings showed melatonin treatment prevented muscle damage by increasing ATP and GSH levels in rats with LPS induced endotoxemia.

Increase in covalent binding of 5-hydroxydiclofenac to hepatic tissues in rats co-treated with lipopolysaccharide and diclofenac: involvement in the onset of diclofenac-induced idiosyncratic hepatotoxicity

Diclofenac (DCF), a nonsteroidal anti-inflammatory drug, is well known to induce idiosyncratic hepatotoxicity. Although there remains much to be elucidated about its onset mechanism, it is widely accepted as a hypothesis that idiosyncratic hepatotoxicity arises from a specific immune response to a hapten formed by covalent binding of drugs or their reactive metabolites to hepatic tissues. In this study, we investigated the effects of covalent binding of DCF reactive metabolites to hepatic tissues using a rat model of liver injury induced by co-treatment with lipopolysaccharide (LPS) at a non-hepatotoxic dose. In studies done in vitro using hepatic microsomes prepared from rats treated with LPS alone, 4'- and 5-hydroxylation activities on DCF metabolism and adducts of reactive metabolites to dansyl glutathione (dGSH) were markedly decreased associated with a decrease in total P450 content. However, in studies done in vivo, the LPS/DCF co-treatment significantly increased adducts of 5-hydroxydiclofenac (5-OH-DCF) to rat hepatic tissues and delayed the elimination of 5-OH-DCF from plasma. Furthermore, we investigated the effects of co-treatment on hepatic GSH level in rats. A decrease of hepatic GSH was observed with the LPS/DCF co-treatment but not with LPS or DCF alone. The results suggest that covalent binding of reactive metabolites via 5-OH-DCF to hepatic tissues may play an important role in the onset of DCF-induced idiosyncratic hepatotoxicity, especially under decreased GSH conditions.

Effect of quercetin on lipid peroxidation and GSH levels in rats exposed to ultraviolet A (UV A)

Effect of quercetin on lipid peroxidation and GSH levels in rats exposed to ultraviolet A (UV A)

Influence of vitamin B 6 status on aspects of lead poisoning in rats

The effects of vitamin B 6 status and lead (Pb) toxicity on aspects of glutathione (GSH) metabolism in rats were examined in a 2 × 2 factorial experiment. The administration of 2000 ppm Pb as Pb acetate 3H 2O significantly ( P<0.05) increased hepatic GSH levels in rats receiving B 6-adequate (+B 6) but decreased GSH in rats fed B 6-deficient (−B 6) diets. The addition of Pb to the +B 6 diet also increased hepatic glutathione reductase (GSSG-R) activity. Plasma pyridoxal phosphate (PLP), cystathionine and valine levels were decreased by the −B 6 diets independent of the presence of Pb. Plasma arginine, alanine, serine and proline levels were increased by Pb in both −B 6 and +B 6 groups. Glycine levels were increased in −B 6 rats only in the absence of Pb while taurine was decreased by Pb only in +B 6 rats. There were significant −B 6 × Pb interactions for hepatic GSH, cysteine and GSSG-R as well as plasma valine, glycine and proline. These results suggest an influence of B 6 status on Pb-induced changes in hepatic GSH, possibly through its role as a co-factor for enzymes involved in amino acid metabolism.

Effect of BSO and phorone on GSH levels in rats with gastric ulcer

Effect of BSO and phorone on GSH levels in rats with gastric ulcer

Effect of Glutathione on Lipogenesis in Liver Slices from Rats Fed on Low Casein Diet

To study the mechanism of fatty infiltration in the liver due to added sulfur-containing amino acids to low casein diet, the effect of sulfur-containing amino acids and glutathione (GSH) on the incorporation of acetate-l-14C into lipid fractions were studied in liver slices from rats fed on 8% casein diet (Basal diet) with or without added methionine (Met). The liver acetyl Co A carboxylase activities of rats on basal diet with or without added Met were similar. Addition of Met, cystine or cysteine to the incubation medium had little effect on lipogenesis of slices. On addition of GSH to liver slices from rats fed on basal diet, lipid formation increased appreciably. On the other hand, addition of GSH to liver slices from rats fed on Met supplemented diet showed no accelerative effect on lipogenesis. Addition of GSH to the incubation medium of liver slices from rats fed on basal diet tended to reduce the incorporation of acetate into the phospholipid fraction and to increase into the fatty acid fraction of liver slices. The content of liver GSH was lower in rats on basal diet than in those on Met supplemented diet. The higher GSH level in rats on Met supplemented diet may be one factor causing fatty infiltration in the liver of these animals.