scholarly journals Changes in Antioxidants in the Brain of Fluoride-Treated Rats

2021 ◽  
pp. 41-48
Author(s):  
Abdulrahman Abdullateef ◽  
Rasheed Abiola Olajide ◽  
Ekpa Emmanuel ◽  
Muhibat Komolafe Bolanle ◽  
Khadijah Umaru
Keyword(s):  
Glutathione Peroxidase ◽  
Wistar Rats ◽  
Defense Mechanism ◽  
Antioxidant Activities ◽  
Reduced Glutathione ◽  
Average Weight ◽  
Glutathione S Transferase ◽  
Severe Problem ◽  
Male Wistar Rats ◽  
The Brain

In recent times, fluorosis is gradually becoming a severe problem throughout the globe due to toxic effects of fluoride (F) on plants and animals. Natural geological sources and increased industrialization have contributed greatly to the increasing incidence of fluoride-induced human and animal toxicities. Adverse effects are mainly through the attenuation of antioxidant defense mechanism and chelation of enzymatic cofactors. This present study was carried out to investigate the changes that occur on antioxidants in the brain of male wistar rats after sub-chronic fluoride exposure at varying doses (10 ppm, 20 ppm and 40 ppm). Twenty-four (24) Male Wistar rats with average weight of 120 g were distributed into 4 groups according to dose administration (Control; 10 ppm, 20 ppm and 40 ppm) of 6 animals each. The control groups were given only distilled water while the Test groups were given sodium fluoride at doses mentioned above for 30 days. Overnight fasted animals from each group were sacrificed on the 30th day and the brain removed for studying the antioxidant activities. Catalase (CAT), reduced glutathione (GSH), glutathione peroxidase (GPx) and glutathione-s-transferase (GST) were measured from the homogenized brain supernatants. Results showed that CAT and GPx decreased in activity in respect to the dose being applied. Decrease in glutathione peroxidase activity was highest at 20 ppm and 40 ppm while Catalase activity showed a decrease at 10 ppm. Reduced glutathione GSH activity increased in the 10 ppm and 20 ppm but decreased at 40 ppm. Other antioxidant activities measured displayed similar trend with much decrease at higher doses. From our results we can say that fluoride toxicity causes changes in antioxidants level. The implications of these findings are herein discussed.

scholarly journals Antioxidant and Hepatoprotective Effect of Cajanus cajan in N-Nitrosodiethylamine-Induced Liver Damage

2019 ◽  
Vol 87 (3) ◽  
pp. 24 ◽  
Author(s):  
Emeka Eze Joshua Iweala ◽  
Winifred Osa Evbakhavbokun ◽  
Emmanuel Ndubisi Maduagwu
Keyword(s):  
Tobacco Smoke ◽  
Cajanus Cajan ◽  
Wistar Rats ◽  
Reduced Glutathione ◽  
Liver Weight ◽  
Treated Group ◽  
Hepatoprotective Effect ◽  
Histopathological Changes ◽  
Glutathione S Transferase ◽  
Male Wistar Rats

N-Nitrosodiethylamine (NDEA) is a nitrosamine derivative with carcinogenic and mutagenic properties which can be found in tobacco smoke, meat and various food products. This study examined the antioxidant and hepatoprotective potential of Cajanus cajan (C. cajan) with respect to hepatotoxicity in male Wistar rats. Administration of NDEA induced hepatotoxicity at 200 mg/kg while C. cajan was administered (200, 400 and 800 mg/kg) for 28 days. NDEA-induced hepatotoxicity significantly (p ≤ 0.05) increased alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malondialdehyde (MDA) and significantly (p ≤ 0.05) decreased reduced glutathione (GSH), albumin (ALB), glutathione S-transferase (GST), catalase (CAT) and superoxide dismutase (SOD). C. cajan-treated groups were seen to have significantly (p ≤ 0.05) decreased ALT and AST and significantly (p < 0.05) increased ALB, GST, GSH, SOD and CAT. The NDEA-treated group also showed a marginal increase in body weight and a significant (p ≤ 0.05) increase in liver weight. The C. cajan treated groups showed a significant (p ≤ 0.05) increase and decrease respectively in body and liver weights. Histopathological changes also substantiated NDEA-induced hepatotoxicity and the hepatoprotective effect of C. cajan on the liver. The results indicate that C. cajan has the potential to ameliorate NDEA-induced hepatotoxicity.

scholarly journals Hepatoprotective effect of aqueous extract of Aframomum melegueta on ethanol-induced toxicity in rats.

2011 ◽  
Vol 58 (3) ◽  
Author(s):  
Sarah O Nwozo ◽  
Babatunji E Oyinloye
Keyword(s):  
Superoxide Dismutase ◽  
Plant Extract ◽  
Antioxidant Activities ◽  
Reduced Glutathione ◽  
Ethanol Administration ◽  
Protective Effects ◽  
Glutathione S Transferase ◽  
Histological Changes ◽  
Male Wistar Rats ◽  
Chronic Ethanol Administration

In recent years there have been remarkable developments in the prevention of diseases, especially with regards to the role of free radicals and antioxidants. Ethanol-induced oxidative stress appears to be one mechanism by which ethanol causes liver injury. The protective effect of aqueous plant extract of Aframomum melegueta on ethanol-induced toxicity was investigated in male Wistar rats. The rats were treated with 45 % ethanol (4.8 g/kg b.w.t.) for 16 days to induce alcoholic diseases in the liver. The activities of alanine aminotransferase, aspartate aminotransferase and triglyceride were monitored and the histological changes in liver examined in order to evaluate the protective effects of the plant extract. Hepatic malondialdehyde and reduced glutathione, as well as superoxide dismutase and glutathione-S-transferase activities were determined for the antioxidant status. Chronic ethanol administration resulted in a statistically significant elevation of serum alanine aminotransferases and triglyceride levels, as well as a decrease in reduced glutathione and superoxide dismutase which was dramatically attenuated by the co-administration of the plant extract. Histological changes were related to these indices. Co-administration of the plant extract suppressed the elevation of lipid peroxidation, restored the reduced glutathion, and enhanced the superoxide dismutase activity. These results highlight the ability of Aframomum melegueta to ameliorate oxidative damage in the liver and the observed effects are associated with its antioxidant activities.

Melatonin prevents and ameliorates lead-induced gonadotoxicity through antioxidative and hormonal mechanisms

2018 ◽  
Vol 34 (9) ◽  
pp. 596-608 ◽  
Author(s):  
Luqman Aribidesi Olayaki ◽  
Isiaka Abdullateef Alagbonsi ◽  
Amin Halimat Abdulrahim ◽  
Wale Johnson Adeyemi ◽  
Muftiat Bakare ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Biochemical Markers ◽  
Wistar Rats ◽  
Reduced Glutathione ◽  
Gonadotropin Releasing Hormone ◽  
Semen Parameters ◽  
Total Antioxidant ◽  
Male Wistar Rats

We investigated the effects of melatonin on sperm parameters and some biochemical markers in lead-exposed male Wistar rats. Lead (50 mg/kg bw/day) and/or melatonin (4 mg/kg or 10 mg/kg bw/day) was administered for 4 weeks, while 2-week lead exposure was preceded by or followed by 2-week treatment with both doses of melatonin in other groups. Lead reduced glutathione, catalase, adjusted testes weight, semen parameters but did not change malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase, and total antioxidant capacity. Though independent of prolactin, lead-induced gonadotoxicity was both centrally and peripherally mediated, as it reduced gonadotropin-releasing hormone and testosterone levels, while gonadotropin levels did not change significantly probably due to negative feedback by elevated estradiol. However, pre-, simultaneous, or posttreatment of lead-exposed rats with melatonin reduced MDA, SOD, and estradiol but dose-dependently increased other parameters. Conclusively, lead causes male gonadotoxicity through oxidative stress and endocrine mechanisms, and these could be dose-dependently prevented and ameliorated by melatonin.

Renal Cortical Slices: An In Vitro Model for Kidney Metabolism and Toxicity

1992 ◽  
Vol 20 (1) ◽  
pp. 71-76
Author(s):  
Andrea Trevisan ◽  
Stefano Maso ◽  
Paola Meneghetti
Keyword(s):  
Wistar Rats ◽  
Reduced Glutathione ◽  
Organic Anion ◽  
Cortical Slice ◽  
Lactate Dehydrogenase Release ◽  
Age Related ◽  
Renal Cortical Slice ◽  
Male Wistar Rats ◽  
Vitro Model

The in vitro renal cortical slice model was used to study: 1) the effects on the kidney of some haloalkanes and haloalkenes using 3-month-old male Wistar rats; 2) influence of age and sex on renal cortical slice indices in non-treated rats; and 3) effects of 1,2-dichloropropane on the slices after pretreatment of 3-month-old male Wistar rats with DL-butathionine-[S,R]-sulphoximine. The most nephrotoxic chemical used was 1,3-dichloropropene, which caused a total depletion in the levels of reduced glutathione, a high peroxidation of lipid (about three thousand-fold with respect to control), a significant release of tubular enzymes into the medium, and loss of organic anion ( p-aminohippurate) accumulation. All the chemicals affected the cytosol more than the brush border. The most remarkable age-related differences in the untreated slices were the progressive decrease of reduced glutathione (p<0.05 from three months of age), and an increase in lactate dehydrogenase release into the medium (p<0.05 from six months of age). By contrast, sex differences were slight. The ‘treatment with 1,2-dichloropropane of slices prepared from rats pretreated with DL-butathionine-[S,R]-sulphoximine significantly increased the depletion of glutathione content (p<0.05) and malondialdehyde release in the medium (p<0.001) caused by the solvent alone.

scholarly journals Impact of Vanadium Complexes Treatment on the Oxidative Stress Factors in Wistar Rats Plasma

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
R. Francik ◽  
M. Krośniak ◽  
M. Barlik ◽  
A. Kudła ◽  
R. Gryboś ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Reduced Glutathione ◽  
The Body ◽  
Stress Factors ◽  
Control Group ◽  
Vanadium Complexes ◽  
Healthy Male ◽  
Reducing Ability ◽  
Male Wistar Rats ◽  
Antioxidant Parameters

The aim of this study was to investigate the clinical efficacy of vanadium complexes on triglycerides (TG), total cholesterol (Chol), uric acid (UA), urea (U), and antioxidant parameters: nonenzymatic (FRAP—ferric reducing ability of plasma, and reduced glutathione—GSH) and enzymatic (glutathione peroxidase—GPx, catalase—CAT, and GPx/CAT ratio) activity in the plasma of healthy male Wistar rats. Three vanadium complexes: [VO(bpy)2]SO4⋅2H2O, [VO(4,4′Me2bpy)2]SO4⋅2H2O, and Na[VO(O2)2(bpy)]⋅8H2O are administered by gavage during 5 weeks in two different diets such as control (C) and high fatty (F) diets. Changes of biochemical and antioxidants parameters are measured in plasma. All three vanadium complexes statistically decrease the body mass growth in comparison to the control and fatty diet. In plasma GSH was statistically increased in all vanadium complexes-treated rats from control and fatty group in comparison to only control group. Calculated GPX/CAT ratio was the highest in the control group in comparison to others.

scholarly journals The subchronic effects of 3,4-methylendioxymethamphetamine on oxidative stress in rat brain

2014 ◽  
Vol 66 (3) ◽  
pp. 1075-1081
Author(s):  
Ivan Simic ◽  
Violeta Iric-Cupic ◽  
Rada Vucic ◽  
Marina Petrovic ◽  
Violeta Mladenovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Rat Brain ◽  
Wistar Rats ◽  
Superoxide Radical ◽  
Reduced Glutathione ◽  
Oxidative Stress Markers ◽  
Sod Activity ◽  
Stress Markers ◽  
Male Wistar Rats

The aim of the present study was to evaluate the subchronic effects of 3,4-methylenedioxymethamphetamine on several oxidative stress markers: index of lipid peroxidation (ILP), superoxide dismutase (SOD) activity, superoxide radical (O2.-) levels, and reduced glutathione (GSH) levels in the frontal cortex, striatum and hippocampus of the rat. The study included 64 male Wistar rats (200-250g). The animals were treated per os with of 5, 10, or 20 mg/kg of 3,4-methylenedioxymethamphetamine (MDMA) every day for 15 days. The subchronic administration of MDMA resulted in an increase in ILP, SOD and O2.-, and a decrease in GSH, from which we conclude that oxidative stress was induced in rat brain.

Oxidative damage and antioxidants in cervical cancer

2020 ◽  
pp. ijgc-2020-001587
Author(s):  
Daciele Paola Preci ◽  
Angélica Almeida ◽  
Anne Liss Weiler ◽  
Maria Luiza Mukai Franciosi ◽  
Andréia Machado Cardoso
Keyword(s):  
Cervical Cancer ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Oxidative Damage ◽  
Cancer Progression ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Enzymatic Antioxidants ◽  
Glutathione S Transferase ◽  
The Impact

The pathogenesis of cervical cancer is related to oxidative damage caused by persistent infection by one of the oncogenic types of human papillomavirus (HPV). This damage comes from oxidative stress, which is the imbalance caused by the increase in reactive oxygen and nitrogen species and impaired antioxidant mechanisms, promoting tumor progression through metabolic processes. The incorporation of HPV into the cellular genome leads to the expression of oncoproteins, which are associated with chronic inflammation and increased production of reactive oxygen species, oxidizing proteins, lipids and DNA. The increase in these parameters is related, in general, to the reduction of circulating levels of enzymatic antioxidants—superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase; and non-enzymatic antioxidants—reduced glutathione, coenzyme Q10 and vitamins A, C and E, according to tumor staging. In contrast, some enzymatic antioxidants suffer upregulation in the tumor tissue as a way of adapting to the oxidative environment generated by themselves, such as glutathione-S-transferase, reduced glutathione, glutathione peroxidase, superoxide dismutase 2, induced nitric oxide synthase, peroxiredoxins 1, 3 and 6, and thioredoxin reductase 2. The decrease in the expression and activity of certain circulatory antioxidants and increasing the redox status of the tumor cells are thus key to cervical carcinoma prognosis. In addition, vitamin deficit is considered a possible modifiable risk factor by supplementation, since the cellular functions can have a protective effect on the development of cervical cancer. In this review, we will discuss the impact of oxidative damage on cervical cancer progression, as well as the main oxidative markers and therapeutic potentialities of antioxidants.

scholarly journals Effect of Antioxidant Treatment on Fibrogenesis in Rats with Carbon Tetrachloride-Induced Cirrhosis

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Silvia Bona ◽  
Lidiane Isabel Filippin ◽  
Fábio Cangeri Di Naso ◽  
Cintia de David ◽  
Bruna Valiatti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Reduced Glutathione ◽  
Thiobarbituric Acid ◽  
Matrix Metalloproteinase 2 ◽  
Glutathione Disulfide ◽  
Antioxidant Treatment ◽  
P450 Enzyme ◽  
Male Wistar Rats ◽  
Increased Activity

Aim. This study aimed to assess the antioxidant activity of quercetin (Q) in an experimental model of cirrhosis induced by CCl4 inhalation. Materials and Methods. We used 25 male Wistar rats (250 g) that were divided into 3 groups: control (CO), CCl4, and CCl4+Q. The rats were subjected to CCl4 inhalation (2x/week) for 16 weeks, and they received phenobarbital in their drinking water at a dose of 0.3 g/dL as a P450 enzyme inducer. Q (50 mg/Kg) was initiated intraperitoneally at 10 weeks of inhalation and lasted until the end of the experiment. Statistical analysis was by ANOVA Student Newman-Keuls (mean±SEM), and differences were considered statistically significant when P<0.05. Results. After treatment with quercetin, we observed an improvement in liver complications, decreased fibrosis, as analyzed by picrosirius for the quantification of collagen, and decreased levels of matrix metalloproteinase 2 (MMP-2) compared with the CCl4 group. It also reduced oxidative stress, as confirmed by the decrease of substances reacting to thiobarbituric acid (TBARS), the increased activity of antioxidant enzymes, and the reduced glutathione ratio and glutathione disulfide (GSH/GSSG). Conclusion. We suggest that the use of quercetin might be promising as an antioxidant therapy in liver fibrosis.

Anxiety-related behavior in hyperhomocysteinemia induced by methionine nutritional overload in rats: role of the brain oxidative stress

2016 ◽  
Vol 94 (10) ◽  
pp. 1074-1082 ◽  
Author(s):  
Dragan Hrncic ◽  
Jelena Mikić ◽  
Aleksandra Rasic-Markovic ◽  
Milica Velimirović ◽  
Tihomir Stojković ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Open Field ◽  
Wistar Rats ◽  
Brain Regions ◽  
Oxidative Status ◽  
Standard Diet ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
The Brain

The aim of this study was to examine the effects of a methionine-enriched diet on anxiety-related behavior in rats and to determine the role of the brain oxidative status in these alterations. Adult male Wistar rats were fed from the 30th to 60th postnatal day with standard or methionine-enriched diet (double content comparing with standard diet: 7.7 g/kg). Rats were tested in open field and light–dark tests and afterwards oxidative status in the different brain regions were determined. Hyperhomocysteinemia induced by methionine-enriched diet in this study decreased the number of rearings, as well as the time that these animals spent in the center of the open field, but increased index of thigmotaxy. Oxidative status was selectively altered in the examined regions. Lipid peroxidation was significantly increased in the cortex and nc. caudatus of rats developing hyperhomocysteinemia, but unaltered in the hippocampus and thalamus. Based on the results of this research, it could be concluded that hyperhomocysteinemia induced by methionine nutritional overload increased anxiety-related behavior in rats. These proanxiogenic effects could be, at least in part, a consequence of oxidative stress in the rat brain.

Differential oxidative stress and DNA damage in rat brain regions and blood following chronic arsenic exposure

2008 ◽  
Vol 24 (4) ◽  
pp. 247-256 ◽  
Author(s):  
D Mishra ◽  
SJS Flora
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Drinking Water ◽  
Wistar Rats ◽  
Arsenic Exposure ◽  
Brain Regions ◽  
Single Strand ◽  
Male Wistar Rats ◽  
Chronic Arsenic Exposure ◽  
The Brain

Chronic arsenic poisoning caused by contaminated drinking water is a wide spread and worldwide problem particularly in India and Bangladesh. One of the possible mechanisms suggested for arsenic toxicity is the generation of reactive oxygen species (ROS). The present study was planned 1) to evaluate if chronic exposure to arsenic leads to oxidative stress in blood and brain – parts of male Wistar rats and 2) to evaluate which brain region of the exposed animals was more sensitive to oxidative injury. Male Wistar rats were exposed to arsenic (50 ppm sodium arsenite in drinking water) for 10 months. The brain was dissected into five major parts, pons medulla, corpus striatum, cortex, hippocampus, and cerebellum. A number of biochemical variables indicative of oxidative stress were studied in blood and different brain regions. Single-strand DNA damage using comet assay was also assessed in lymphocytes. We observed a significant increase in blood and brain ROS levels accompanied by the depletion of GSH/GSSG ratio and glucose-6-phosphate dehydrogenase (G6PD) activity in different brain regions of arsenic-exposed rats. Chronic arsenic exposure also caused significant single-strand DNA damage in lymphocytes as depicted by comet with a tail in arsenic-exposed cells compared with the control cells. On the basis of results, we concluded that the cortex region of the brain was more sensitive to oxidative injury compared with the other regions studied. The present study, thus, leads us to suggest that arsenic induces differential oxidative stress in brain regions with cortex followed by hippocampus and causes single-strand DNA damage in lymphocytes.

Sign in / Sign up

Export Citation Format

Share Document