Effect of the Carotenoid-Producing Alga, Dunaliella bardawil, on CCl4-Induced Toxicity in Rats

2007 ◽  
Vol 26 (2) ◽  
pp. 159-167 ◽  
Author(s):  
A. Vanitha ◽  
K. N. Chidambara Murthy ◽  
Vinod Kumar ◽  
G. Sakthivelu ◽  
Jyothi M. Veigas ◽  
...  
Keyword(s):  
Liver Toxicity ◽  
Day Treatment ◽  
Protective Action ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protective Effects ◽  
Mean Values ◽  
Dunaliella Bardawil ◽  
Liver Histopathology ◽  
Dna Strand

Dunaliella bardawil is a carotenoid-producing alga that is being considered for use in nutraceuticals. To evaluate potential protective effects of consumption of this alga, rats were treated with two different doses of D. bardawil (2.5 and 5.0 g kg–1 body weight [bw]) as a biomass suspension daily for 14 days. Animals were tested against Carbon tetrachloride (CCl4; 2 ml kg–1)–induced liver toxicity as measured by various biochemical marker enzymes in liver and blood. All measurements were taken 6 h following the single dose of CCl4. The results of this study show that there was a slight, but statistically significant mean serum enzyme values, with D. bardawil treatment, compared to higher mean values in animals receiving CCl4 alone. Lipid peroxidation is measured by thiobarbituric acid–reactive substance (TBARS) activity was likewise slightly less elevated with algae treatment. The results also demonstrated protection against DNA strand breaks in hepatocytes, as measured by single cell gel electrophoresis. Liver histopathology was less severe with D. bardawil treatment, supporting the apparent protective action of 14-day treatment on hepatic oxidative injury.

scholarly journals Effect of Eclipta alba and Ocimum sanctum on haloperidol induced parkinsonism

2018 ◽  
Vol 8 (5) ◽  
pp. 288-293
Author(s):  
Harmel Singh Chahal ◽  
Shailendra Sharma
Keyword(s):  
Oxidative Stress ◽  
Protective Action ◽  
Thiobarbituric Acid ◽  
Brain Homogenate ◽  
Substantia Nigra Pars Compacta ◽  
Ocimum Sanctum ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Eclipta Alba ◽  
Tnf Α

The aim of the study is protective effect of compound Eclipta alba and Ocimum sanctum on Parkinsonism induced mice by haloperidol injection. Parkinsonism is neurodegenerative disease due to the deficiency of dopamine in brain. The pathological hallmark of Parkinson’s disease in the cell loss within substantia nigra pars compacta (SNpc) region and the disease is charactrised by bradykinesia, rigidity, postural instability, orofacial dyskinesia, muscular stiffness and tremor1. Mice were injected 1mg/kg haloperidol and then treated with test and standard substance for 15 days. The impairment in catatonia in mice were tested using catatonic activity. Biochemical analysis of brain homogenate was performed so ass to assess brain Thiobarbituric acid reactive substance (TBARS) level and reduced glutathione (GSH) and TNF-α level were measured to assess total oxidative stress. EA 300mg/kg and OS 400mg/kg show slightly change in catatonic activity in mice while EA 600mg/kg and 800mg/kg significantly change in catatonic activity. Furthermore, Eclipta alba and Ocimum sanctum prevent the haloperidol induced changes in the level of brain TBARS, GSH and TNF-α. From the results we conclude that Eclipta alba and Ocimum sanctum has protective action against impairment in catatonic activity and pathological damage due to oxidative stress induced by intraperitoneally injection of haloperidol in mice.        Keywords: Eclipta alba, Ocimum Sanctum, Parkinsonism, Anti-oxidant.

Protective effects of Gingko biloba on thioacetamide-induced fulminant hepatic failure in rats

2006 ◽  
Vol 25 (12) ◽  
pp. 705-713 ◽  
Author(s):  
M M M Harputluoglu ◽  
U Demirel ◽  
H Ciralik ◽  
I Temel ◽  
S Firat ◽  
...  
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Radical Scavenging ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protective Effects ◽  
Liver Necrosis ◽  
Gingko Biloba ◽  
Liver Tbars

Gingko biloba (GB) has antioxidant and platelet-activating factor (PAF) antagonistic effects. We investigated the protective effects of GB on thioacetamide (TAA)induced fulminant hepatic failure in rats. Fulminant hepatic failure was induced in treatment groups by three intraperitoneal (ip) injections of TAA (350 mg/kg) at 24-hour intervals. Treatments with GB (100 mg/kg per day, orally) and N-acetylcysteine (20 mg/kg twice daily, sc) were initiated 48 hours prior to TAA administration. The liver was removed for histopathological examinations. Serum and liver thiobarbituric acid-reactive substance (TBARS) levels were measured for assessment of oxidative stress. Liver necrosis and inflammation scores and serum and liver TBARS levels were significantly higher in the TAA group compared to the control group (P <0.001,<0.001, 0.001,<0.001, respectively). Liver necrosis and inflammation scores and liver TBARS levels were significantly lower in the GB group compared to the TAA group (P <0.001,<0.001 and 0.01, respectively). GB ameliorated hepatic damage in TAA-induced fulminant hepatic failure. This may be due to the free radical-scavenging effects of GB.

scholarly journals Protective effects of molsidomine against doxorubicin-induced renal damage in rats

2016 ◽  
Vol 39 (1) ◽  
pp. 7 ◽  
Author(s):  
Fatih Oguz ◽  
Ali Beytur ◽  
Ediz Sarihan ◽  
Hilal K Oguz ◽  
Recep Bentli ◽  
...  
Keyword(s):  
Renal Damage ◽  
Reduced Glutathione ◽  
Kidney Injury ◽  
Thiobarbituric Acid ◽  
Kidney Damage ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protective Effects ◽  
Reactive Substance ◽  
Group 4

Purpose: The purpose of this study was to investigate the therapeutic and protective effects of molsidomine (MLS) against doxorubicin (DOX)-induced renal damage in rats. Methods: Forty rats were randomly divided into five groups (control, MLS, DOX, DOX+MLS and MLS+DOX groups). Thiobarbituric acid reactive substance (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitric oxide (NO) and glutathione peroxidase (GPx) levels were determined from kidney tissues and blood urea nitrogen (BUN), creatinine (Cr) and albumin (Alb) levels also determined. Results: DOX treatment caused a significant increase in TBARS levels and a significant decrease in the GSH and CAT levels compared with the control group. In comparison, MLS administration before DOX injection caused a significant decrease in TBARS levels and also increases in GSH and CAT levels, whereas treatment of MLS after DOX injection did not show any beneficial effect on these parameters. All groups showed a significant increase in NO levels compared to the control group. There were no significant differences among the all groups for BUN and Cr levels. Serum level of Alb decreased in the DOX-treated groups when compared with control and MLS groups. The histopathological findings were in accordance with the biochemical results. MLS treatment reversed the DOX-induced kidney damage in group 4. MLS treatment before DOX injection exerted a protective effect against DOX-induced kidney damage. Conclusions: MLS shows promise as a possible therapeutic intervention for the prevention of kidney injury associated with DOX treatment. Additional studies are warranted.

scholarly journals Protective Effects of Inflammation of Curcumae Longae Rhizoma 30% EtOH Extract on Acute Reflux Esophagitis Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Jin A. Lee ◽  
Mi-Rae Shin ◽  
Min Ju Kim ◽  
Ji Hye Lee ◽  
Hae-Jin Park ◽  
...  
Keyword(s):  
Reflux Esophagitis ◽  
Stomach Contents ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Related Factors ◽  
Etoh Extract

Gastroesophageal reflux disease (GERD) is induced by the reflux of stomach contents or gastric acid, pepsin into the esophagus for prolonged periods of time due to defection of the lower esophageal sphincter. Reflux esophagitis is a disease found in less than 50% of GERD patients. This study is aimed at evaluating the protective effect of Curcumae longae Rhizoma 30% EtOH extract (CLR) in acute reflux esophagitis (ARE) rats. CLR measured antioxidant activity through in vitro experiments. Based on the results, we performed experiments in vivo. Before 90 min ARE induction, CLR was administered orally by concentration. ARE was derived by linking the metastatic junction between pylorus and forestomach and corpus in Sprague-Dawley rats. And rats were sacrificed 5 h after surgery. We analyzed the expression of antioxidant and inflammatory-related markers by western blot and observed the production of alanine aminotransferase (ALT), aspartate aminotransferase (AST), reactive oxygen species (ROS), peroxynitrite (ONOO-), and thiobarbituric acid reactive substance (TBARS). The administration of CLR reduced esophagus tissue damage in rats with acute reflux esophagitis and decreased the elevated ALT, AST, ROS, ONOO-, and TBARS. In addition, CLR effectively increased antioxidant-related factors and reduced inflammatory protein. Overall, these results suggest that CLR would be used as a therapeutic material in protection and treatment for ARE. Overall, CLR treatment informed that markedly ameliorated inactivation of NF-κB led to the inhibition of the expressions of proinflammatory proteins. These results suggest that CLR would be used as a therapeutic material in protection and treatment for ARE.

The impact of Crocus sativus stigma against methotrexate-induced liver toxicity in rats

2019 ◽  
Vol 17 (2) ◽  
Author(s):  
Reyhane Hoshyar ◽  
Ahmadreza Sebzari ◽  
Mohadeseh Balforoush ◽  
Masoomeh Valavi ◽  
Mehran Hosseini
Keyword(s):  
Plasma Levels ◽  
Liver Toxicity ◽  
Post Treatment ◽  
Crocus Sativus ◽  
Protective Effects ◽  
Sod Activity ◽  
Morphological Alterations ◽  
Liver Histopathology ◽  
Male Wistar Rats ◽  
The Impact

AbstractBackgroundThe adverse effects of methotrexate (MTX) mainly hepatotoxicity restrict its clinical use. This study was designed to investigate the protective effects of saffron (Crocus sativus) (CS) extract on MTX-induced hepatotoxicity.MethodsTwenty-eight male Wistar rats randomly divided into four equal groups. Except for control, all groups received a single intraperitoneal (i.p.) injection of MTX on the 3rd day of study. The CS extract was given (80 mg/kg i.p.) to rats 3 days before MTX and continued for the next 7 days (Pre&Post-CS group) or administrated after MTX injection and lasted for 7 days (Post-CS group). On the 11th day, all rats were sacrificed and their plasma levels of liver enzymes including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were determined. Also, liver histopathology and hepatic levels of malondialdehyde (MDA), nitric oxide (NO) and super oxidase dismutase (SOD) were evaluated.ResultsThe results showed that MTX significantly incremented plasma levels of AST, ALT, ALP and LDH (all p<0.001) and hepatic MDA and NO levels; whereas, decreased SOD activity. Histological alterations such as early fatty changes were evident in the MTX group. Administration of CS extract at both methods could ameliorate liver enzyme elevation, oxidative/nitrosative stresses and morphological alterations of the liver. Pre-and-post treatment with CS extract showed better protective effects than only post-treatment.ConclusionThe present findings provide showing CS could effectively alleviate MTX-induced hepatotoxicity in rats. Further investigations are recommended to determine the exact mechanisms underlying the hepatoprotective potential of saffron.

scholarly journals The Bioactive Compound Contents and Potential Protective Effects of Royal Jelly Protein Hydrolysates against DNA Oxidative Damage and LDL Oxidation

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 580
Author(s):  
Shu-Hua Chiang ◽  
Kia-Min Yang ◽  
Shiann-Cherng Sheu ◽  
Chih-Wei Chen
Keyword(s):  
Oxidative Damage ◽  
Royal Jelly ◽  
Density Lipoprotein ◽  
Thiobarbituric Acid ◽  
Ldl Oxidation ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protective Effects ◽  
Dna Oxidative Damage ◽  
Royal Jelly Protein

In this study, the inhibition of DNA oxidative damage and low-density lipoprotein (LDL) oxidation of royal jelly protein (RJP) hydrolysates obtained from two commercial proteases were investigated. The results showed that the inhibition of DNA oxidative damage induced by the Fenton reaction, RJP, RJPs hydrolyzed by alcalase (RJP-A), RJPs hydrolyzed by flavourzyme (RPJ-F) and RJP two-stage hydrolysates (RPJ-AF) all had the effect of inhibiting deoxyribose oxidative damage. The inhibition effect of RJP, RJP-A, RJP-F and RJP-AF (1.0 mg/mL) were 47.06%, 33.70%, 24.19% and 43.09%, respectively. In addition, studies have also found that both RJP and RJP hydrolysates can reduce the production of 8-OH-2′-dG and the order of its inhibitory ability is RJP-AF ≒ RJP-A > RJP-F > RJP. The inhibition of DNA damage induced by bleomycin-Fe3+/ascorbic acid (Asc) with the addition of RJP, RJP-A, RPJ-F and RPJ-AF were 17.16%, 30.88%, 25.00% and 37.25%, respectively. The results of LDL oxidation inhibition showed that RJP-AF (1 mg/mL) not only had the most effective inhibitory Cu2+-induced LDL oxidation to produce a thiobarbituric acid reactive substance (TBARS) but also extended the lag time of conjugated diene formation to 300 min, which was 3.3 times that of the control group.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

Synthesis and Biological Evaluation of Scutellarein Alkyl Derivatives as Preventing Neurodegenerative Agents with Improved Lipid Soluble Properties

2019 ◽  
Vol 15 (7) ◽  
pp. 771-780
Author(s):  
He-Min Li ◽  
Ting Gu ◽  
Wen-Yu Wu ◽  
Shao-Peng Yu ◽  
Tian-Yuan Fan ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Neuronal Damage ◽  
Thiobarbituric Acid ◽  
Rat Hepatocytes ◽  
Biological Evaluation ◽  
Thiobarbituric Acid Reactive Substance ◽  
Alkyl Derivatives ◽  
Promising Therapeutic Approach ◽  
Microsomal Membranes

Background: Exogenous antioxidants are considered as a promising therapeutic approach to treat neurodegenerative diseases since they could prevent and/or minimize the neuronal damage by oxidation. Objective: Three series of lipophilic compounds structurally based on scutellarein (2), which is one metabolite of scutellarin (1) in vivo, have been designed and synthesized. Methods: Their antioxidant activity was evaluated by detecting the 2-thiobarbituric acid reactive substance (TBARS) produced in the ferrous salt/ascorbate-induced autoxidation of lipids, which were present in microsomal membranes of rat hepatocytes. The lipophilicity of these compounds indicated as partition coefficient between n-octanol and buffer was investigated by ultraviolet (UV) spectrophotometer. Results: This study indicated that compound 5e which had a benzyl group substituted at the C4'- OH position showed a potent antioxidant activity and good lipophilicity. Conclusion: 5e could be an effective candidate for preventing or reducing the oxidative status associated with the neurodegenerative processes.

scholarly journals Hepatoprotective effect of galangin on carbon tetrachloride-induced hepatotoxicity via the LKB1/AMPK pathway

2021 ◽  
Vol 19 ◽  
pp. 205873922110008
Author(s):  
Meng Chen ◽  
Xinyan Song ◽  
Jifang Jiang ◽  
Lei Xing ◽  
Pengfei Wang
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Toxicity ◽  
Corn Oil ◽  
Histopathological Examination ◽  
Hepatoprotective Effect ◽  
Control Group ◽  
Group Model ◽  
Protective Effects ◽  
Model Group ◽  
Expression Levels

To investigate the protective effects of galangin on liver toxicity induced by carbon tetrachloride (CCl4) in mice. Mouse hepatotoxicity model was established by intraperitoneal injection (i.p.) of 10 ml/kg body weight CCl4 that diluted with corn oil to a proportion of 1:500 on Kunming mice. The mice were randomly divided into five groups named control group, model group, and 1, 5, and 10 mg/kg galangin group. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA. Liver histopathological examination was observed via optical microscopy. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and glutathion (GSSG) were analyzed to assess oxidative stress. Finally, western blot assay was carried out to analyse the expression levels of total AMP-activated protein kinase (AMPK), phospho-AMPK (p-AMPK), total liver kinase B1 (LKB1), and phospho-LKB1 (p-LKB1). Compared with the control group, in the model group, the levels of AST, ALT, MDA, and GSSG increased significantly ( p < 0.01); the activity of SOD and GSH decreased significantly ( p < 0.01); and the histopathological examination revealed liver necrosis. However, treatment with galangin (5 and 10 mg/kg) significantly reversed these CCl4-induced liver damage indicators. Furthermore, treatment with galangin (10 mg/kg) significantly increased the p-AMPK and p-LKB1 expression levels ( p < 0.01). This study supports the hepatoprotective effect of galangin against hepatotoxicity, perhaps occurring mainly through the LKB1/AMPK-mediated pathway.

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