Amelioration of ferric nitrilotriacetate-induced hepatotoxicity in Wistar rats by diallylsulfide

2015 ◽  
Vol 35 (3) ◽  
pp. 259-266 ◽  
Author(s):  
S Ansar ◽  
M Iqbal

Garlic contains diallylsulfide (DAS) and other structurally related compounds that are widely believed to be active agents in preventing cancer. This study shows the effect of DAS (a phenolic antioxidant used in foods, cosmetics, and pharmaceutical products) on ferric nitrilotriacetate (Fe-NTA)-induced hepatotoxicity in rats. Male albino rats of Wistar strain weighing 125–150 g were given a single dose of Fe-NTA (9 mg kg−1 body weight, intraperitoneally) after 1 week of treatment with 100 and 200 mg kg−1 DAS in corn oil respectively administered through the gavage. Fe-NTA administration led to 2.5-fold increase in the values of both alanine transaminase and aspartate aminotransferase, respectively, and 3.2-fold increase in the activity of lactate dehydrogenase, microsomal lipid peroxidation to approximately 2.0-fold compared to saline-treated control. The activities of glutathione (GSH) and other antioxidant enzymes decreased to a range of 2.2–2.5-fold. These changes were reversed significantly ( p < 0.001) in animals receiving a pretreatment of DAS. DAS protected against hepatic lipid peroxidation, hydrogen peroxide generation, preserved GSH levels, and GSH metabolizing enzymes to 60–80% as compared to Fe-NTA alone-treated group. Present data suggest that DAS can ameliorate the toxic effects of Fe-NTA and suppress oxidant-induced tissue injury and hepatotoxicity in rats.

2017 ◽  
Vol 95 (4) ◽  
pp. 524-530 ◽  
Author(s):  
Mabrouk Attia Abd Eldaim ◽  
Ahmed Shaban Abd Elrasoul ◽  
Samy Ahmed Abd Elaziz

This study was carried out to evaluate the possible mechanisms through which an aqueous extract from MO leaves demonstrates hepatoprotective effects in alloxan-induced diabetic rats. Eighty albino rats were assigned to 4 groups. The control group was orally administered sterile saline. The second group was injected with alloxan (150 mg/kg body mass (b.m.)) by intraperitoneal injection (i.p.). The third group was given MO (250 mg/kg b.m.) orally, daily. The fourth group was injected with alloxan, as for the second group, and administrated an aqueous extract of MO leaves, as for the third group. Alloxan induced degenerative changes in hepatic and pancreatic tissues, increased hepatic lipid peroxidation, and increased gene expression of PC and caspase 3. However, it decreased the activities of hepatic SOD and CAT, and gene expression of GS. In contrast, the MO extract prevented changes to the histoarchitecture of hepatic and pancreatic tissues and normalized the reduced hepatic levels of glutathione, as well as the activities of SOD and CAT, and the gene expression of GS, while reducing blood glucose levels, hepatic lipid peroxidation, and the gene expression of PC and caspase 3. This study indicated that an aqueous extract of MO leaves can be a potent antioxidant and used as an hepatoprotective agent.


1998 ◽  
Vol 17 (3) ◽  
pp. 163-171 ◽  
Author(s):  
Mohammad Iqbal ◽  
Hassan Rezazadeh ◽  
Sabah Ansar ◽  
Mohammad Athar

Ferric nitrilotriacetate (Fe-NTA) is a potent nephrotoxic agent. In this communication, we show the modulatory effect of DL-a-tocopherol (Vitamin-E) on ferric nitrilotriacetate (Fe-NTA)-induced renal oxidative stress, toxicity and hyperproliferative response in rats. Fe-NTA-treatment enhances the susceptibility of renal microsomal membrane for iron-ascorbate-induced lipid peroxidation and hydrogen peroxide generation which are accompanied by a decrease in the activities of renal antioxidant enzymes, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and depletion in the level of renal glutathione. Parallel to these changes, a sharp increase in blood urea nitrogen and serum creatinine has been observed. In addition, Fe-NTA-treatment also enhances renal ornithine decarboxylase activity (ODC) and increases [3H]thymidine incorporation in renal DNA. Prophylactic treatment of animals with Vit.E daily for 1 week prior to the administration of Fe-NTA resulted in the diminution of Fe-NTA-mediated damage. Enhanced susceptibility of renal microsomal membrane for lipid peroxidation induced by iron-ascorbate and hydrogen peroxide generation were significantly reduced (P50.05). In addition, the depleted level of glutathione and inhibited activities of antioxidant enzymes recovered to significant levels (P50.05). Similarly, the enhanced blood urea nitrogen and serum creatinine levels which are indicative of renal injury showed a reduction of about 50% at a higher dose of Vit.E. The pretreatment of rats with Vit.E reduced the Fe-NTA-mediated induction in ODC activity and enhancement in [3H]thymidine incorporation in DNA. The protective effect of Vit.E was dose dependent. In summary, our data suggest that Vit.E is an effective chemopreventive agent in kidney and may suppress Fe-NTA-induced renal toxicity.


2020 ◽  
Vol 21 (1) ◽  
pp. 36-45
Author(s):  
Huda Elbaz ◽  
Mohamed Hamed ◽  
Fatma Abdelhamid ◽  
Osama Abdalla

Objective: To evaluate the effect of cefepime on hematological changes, immunological disorders and hepatic oxidative damage in rats experimentally infected with E.coli ATCC 25922. Design: Randomized controlled experimental study. Animals: Thirty-two adult male albino rats weighting150-200 g. Procedures: Rats used for this study were randomly assigned into 4 equal groups: the control one, E.coli infected group (1×108CFU/I/P/once), the cefepime treated group (45 mg/kg bw/I/M/day) for 5 days and the E.coli infected group that treated with cefepime 24h after bacterial inoculation as previously described. Hematological and immunological parameters, liver function biomarkers and hepatic oxidative stress and antioxidant markers were determined. Results: Our result revealed that E.coli infection induced a significant elevation in the erythrocytes count, hemoglobin concentration, PCV% and total leukocytic count (TLC) (P < 0.05). In the same respect, liver function biomarkers, serum glucose, total cholesterol, and triglyceride levels as well hepatic malondialdehyde (MDA), nitric oxide (NO), TNF-α, IL-10, and lysozyme activity were significantly increased compared to the control rats (P < 0.05). In contrast, hepatic reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were decreased significantly (P < 0.05). Cefepime treatment in E.coli + CFPM group reduced the elevated eythrogram, TLC and liver function biomarkers. Cefepime also ameliorated the oxidative damage and inflammatory response induced by E.coli infection. Conclusion and clinical relevance: Cefepime is safe when administered in a fixed-dose and possess antioxidant that contributes to improve efficacy against adverse effect induced by E.coli ATCC 25922 infection.


2020 ◽  
Vol 21 (1) ◽  
pp. 36-45
Author(s):  
Huda Elbaz

Objective: To evaluate the effect of cefepime on hematological changes, immunological disorders and hepatic oxidative damage in rats experimentally infected with E.coli ATCC 25922. Design: Randomized controlled experimental study. Animals: Thirty-two adult male albino rats weighting150-200 g. Procedures: Rats used for this study were randomly assigned into 4 equal groups: the control one, E.coli infected group (1×108CFU/I/P/once), the cefepime treated group (45 mg/kg bw/I/M/day) for 5 days and the E.coli infected group that treated with cefepime 24h after bacterial inoculation as previously described. Hematological and immunological parameters, liver function biomarkers and hepatic oxidative stress and antioxidant markers were determined. Results: Our result revealed that E.coli infection induced a significant elevation in the erythrocytes count, hemoglobin concentration, PCV% and total leukocytic count (TLC) (P < 0.05). In the same respect, liver function biomarkers, serum glucose, total cholesterol, and triglyceride levels as well hepatic malondialdehyde (MDA), nitric oxide (NO), TNF-α, IL-10, and lysozyme activity were significantly increased compared to the control rats (P < 0.05). In contrast, hepatic reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were decreased significantly (P < 0.05). Cefepime treatment in E.coli + CFPM group reduced the elevated eythrogram, TLC and liver function biomarkers. Cefepime also ameliorated the oxidative damage and inflammatory response induced by E.coli infection. Conclusion and clinical relevance: Cefepime is safe when administered in a fixed-dose and possess antioxidant that contributes to improve efficacy against adverse effect induced by E.coli ATCC 25922 infection.


Author(s):  
Raghavendra Mitta ◽  
Sushmitha Duddu ◽  
Raghuveer Yadav Pulala ◽  
Pradeepkumar Bhupalam ◽  
Venkatakirankumar Mandlem ◽  
...  

AbstractObjectivesThe main objective of the present study is to evaluate the mitigative effect of hydroalcoholic extract of Momordica cymbalaria fruits against sodium fluoride (NaF) induced hepatotoxicity.MethodsIn this study, Wistar male albino rats were randomly divided into five groups of six rats each. Group I and II served as normal and toxic controls. Group III as plant control received extract at a dose of 400 mg/kg b. wt, p.o and Groups IV and V as treatment groups received extract at a dose 200 and 400 mg/kg b. wt, p.o for 30 days. All groups except Groups I and III received 100 ppm of NaF through drinking water. After completion of the study, blood collected for the estimation of liver blood serum biomarkers such as aspartate aminotransferases (AST), alanine aminotransferases (ALT), alkaline Phosphatase (ALP), direct and total bilirubin, total protein and albumin. The liver tissue homogenate was for estimation of lipid peroxidation, catalase, and reduced glutathione levels.ResultsThe results showed that NaF intoxication caused elevation of liver blood serum levels and lipid peroxidation; decreased levels of serum total protein, albumin and liver reduced glutathione, and catalase observed. The treatment groups showed decreased elevated serum biomarkers (ALT, AST, and ALP), liver lipid peroxidation and increased serum total protein and albumin, liver reduced glutathione and catalase levels in a dose-dependent manner. Histopathological studies also further strongly supported for mitigative effects of the plant.ConclusionsIn conclusion, our findings of the study indicated that M. cymbalaria fruits were a potential drug candidate in the treatment of NaF induced hepatotoxicity.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Chiemeka Lynda Umenwanne ◽  
Martins Obinna Ogugofor ◽  
Obioma U. Njoku

Abstract Background Cardiovascular diseases have continued to be the leading cause of death globally. In addition, some of the drugs used in the treatment of the diseases present some adverse effects which limit the usefulness of such drugs. Thus, there is a need for novel drugs whose side effect is either minimal or non-existent. The presence of bioactive compounds in Cola hispida leaf is of great significance in the treatment and management of cardiovascular conditions. This study investigated the cardio-protective potential against doxorubicin (Dox)-induced cardiac infarction in rats. Results Dox induction resulted to muscle fiber degeneration in Dox-treated rats hence revealed significant (p < 0.05) elevation in the serum level of cardio biomarker enzymes and lipid peroxidation profile while significant (p < 0.05) fall in cardiac enzymatic antioxidant levels were observed relative to the normal control. Pre-treatment with ethyl acetate fraction of Cola hispida leaf expressed cardio-protective potentials against Dox-induced cardiotoxicity by significantly (p < 0.05) lowering the levels of cardiac biomarker enzymes towards normal, building up the activities of subdued antioxidant enzymes and depleting its malondialdehyde level. Histopathology photomicrograph of the heart tissues expressed myxomatous degeneration but was ameliorated through the administration of the fraction. Conclusion In accordance with the findings from this study, the administration of ethyl acetate fraction of Cola hispida leaf is effective against Dox-induced redox imbalance due to its enriched antioxidant phytoconstituents.


1986 ◽  
Vol 251 (5) ◽  
pp. F839-F843 ◽  
Author(s):  
M. S. Paller ◽  
R. P. Hebbel

After renal ischemia, oxygen free radicals are formed and produce tissue injury, in large part, through peroxidation of polyunsaturated fatty acids. We used an in vivo method to monitor lipid peroxidation after renal ischemia, the measurement of ethane in expired gas, to determine the time course of lipid peroxidation and the effect of several agents to limit lipid peroxidation after renal ischemia. In anesthetized rats there was no significant increase in ethane production during 60 min of renal ischemia. During the first 10 min of renal reperfusion, there was a prompt increase in ethane production from 2.9 +/- 1.3 to 6.3 +/- 1.9 pmol/min (P less than 0.05). Ethane production was significantly increased during the first 50 min of reperfusion and then rapidly tapered to base-line levels. Preischemic administration of allopurinol to prevent superoxide radical generation or the superoxide radical scavenger superoxide dismutase prevented the increase in ethane production during postischemic reperfusion. These studies confirm that there is increase lipid peroxidation following renal ischemia that can be prevented by agents which limit the formation or accumulation of oxygen free radicals. This in vivo method for measuring lipid peroxidation could also be employed to study the effects of ischemia on lipid peroxidation in other organs, as well as to monitor lipid peroxidation in other forms of injury.


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