FK228 Ameliorates the Liver Toxicity and Oxidative Stress on Thiram-Induced Tibial Dyschondroplasia in Chicken

Methamphetamine intoxication can cause acute hepatic failure. Chlorogenic and caftaric acids are the major dietary polyphenols present in various foods. The aim of this study was to evaluate the protective role of chlorogenic and caftaric acids in liver toxicity and oxidative stress induced by methamphetamine in rats. Thirty-two male albino rats were divided into 4 equal groups. Group 1, which was control group, was injected (i.p) with saline (1 mL/kg) twice a day over seven-day period. Groups 2, 3, and 4 were injected (i.p) with methamphetamine (10 mg/kg) twice a day over seven-day period, where groups 3 and 4 were injected (i.p) with 60 mg/kg chlorogenic acid and 40 mg/kg caftaric acid, respectively, one day before methamphetamine injections. Methamphetamine increased serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, bilirubin, cholesterol, low-density lipoprotein, and triglycerides. Also, malondialdehyde in serum, liver, and brain and plasma and liver nitric oxide levels were increased while methamphetamine induced a significant decrease in serum total protein, albumin, globulin, albumin/globulin ratio, brain serotonin, norepinephrine and dopamine, blood and liver superoxide dismutase, and glutathione peroxidase levels. Chlorogenic and caftaric acids prior to methamphetamine injections restored all the above parameters to normal values. In conclusion, chlorogenic and caftaric acids before methamphetamine injections prevented liver toxicity and oxidative stress where chlorogenic acid was more effective.

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Silibinin mitigates zidovudine-induced hepatocellular degenerative changes, oxidative stress and hyperlipidaemia in rats

Human & Experimental Toxicology ◽

10.1177/0960327114567765 ◽

2015 ◽

Vol 34 (11) ◽

pp. 1031-1042 ◽

Cited By ~ 8

Author(s):

R Raghu ◽

B Jesudas ◽

G Bhavani ◽

D Ezhilarasan ◽

S Karthikeyan

Keyword(s):

Oxidative Stress ◽

Liver Toxicity ◽

Parenchymal Cell ◽

Radical Scavenging ◽

Simultaneous Treatment ◽

Protein Thiols ◽

Radical Scavenging Properties ◽

Withdrawal Of Therapy ◽

Inflammatory Changes ◽

And Oxidative Stress

Prolonged zidovudine (AZT) treatment in HIV-infected and AIDS patients is shown to induce liver toxicity leading to complications. Therapeutic regimen that could encounter this adverse effect is unavailable and management of toxicity is often symptomatic or is limited to withdrawal of therapy. In the present investigation, we evaluated the alleviating properties of silibinin (SBN), a flavanolignan obtained from Silybum marianum against subacute AZT-induced hepatotoxicity and oxidative stress in rats. AZT treatment (50 mg/kg body weight (b.w.) periorally (p.o.), daily for 45 days) caused highly significant increases in alanine transaminase, alkaline phosphatase, argininosuccinic acid lyase and bilirubin in serum. Oxidative stress is shown by a highly significant increase in lipid peroxidase and total carbonyl content and decrease in catalase and protein thiols in the liver tissue. Hyperlipidaemia is indicated by highly significant increase in total lipids and free fatty acid in serum. Evaluation of liver by haematoxylin and eosin staining shows parenchymal cell enlargement, inflammatory changes and increase in sinusoidal spaces. Simultaneous treatment of SBN (100 mg/kg b.w. p.o., daily for 45 days) significantly protected the liver against hepatotoxicity, oxidative stress and hyperlipidaemia induced by AZT, and this alleviating property is attributed to hepatoprotective, membrane-stabilizing, antioxidant and free radical scavenging properties of SBN.

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Pre-administration of turmeric prevents methotrexate-induced liver toxicity and oxidative stress

BMC Complementary and Alternative Medicine ◽

10.1186/s12906-015-0773-6 ◽

2015 ◽

Vol 15 (1) ◽

Cited By ~ 37

Author(s):

Adel Rezaei Moghadam ◽

Soheil Tutunchi ◽

Ali Namvaran-Abbas-Abad ◽

Mina Yazdi ◽

Fatemeh Bonyadi ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Toxicity ◽

And Oxidative Stress

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Protective Effect of Quercetin on Chloroquine-Induced Oxidative Stress and Hepatotoxicity in Mice

Malaria Research and Treatment ◽

10.1155/2013/141734 ◽

2013 ◽

Vol 2013 ◽

pp. 1-10 ◽

Cited By ~ 10

Author(s):

Shrawan Kumar Mishra ◽

Prabhat Singh ◽

Srikanta Kumar Rath

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Prophylactic Treatment ◽

Liver Toxicity ◽

Specific Pattern ◽

The Body ◽

Oxygen Species ◽

Antimalarial Therapy ◽

And Oxidative Stress

The present study was aimed to find out the protective effect of quercetin on hepatotoxicity resulting by commonly used antimalarial drug chloroquine (CQ). Swiss albino mice were administered with different amounts of CQ ranging from human therapeutic equivalent of 360 mg/kg body wt. to as high as 2000 mg/kg body wt. We observed statistically significant generation of reactive oxygen species, liver toxicity, and oxidative stress. Our observation of alterations in biochemical parameters was strongly supported by real-time PCR measurement of mRNA expression of key biochemical enzymes involved in hepatic toxicity and oxidative stress. However, the observed hepatotoxicity and accompanying oxidative stress following CQ administration show dose specific pattern with little or apparently no effect at therapeutic dose while having severe effects at higher dosages. We further tested quercetin, an antioxidant flavanoid, against CQ-induced hepatoxicity and found encouraging results as quercetin was able to drastically reduce the oxidative stress and hepatotoxicity resulting at higher dosages of CQ administration. In conclusion, our study strongly suggests co administration of antioxidant flavonoid like quercetin along with CQ for antimalarial therapy. This is particularly important when CQ is administered as long-term prophylactic treatment for malaria as chronic exposure has shown to be resulting in higher dose level of drug in the body.

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Zidovudine and isoniazid induced liver toxicity and oxidative stress: Evaluation of mitigating properties of silibinin

Environmental Toxicology and Pharmacology ◽

10.1016/j.etap.2016.07.014 ◽

2016 ◽

Vol 46 ◽

pp. 217-226 ◽

Cited By ~ 12

Author(s):

Ramanathan Raghu ◽

Sivanesan Karthikeyan

Keyword(s):

Oxidative Stress ◽

Liver Toxicity ◽

Stress Evaluation ◽

And Oxidative Stress

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Silymarin mitigates diclofenac-induced liver toxicity through inhibition of inflammation and oxidative stress in male rats

Journal of Herbmed Pharmacology ◽

10.15171/jhp.2019.34 ◽

2019 ◽

Vol 8 (3) ◽

pp. 231-237 ◽

Cited By ~ 2

Author(s):

Pantea Ramezannezhad ◽

Ali Nouri ◽

Esfandiar Heidarian

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Total Bilirubin ◽

Liver Toxicity ◽

Treated Group ◽

Male Rats ◽

Control Group ◽

Tnf Α ◽

Ameliorative Effect ◽

And Oxidative Stress

Introduction: Diclofenac (DIC) is one of the compounds derived from acetic acid which isknown for its anti-inflammatory and analgesic attributes. Silymarin is a flavonoid compoundwhich is derivate from Silybum marianum seeds. This research was done to assess the protectiverole of silymarin against liver toxicity induced by DIC in male rats.Methods: Randomly, 40 male Wistar rats were assigned into five groups as follows: Group 1:control group, Group 2: DIC-only treated (50 mg/kg, i.p), Group 3: silymarin-only treated (200mg/kg, p.o); Groups 4 and 5: DIC (50 mg/kg, i.p) plus silymarin (100 mg/kg and 200 mg/kg, p.o,respectively) treated. Various biochemical, molecular, and histological parameters were evaluatedin serum and tissue.Results: In the DIC-only treated group, the levels of liver glutathione peroxidase (GPx), superoxidedismutase (SOD), intracellular glutathione (GSH) and catalase (CAT) significantly diminished andthe levels of total bilirubin, alkaline phosphatase (ALP), nitrite, alanine aminotransferase (ALT),malondialdehyde (MDA), serum tumor necrosis factor-α (TNF-α), aspartate aminotransferase(AST), and TNF-α gene expression were remarkably elevated relative to control animals. In otherhands, treatment with silymarin caused a noticeable elevation in GPx, SOD, GSH, CAT and aremarkable reduction in levels of total bilirubin, ALP, nitrite content, ALT, MDA, serum TNF-α,AST and TNF-α gene expression relative to DIC-only treated group. Histopathological injurieswere also improved by silymarin administration.Conclusion: The results confirm that silymarin has an ameliorative effect on liver toxicity inducedby DIC and oxidative stress in male rats.

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