Stress In Liver Tissue Of Rats Research Articles

Red Seaweed (Hypnea Bryodies and Melanothamnus Somalensis) Extracts Counteracting Azoxymethane-Induced Hepatotoxicity in Rats

Background:Azoxymethane (AOM) is a well-known colon cancer-inducing agent in experimental animals via mechanisms that include oxidative stress in rat colon and liver tissue. Few studies have investigated AOM-induced oxidative stress in rat liver tissue. Red seaweeds of the genera Hypnea Bryodies and Melanothamnus Somalensis are rich in polyphenolic compounds that may suppress cancer through antioxidant properties, yet limited research has been carried out to investigate their anti-carcinogenic and antioxidant influence against AOM-induced oxidative stress in rat liver.Objective:This study aims to determine protective effects of red seaweed (Hypnea Bryodies and Melanothamnus Somalensis) extracts against AOM-induced hepatotoxicity and oxidative stress.Materials and Methods:Sprague–Dawley rats received intraperitoneal injections of AOM, 15 mg/kg body weight, once a week for two consecutive weeks and then orally administered red seaweed (100 mg/kg body-weight) extracts for sixteen weeks. At the end of the experiment all animals were overnight fasted then sacrificed and blood and liver tissues were collected.Results:AOM treatment significantly decreased serum liver markers and induced hepatic oxidative stress as evidenced by increased liver tissue homogenate levels of nitric oxide and malondialdehyde, decreased total antioxidant capacity and glutathione, and inhibition of antioxidant enzymes (catalase, glutathione peroxidase, glutathione S-transferase, glutathione reductase and superoxide dismutase). Both red seaweed extracts abolished the AOM-associated oxidative stress and protected against liver injury as evidenced by increased serum levels of liver function markers. In addition, histological findings confirmed protective effects of the two red seaweed extracts against AOM-induced liver injury.Conclusion:Our findings indicate that red seaweed (Hypnea Bryodies and Melanothamnus Somalensis) extracts counteracted oxidative stress-induced hepatotoxicity in a rat model of colon cancer.

Dose-dependent protective effect of L-carnitine on oxidative stress in the livers of hyperthyroid rats.

The present study was designed to investigate the dose-dependent protective effect of L-carnitine (LC) on thyroid hormone-induced oxidative stress in rat liver tissue. Twenty-one male Sprague Dawley rats were divided into four groups: control, hyperthyroidism, hyperthyroidism plus L-carnitine 100, and hyperthyroidism plus L-carnitine 500. Hyperthyroidism was induced in rats by injecting 250 μg of L-thyroxine/kg body weight/day for twenty consecutive days. The activities of catalase (CAT), glutathione peroxidase (GPX) and myeloperoxidase (MPO) and the level of malondialdehyde (MDA) were measured in liver homogenates. The liver CAT, GPX and MPO activities were significantly lower in the hyperthyroid rats than in the control group. Treating hyperthyroid rats with both low-dose (100 mg/kg) and high-dose (500 mg/kg) L-carnitine for 10 days resulted in a marked increase in the activities of the antioxidant enzymes in the liver tissue. The present study indicates that the low-dose L-carnitine application was sufficient to prevent L-thyroxine-induced oxidative stress in rat livers.

Effects of Lycium Barbarum Aqueous and Ethanol Extracts on High-Fat-Diet Induced Oxidative Stress in Rat Liver Tissue

This study evaluated the protective effects of aqueous extract of Lycium barbarum (LBAE) and ethanol extract of Lycium barbarum (LBEE) on blood lipid levels, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) activities and liver tissue antioxidant enzyme activities in rats fed a high fat diet (HF). The rats were randomly divided into seven groups of ten rats each and fed a different diet for eight weeks as follows: One group (NC group) was fed a standard diet, one group was fed a high-fat diet (HF group), one group was fed a high-fat diet and orally fed with 20 mg/kg b.w. simvastatin (HF + simvastatin group), and the other group was fed the high fat diet and orally fed with 50 mg/kg b.w. or 100 mg/kg b.w. LBAE (HF + LBAE), or 50 mg/kg b.w. or 100 mg/kg b.w. LBEE (HF + LBEE), respectively. After eight weeks, the HF diet caused deleterious metabolic effects. Rats fed the HF diet alone showed increased hepatocellular enzyme activities in plasma, a significant decline in antioxidant enzyme activities, and elevated liver lipid peroxidation indices. LBAE and LBEE administration significantly reduced liver damage and oxidative changes, and brought back the antioxidants and lipids towards normal levels. These data suggest that these antioxidants protect against toxicity parameters in HF rats.