Comparison of Protective Effects of Omega3 Fish Oil and Aqueous Extract of Glycyrrhiza glabra Root on Thioacetamide Induced Lipid Toxicity in Male Rats

Davood Moghadamnia,Mokhtar Mokhtari,Saeed Khatamsaz

doi:10.13005/bpj/917

Davood Moghadamnia, Mokhtar Mokhtari + Show 1 more

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https://doi.org/10.13005/bpj/917

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Abstract

Introduction Thioacetamide (TAA) is an experimental hepatoxin(Staňková et al,2010)which is a thiono-sulfur containing compound with liver damaging and carcinogenic activity.Shortly after administration,TAA undergoes metabolism to acetamide and thioacetamide-S-oxide by the mixed function oxid

Highlights

Thioacetamide (TAA) is an experimental hepatoxin1which is a thiono-sulfur containing compound with liver damaging and carcinogenic activity.Shortly after administration,TAA undergoes metabolism to acetamide and thioacetamide-Soxide by the mixed function oxidase system[2].TAA is the most potent nephrotoxic substance because of its repid elimination and cumulative injury when it is given intermittently,presumably by free radicalmediated lipid[3,4].Metabolic studies of TAA-induced tissue damage suggest that TAA is metabolized by the mixed function oxidase system to its toxic metabolites sulfine(sulfoxide) and sulfene(sulfone) which distributed among serveral organs including plasma,liver,kidney,bone marrow, adernals and other tissues[5].MOGHADAMNIA et al, Biomed. & Pharmacol
Pretreatmen with 100,300 mg/kg of aqueous extract of Glycyrrhiza glabra root significant increased the serum levels of total cholesterol comparing with thioacetamide group (P
Pretreatmen with the aqueous extract of Glycyrrhiza glabra root at all doses increased the serum levels of FBS comparing with thioacetamide group but there was no significant difference(P

Summary

INTRODUCTION

Thioacetamide (TAA) is an experimental hepatoxin1which is a thiono-sulfur containing compound with liver damaging and carcinogenic activity.Shortly after administration,TAA undergoes metabolism to acetamide and thioacetamide-Soxide by the mixed function oxidase system[2].TAA is the most potent nephrotoxic substance because of its repid elimination and cumulative injury when it is given intermittently,presumably by free radicalmediated lipid[3,4].Metabolic studies of TAA-induced tissue damage suggest that TAA is metabolized by the mixed function oxidase system to its toxic metabolites sulfine(sulfoxide) and sulfene(sulfone) which distributed among serveral organs including plasma,liver,kidney,bone marrow, adernals and other tissues[5]. Each rat of the group received 300 mg/kg of omega 3 fish oil supplements orally per day for 3 months and 150 mg/kg of TAA intrapertionealy in a single dose for 3months.Experimental group 4. Each rat of the group received 100 mg/kg of aqueous extract of glycyrrhiza glabra root orally per day for 3 months and 150 mg/kg of TAA intrapertionealy in a single dose for 3months.Experimental group 5. Each rat of the group received 300 mg/kg of aqueous extract of glycyrrhiza glabra root orally per day for 3 months and 150 mg/kg of TAA intrapertionealy in a single dose for 3months . By the end of experimental periods,rats were scarified under diethyl ether anesthesia at fasting state.The portion of blood samples were collected and allowed to coagulate at room temperature;other portion of blood added to it,EDTA(ethylene diamine tetracetic acid) and centrifuged at 5000r.p.m for 15 minutes.The clear,none-haemolysed supernatant sera and plasma were quickly removed divided into four portions for each individual,and stored at -20c for subsequent analysis[19,20]

MATERIALS AND METHODS

RESULTS AND DISCUSSION

CONCLUSION

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