Chlorogenic and caftaric acids in liver toxicity and oxidative stress induced by methamphetamine.

Khaled M M Koriem,Rowan E Soliman

doi:10.1155/2014/583494

Khaled M M Koriem, Rowan E Soliman

Open Access

https://doi.org/10.1155/2014/583494

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Abstract

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.

Highlights

Methamphetamine (METH) is a potent addictive psychostimulant, commonly referred to as “speed,” “crystal,” “crank,” “go,” and “ice.” It is reportedly being abused by approximately 35 million people worldwide [1]
The pretreatment with chlorogenic or caftaric acid prior to METH injections inhibits (P > 0.05) the increase in AST, ALT, alkaline phosphatase (ALP), and bilirubin as compared to the METH-injected rats where chlorogenic acid was more potent than caftaric acid
It is obvious that METH caused a significant decrease (P < 0.05) in serum total protein, albumin, globulin levels, and albumin/globulin ratio as compared with control rats

Summary

Introduction

Methamphetamine (METH) is a potent addictive psychostimulant, commonly referred to as “speed,” “crystal,” “crank,” “go,” and “ice.” It is reportedly being abused by approximately 35 million people worldwide [1]. It has been reported that approximately 5.8% of Americans, aged 12 years or older, have used METH at least once in their lifetime [2]. A dramatic increase in METH-related emergency department visits is alarming, with >50% involving young adults aged 18–34 years [3]. Individuals with METH-related disorders have a higher risk of schizophrenia than those with other drug use disorders and these effects explained by shared etiological mechanisms are involved in the development of schizophrenia [19]. Tokunaga et al [21] studied changes in renal function and found that repeated METH administration induced oxidative DNA injury to the kidney, as a chronic or subacute influence

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