Effects of excessive dietary methionine on oxidative stress and dyslipidemia in chronic ethanol-treated rats.
- Author:
Seon Young KIM
1
;
Hyewon KIM
;
Hyesun MIN
Author Information
- Publication Type:Original Article
- Keywords: Ethanol; DL-Methionine supplementation; oxidative stress; plasma lipids; aminothiols
- MeSH: Alanine Transaminase; Animals; Aspartate Aminotransferases; Cholesterol; Cysteine; Diet; Dyslipidemias*; Ethanol; Folic Acid; Glutathione; Homocysteine; Humans; Hyperhomocysteinemia; Male; Malondialdehyde; Methionine*; Oxidative Stress*; Plasma; Rats*; Rats, Wistar; S-Adenosylhomocysteine; S-Adenosylmethionine; Triglycerides
- From:Nutrition Research and Practice 2015;9(2):144-149
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/OBJECTIVE: The aim of this study was to examine the effect of high dietary methionine (Met) consumption on plasma and hepatic oxidative stress and dyslipidemia in chronic ethanol fed rats. MATERIALS/METHODS: Male Wistar rats were fed control or ethanol-containing liquid diets supplemented without (E group) or with DL-Met at 0.6% (EM1 group) or 0.8% (EM2 group) for five weeks. Plasma aminothiols, lipids, malondialdehyde (MDA), alanine aminotransferase (ALT), and aspartate aminotransferase were measured. Hepatic folate, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) were measured. RESULTS: DL-Met supplementation was found to increase plasma levels of homocysteine (Hcy), triglyceride (TG), total cholesterol (TC), and MDA compared to rats fed ethanol alone and decrease plasma ALT. However, DL-Met supplementation did not significantly change plasma levels of HDL-cholesterol, cysteine, cysteinylglycine, and glutathione. In addition, DL-Met supplementation increased hepatic levels of folate, SAM, SAH, and SAM:SAH ratio. Our data showed that DL-Met supplementation can increase plasma oxidative stress and atherogenic effects by elevating plasma Hcy, TG, and TC in ethanol-fed rats. CONCLUSION: The present results demonstrate that Met supplementation increases plasma oxidative stress and atherogenic effects by inducing dyslipidemia and hyperhomocysteinemia in ethanol-fed rats.
